From Wikipedia, the free encyclopedia
(Redirected from Sexual impotence)
Erectile dysfunction (ED or (male) impotence) is a sexual dysfunction characterized by the inability to develop or maintain an erection of the penis sufficient for satisfactory sexual performance.
An erection occurs due to hydraulic effects due to blood entering and being retained in sponge-like bodies inside the penis. During intercourse, the process is initiated when sexual arousal is transmitted from the brain to nerves in the pelvis. There are various and often multiple underlying causes, some of which are treatable medical conditions. The most important organic causes are cardiovascular disease and diabetes, neurological problems (for example, trauma from prostatectomy surgery), hormonal insufficiencies (hypogonadism) and drug side effects. It is important to realise that erectile dysfunction can signal underlying risk for cardiovascular disease.
There is often a contributing and complicating and sometimes a primary psychological or relational problem. Psychological impotence is where erection or penetration fails due to thoughts or feelings (psychological reasons) rather than physical impossibility; this can often be helped. Notably in psychological impotence, there is a strong response to placebo treatment. Erectile dysfunction, tied closely as it is to cultural notions of potency, success and masculinity, can have severe psychological consequences. There is a strong culture of silence and inability to discuss the matter. In reality, it has been estimated that around 1 in 10 men will experience recurring impotence problems at some point in their lives.
Besides treating the underlying causes and psychological consequences, the first line treatment of erectile dysfunction consists of a trial of PDE5 inhibitor drugs (the first of which was sildenafil or Viagra). In some cases, treatment can involve prostaglandin tablets in the urethra, intracavernous injections with a fine needle into the penis that cause swelling, a penile prosthesis, a penis pump or vascular reconstructive surgery.
The Latin term impotentia coeundi describes simple inability to insert the penis into the vagina. It is now mostly replaced by more precise terms. The study of erectile dysfunction within medicine is covered by andrology, a sub-field within urology.
venerdì 6 marzo 2009
sabato 24 gennaio 2009
Blood Pressure (last part) : Pathophysiology
from Wikipedia.org
Arterial hypertension in itself it is not generally an acute problem; see hypertensive emergency. But because of its long-term indirect effects (and also as an indicator of other problems) it is a serious worry to physicians diagnosing it.
Main complications of persistent high blood pressure.
All levels of arterial pressure put mechanical stress on the arterial walls. Higher pressures increase heart workload and progression of unhealthy tissue growth (atheroma) that develops within the walls of arteries. The higher the pressure, the more stress that is present and the more atheroma tend to progress and the heart muscle tends to thicken, enlarge and become weaker over time.
Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysms, and is the leading cause of chronic renal failure. Even moderate elevation of arterial pressure leads to shortened life expectancy. At severely high pressures, mean arterial pressures 50% or more above average, a person can expect to live no more than a few years unless appropriately treated.
In the past, most attention was paid to diastolic pressure; but nowadays it is recognised that both high systolic pressure and high pulse pressure (the numerical difference between systolic and diastolic pressures) are also risk factors. In some cases, it appears that a decrease in excessive diastolic pressure can actually increase risk, due probably to the increased difference between systolic and diastolic pressures (see the article on pulse pressure).
Low arterial pressure
Blood pressure that is too low is known as hypotension. The similarity in pronunciation with hypertension can cause confusion. Hypotension is a medical concern only if it causes signs or symptoms, such as dizziness, fainting, or in extreme cases, shock.
When arterial pressure and blood flow decrease beyond a certain point, the perfusion of the brain becomes critically decreased (i.e., the blood supply is not sufficient), causing lightheadedness, dizziness, weakness or fainting.
However, people who function well, while maintaining low arterial pressures have lower rates of cardiovascular disease events than people with normal arterial pressures.
Sometimes the arterial pressure drops significantly when a patient stands up from sitting. This is known as orthostatic hypotension (postural hypotension); gravity reduces the rate of blood return from the body veins below the heart back to the heart, thus reducing stroke volume and cardiac output.
When people are healthy, the veins below their heart quickly constrict and the heart rate increases to minimize and compensate for the gravity effect. This is carried out involuntarily by the autonomic nervous system. The system usually requires a few seconds to fully adjust and if the compensations are too slow or inadequate, the individual will suffer reduced blood flow to the brain, dizziness and potential blackout. Increases in G-loading, such as routinely experienced by acrobatic jet pilots 'pulling Gs', greatly increases this effect. Repositioning the body perpendicular to gravity largely eliminates the problem.
Other causes of low arterial pressure include:
* Sepsis
* Hemorrhage - blood loss
* Toxins including toxic doses of blood pressure medicine
* Hormonal abnormalities, such as Addison's disease
Shock is a complex condition which leads to critically decreased perfusion. The usual mechanisms are loss of blood volume, pooling of blood within the veins reducing adequate return to the heart and/or low effective heart pumping. Low arterial pressure, especially low pulse pressure, is a sign of shock and contributes to and reflects decreased perfusion.
If there is a significant difference in the pressure from one arm to the other, that may indicate a narrowing (for example, due to aortic coarctation, aortic dissection, thrombosis or embolism) of an artery.
Venous pressure
Venous pressure is the vascular pressure in a vein or in the atria of the heart. It is much less than arterial pressure, with common values of 5 mmHg in the right atrium and 8 mmHg in the left atrium. Measurement of pressures in the venous system and the pulmonary vessels plays an important role in intensive care medicine but requires an invasive central venous catheter.
mercoledì 17 dicembre 2008
Blood Pressure (third part): Physiology
The physics of the circulatory system is very complex. That said, there are many physical factors that influence arterial pressure. Each of these may in turn be influenced by physiological factors, such as diet, exercise, disease, drugs or alcohol, obesity, excess weight and so-forth.
Some physical factors are:
* Rate of pumping. In the circulatory system, this rate is called heart rate, the rate at which blood (the fluid) is pumped by the heart. The volume of blood flow from the heart is called the cardiac output which is the heart rate (the rate of contraction) multiplied by the stroke volume (the amount of blood pumped out from the heart with each contraction). The higher the heart rate, the higher the arterial pressure, assuming no reduction in stroke volume.
* Volume of fluid or blood volume, the amount of blood that is present in the body. The more blood present in the body, the higher the rate of blood return to the heart and the resulting cardiac output. There is some relationship between dietary salt intake and increased blood volume, potentially resulting in higher arterial pressure, though this varies with the individual and is highly dependent on autonomic nervous system response.
* Resistance. In the circulatory system, this is the resistance of the blood vessels. The higher the resistance, the higher the arterial pressure upstream from the resistance to blood flow. Resistance is related to vessel radius (the larger the radius, the lower the resistance), vessel length (the longer the vessel, the higher the resistance), as well as the smoothness of the blood vessel walls. Smoothness is reduced by the buildup of fatty deposits on the arterial walls. Substances called vasoconstrictors can reduce the size of blood vessels, thereby increasing blood pressure. Vasodilators (such as nitroglycerin) increase the size of blood vessels, thereby decreasing arterial pressure. Resistance, and its relation to volumetric flow rate (Q) and pressure difference between the two ends of a vessel are described by Poiseuille's Law.
* Viscosity, or thickness of the fluid. If the blood gets thicker, the result is an increase in arterial pressure. Certain medical conditions can change the viscosity of the blood. For instance, low red blood cell concentration, anemia, reduces viscosity, whereas increased red blood cell concentration increases viscosity. Viscosity also increases with blood sugar concentration—visualize pumping syrup. It had been thought that aspirin and related "blood thinner" drugs decreased the viscosity of blood, but studies found[22] that they act by reducing the tendency of the blood to clot instead.
In practice, each individual's autonomic nervous system responds to and regulates all these interacting factors so that, although the above issues are important, the actual arterial pressure response of a given individual varies widely because of both split-second and slow-moving responses of the nervous system and end organs. These responses are very effective in changing the variables and resulting blood pressure from moment to moment.
[edit] Mean arterial pressure
The mean arterial pressure (MAP) is the average over a cardiac cycle and is determined by the cardiac output (CO), systemic vascular resistance (SVR), and central venous pressure (CVP),[23]
\! MAP = (CO \cdot SVR) + CVP
MAP can be approximately determined from measurements of the systolic pressure \! P_{sys} and the diastolic pressure \! P_{dias} while there is a normal resting heart rate,[23]
\! MAP \approxeq P_{dias} + \frac{1}{3} (P_{sys} - P_{dias})
[edit] Pulse pressure
The up and down fluctuation of the arterial pressure results from the pulsatile nature of the cardiac output, i.e. the heartbeat. The pulse pressure is determined by the interaction of the stroke volume of the heart, compliance (ability to expand) of the aorta, and the resistance to flow in the arterial tree. By expanding under pressure, the aorta absorbs some of the force of the blood surge from the heart during a heartbeat. In this way the pulse pressure is reduced from what it would be if the aorta wasn't compliant.[24]
The pulse pressure can be simply calculated from the difference of the measured systolic and diastolic pressures,[24]
\! P_{pulse} = P_{sys} - P_{dias}
[edit] Vascular resistance
The larger arteries, including all large enough to see without magnification, are low resistance conduits (assuming no advanced atherosclerotic changes) with high flow rates that generate only small drops in pressure. For instance, with a subject in the supine position, blood travelling from the heart to the toes typically only experiences a 5 mmHg drop in mean pressure.
[edit] Vascular pressure wave
Modern physiology developed the concept of the vascular pressure wave (VPW). This wave is created by the heart during the systole and originates in the ascending aorta. Much faster than the stream of blood itself, it is then transported through the vessel walls to the peripheral arteries. There the pressure wave can be palpated as the peripheral pulse. As the wave is reflected at the peripheral veins it runs back in a centripetal fashion. Where the crests of the reflected and the original wave meet, the pressure inside the vessel is higher than the true pressure in the aorta. This concept explains why the arterial pressure inside the peripheral arteries of the legs and arms is higher than the arterial pressure in the aorta,[25][26][27] and in turn for the higher pressures seen at the ankle compared to the arm with normal ankle brachial pressure index values.
[edit] Regulation
The endogenous regulation of arterial pressure is not completely understood. Currently, three mechanisms of regulating arterial pressure have been well-characterized:
* Baroreceptor reflex: Baroreceptors detect changes in arterial pressure and send signals ultimately to the medulla of the brain stem. The medulla, by way of the autonomic nervous system, adjusts the mean arterial pressure by altering both the force and speed of the heart's contractions, as well as the total peripheral resistance. The most important arterial baroreceptors are located in the left and right carotid sinuses and in the aortic arch.[28]
* Renin-angiotensin system (RAS): This system is generally known for its long-term adjustment of arterial pressure. This system allows the kidney to compensate for loss in blood volume or drops in arterial pressure by activating an endogenous vasoconstrictor known as angiotensin II.
* Aldosterone release: This steroid hormone is released from the adrenal cortex in response to angiotensin II or high serum potassium levels. Aldosterone stimulates sodium retention and potassium excretion by the kidneys. Since sodium is the main ion that determines the amount of fluid in the blood vessels by osmosis, aldosterone will increase fluid retention, and indirectly, arterial pressure.
These different mechanisms are not necessarily independent of each other, as indicated by the link between the RAS and aldosterone release. Currently, the RAS system is targeted pharmacologically by ACE inhibitors and angiotensin II receptor antagonists. The aldosterone system is directly targeted by spironolactone, an aldosterone antagonist. The fluid retention may be targeted by diuretics; the antihypertensive effect of diuretics is due to its effect on blood volume. Generally, the baroreceptor reflex is not targeted in hypertension because if blocked, individuals may suffer from orthostatic hypotension and fainting.
Some physical factors are:
* Rate of pumping. In the circulatory system, this rate is called heart rate, the rate at which blood (the fluid) is pumped by the heart. The volume of blood flow from the heart is called the cardiac output which is the heart rate (the rate of contraction) multiplied by the stroke volume (the amount of blood pumped out from the heart with each contraction). The higher the heart rate, the higher the arterial pressure, assuming no reduction in stroke volume.
* Volume of fluid or blood volume, the amount of blood that is present in the body. The more blood present in the body, the higher the rate of blood return to the heart and the resulting cardiac output. There is some relationship between dietary salt intake and increased blood volume, potentially resulting in higher arterial pressure, though this varies with the individual and is highly dependent on autonomic nervous system response.
* Resistance. In the circulatory system, this is the resistance of the blood vessels. The higher the resistance, the higher the arterial pressure upstream from the resistance to blood flow. Resistance is related to vessel radius (the larger the radius, the lower the resistance), vessel length (the longer the vessel, the higher the resistance), as well as the smoothness of the blood vessel walls. Smoothness is reduced by the buildup of fatty deposits on the arterial walls. Substances called vasoconstrictors can reduce the size of blood vessels, thereby increasing blood pressure. Vasodilators (such as nitroglycerin) increase the size of blood vessels, thereby decreasing arterial pressure. Resistance, and its relation to volumetric flow rate (Q) and pressure difference between the two ends of a vessel are described by Poiseuille's Law.
* Viscosity, or thickness of the fluid. If the blood gets thicker, the result is an increase in arterial pressure. Certain medical conditions can change the viscosity of the blood. For instance, low red blood cell concentration, anemia, reduces viscosity, whereas increased red blood cell concentration increases viscosity. Viscosity also increases with blood sugar concentration—visualize pumping syrup. It had been thought that aspirin and related "blood thinner" drugs decreased the viscosity of blood, but studies found[22] that they act by reducing the tendency of the blood to clot instead.
In practice, each individual's autonomic nervous system responds to and regulates all these interacting factors so that, although the above issues are important, the actual arterial pressure response of a given individual varies widely because of both split-second and slow-moving responses of the nervous system and end organs. These responses are very effective in changing the variables and resulting blood pressure from moment to moment.
[edit] Mean arterial pressure
The mean arterial pressure (MAP) is the average over a cardiac cycle and is determined by the cardiac output (CO), systemic vascular resistance (SVR), and central venous pressure (CVP),[23]
\! MAP = (CO \cdot SVR) + CVP
MAP can be approximately determined from measurements of the systolic pressure \! P_{sys} and the diastolic pressure \! P_{dias} while there is a normal resting heart rate,[23]
\! MAP \approxeq P_{dias} + \frac{1}{3} (P_{sys} - P_{dias})
[edit] Pulse pressure
The up and down fluctuation of the arterial pressure results from the pulsatile nature of the cardiac output, i.e. the heartbeat. The pulse pressure is determined by the interaction of the stroke volume of the heart, compliance (ability to expand) of the aorta, and the resistance to flow in the arterial tree. By expanding under pressure, the aorta absorbs some of the force of the blood surge from the heart during a heartbeat. In this way the pulse pressure is reduced from what it would be if the aorta wasn't compliant.[24]
The pulse pressure can be simply calculated from the difference of the measured systolic and diastolic pressures,[24]
\! P_{pulse} = P_{sys} - P_{dias}
[edit] Vascular resistance
The larger arteries, including all large enough to see without magnification, are low resistance conduits (assuming no advanced atherosclerotic changes) with high flow rates that generate only small drops in pressure. For instance, with a subject in the supine position, blood travelling from the heart to the toes typically only experiences a 5 mmHg drop in mean pressure.
[edit] Vascular pressure wave
Modern physiology developed the concept of the vascular pressure wave (VPW). This wave is created by the heart during the systole and originates in the ascending aorta. Much faster than the stream of blood itself, it is then transported through the vessel walls to the peripheral arteries. There the pressure wave can be palpated as the peripheral pulse. As the wave is reflected at the peripheral veins it runs back in a centripetal fashion. Where the crests of the reflected and the original wave meet, the pressure inside the vessel is higher than the true pressure in the aorta. This concept explains why the arterial pressure inside the peripheral arteries of the legs and arms is higher than the arterial pressure in the aorta,[25][26][27] and in turn for the higher pressures seen at the ankle compared to the arm with normal ankle brachial pressure index values.
[edit] Regulation
The endogenous regulation of arterial pressure is not completely understood. Currently, three mechanisms of regulating arterial pressure have been well-characterized:
* Baroreceptor reflex: Baroreceptors detect changes in arterial pressure and send signals ultimately to the medulla of the brain stem. The medulla, by way of the autonomic nervous system, adjusts the mean arterial pressure by altering both the force and speed of the heart's contractions, as well as the total peripheral resistance. The most important arterial baroreceptors are located in the left and right carotid sinuses and in the aortic arch.[28]
* Renin-angiotensin system (RAS): This system is generally known for its long-term adjustment of arterial pressure. This system allows the kidney to compensate for loss in blood volume or drops in arterial pressure by activating an endogenous vasoconstrictor known as angiotensin II.
* Aldosterone release: This steroid hormone is released from the adrenal cortex in response to angiotensin II or high serum potassium levels. Aldosterone stimulates sodium retention and potassium excretion by the kidneys. Since sodium is the main ion that determines the amount of fluid in the blood vessels by osmosis, aldosterone will increase fluid retention, and indirectly, arterial pressure.
These different mechanisms are not necessarily independent of each other, as indicated by the link between the RAS and aldosterone release. Currently, the RAS system is targeted pharmacologically by ACE inhibitors and angiotensin II receptor antagonists. The aldosterone system is directly targeted by spironolactone, an aldosterone antagonist. The fluid retention may be targeted by diuretics; the antihypertensive effect of diuretics is due to its effect on blood volume. Generally, the baroreceptor reflex is not targeted in hypertension because if blocked, individuals may suffer from orthostatic hypotension and fainting.
giovedì 27 novembre 2008
Blood Pressure (second part): Classification
Normal values
While average values for arterial pressure could be computed for any given population, there is often a large variation from person to person; arterial pressure also varies in individuals from moment to moment. Additionally, the average of any given population may have a questionable correlation with its general health, thus the relevance of such average values is equally questionable. However, in a study of 100 subjects with no known history of hypertension, an average blood pressure of 112/64 mmHg was found,[15] which is in the normal range.
In children the normal ranges are lower than for adults.[16] In the elderly, blood pressure tends to be higher than normal adult values, largely because of reduced flexibility of the arteries. Factors such as age, gender and race[citation needed] influence blood pressure values. Pressure also varies with exercise, emotional reactions, sleep, digestion and time of day.
Differences between left and right arm blood pressure measurements tend to be random and average to nearly zero if enough measurements are taken. However, in a small percentage of cases there is a consistently present difference greater than 10 mmHg which may need further investigation, e.g. for obstructive arterial disease.[17] [18]
The risk of cardiovascular disease increases progressively throughout the range of higher arterial pressure that begins at 115/75 mmHg.[19] In the past, hypertension was only diagnosed if secondary signs of high arterial pressure were present, along with a prolonged high systolic pressure reading over several visits. In the US, this reactive stance has been soundly rejected in light of recent evidence. However in the UK, patients’ readings are still considered normal up to 140/90 mmHg.[20]
Clinical trials demonstrate that people who maintain arterial pressures at the low end of these pressure ranges have much better long term cardiovascular health. The principal medical debate concerns the aggressiveness and relative value of methods used to lower pressures into this range for those who do not maintain such pressure on their own. Elevations, more commonly seen in older people, though often considered normal, are associated with increased morbidity and mortality. The clear trend from double blind clinical trials (for the better strategies and agents) demonstrates that lower arterial pressure correlates with lower rates of disease.[citation needed]
from wikipedia.org
While average values for arterial pressure could be computed for any given population, there is often a large variation from person to person; arterial pressure also varies in individuals from moment to moment. Additionally, the average of any given population may have a questionable correlation with its general health, thus the relevance of such average values is equally questionable. However, in a study of 100 subjects with no known history of hypertension, an average blood pressure of 112/64 mmHg was found,[15] which is in the normal range.
In children the normal ranges are lower than for adults.[16] In the elderly, blood pressure tends to be higher than normal adult values, largely because of reduced flexibility of the arteries. Factors such as age, gender and race[citation needed] influence blood pressure values. Pressure also varies with exercise, emotional reactions, sleep, digestion and time of day.
Differences between left and right arm blood pressure measurements tend to be random and average to nearly zero if enough measurements are taken. However, in a small percentage of cases there is a consistently present difference greater than 10 mmHg which may need further investigation, e.g. for obstructive arterial disease.[17] [18]
The risk of cardiovascular disease increases progressively throughout the range of higher arterial pressure that begins at 115/75 mmHg.[19] In the past, hypertension was only diagnosed if secondary signs of high arterial pressure were present, along with a prolonged high systolic pressure reading over several visits. In the US, this reactive stance has been soundly rejected in light of recent evidence. However in the UK, patients’ readings are still considered normal up to 140/90 mmHg.[20]
Clinical trials demonstrate that people who maintain arterial pressures at the low end of these pressure ranges have much better long term cardiovascular health. The principal medical debate concerns the aggressiveness and relative value of methods used to lower pressures into this range for those who do not maintain such pressure on their own. Elevations, more commonly seen in older people, though often considered normal, are associated with increased morbidity and mortality. The clear trend from double blind clinical trials (for the better strategies and agents) demonstrates that lower arterial pressure correlates with lower rates of disease.[citation needed]
from wikipedia.org
giovedì 6 novembre 2008
Blood Pressure (first part): measurament
Blood pressure
From Wikipedia, the free encyclopedia
Blood pressure refers to the force exerted by circulating blood on the walls of blood vessels, and constitutes one of the principal vital signs. The pressure of the circulating blood decreases as blood moves through arteries, arterioles, capillaries, and veins; the term blood pressure generally refers to arterial pressure, i.e., the pressure in the larger arteries, the blood vessels that take blood away from the heart. Arterial pressure is most commonly measured via a sphygmomanometer, which historically used the height of a column of mercury to reflect the circulating pressure (see Non-invasive measurement). Today blood pressure values are still reported in millimetres of mercury (mmHg), though aneroid and electronic devices do not use mercury.
For each heartbeat, blood pressure varies between systolic and diastolic pressures. Systolic pressure is peak pressure in the arteries, which occurs near the beginning of the cardiac cycle when the ventricles are contracting. Diastolic pressure is minimum pressure in the arteries, which occurs near the end of the cardiac cycle when the ventricles are filled with blood. An example of normal measured values for a resting, healthy adult human is 115 mmHg systolic and 75 mmHg diastolic (written as 115/75 mmHg, and spoken as "one fifteen over seventy-five"). Pulse pressure is the difference between systolic and diastolic pressures.
Systolic and diastolic arterial blood pressures are not static but undergo natural variations from one heartbeat to another and throughout the day (in a circadian rhythm). They also change in response to stress, nutritional factors, drugs, disease, exercise, and momentarily from standing up. Sometimes the variations are large. Hypertension refers to arterial pressure being abnormally high, as opposed to hypotension, when it is abnormally low. Along with body temperature, blood pressure measurements are the most commonly measured physiological parameters.
Measurement
Arterial pressures can be measured invasively (by penetrating the skin and measuring inside the blood vessels) or non-invasively. The former is usually restricted to a hospital setting.
Units
The predominantly used unit for blood pressure measurement is mmHg (millimeter of mercury). Sometimes the unit kPa (kilopascal) is used, where 1 kPa = 7.50 mmHg.
Noninvasive measurement
The noninvasive auscultatory (from the Latin for listening) and oscillometric measurements are simpler and quicker than invasive measurements, require less expertise in fitting, have virtually no complications, and are less unpleasant and painful for the patient. However, non-invasive measures may yield somewhat lower accuracy and small systematic differences in numerical results. Non-invasive measurement methods are more commonly used for routine examinations and monitoring.
Palpation methods
A minimum systolic value can be roughly estimated without any equipment by palpation, most often used in emergency situations. Palpation of a radial pulse indicates a minimum blood pressure of 80 mmHg, a femoral pulse indicates at least 70 mmHg, and a carotid pulse indicates a minimum of 60 mmHg. However, one study indicated that this method was not accurate enough and often overestimated patients' systolic blood pressure.[1] A more accurate value of systolic blood pressure can be obtained with a sphygmomanometer and palpating for when a radial pulse returns.[2] Because a diastolic pressure cannot be obtained by this method, blood pressures obtained by palpation are noted as "/P".[3]
Auscultatory methods
Auscultatory method aneroid sphygmomanometer with stethoscope
Mercury manometer
The auscultatory method uses a stethoscope and a sphygmomanometer. This comprises an inflatable (Riva-Rocci) cuff placed around the upper arm at roughly the same vertical height as the heart, attached to a mercury or aneroid manometer. The mercury manometer, considered to be the gold standard for arterial pressure measurement, measures the height of a column of mercury, giving an absolute result without need for calibration, and consequently not subject to the errors and drift of calibration which affect other methods. The use of mercury manometers is often required in clinical trials and for the clinical measurement of hypertension in high risk patients, such as pregnant women.
A cuff of appropriate size is fitted and inflated manually by repeatedly squeezing a rubber bulb until the artery is completely occluded. Listening with the stethoscope to the brachial artery at the elbow, the examiner slowly releases the pressure in the cuff. When blood just starts to flow in the artery, the turbulent flow creates a "whooshing" or pounding (first Korotkoff sound). The pressure at which this sound is first heard is the systolic blood pressure. The cuff pressure is further released until no sound can be heard (fifth Korotkoff sound), at the diastolic arterial pressure. Sometimes, the pressure is palpated (felt by hand) to get an estimate before auscultation.
Oscillometric methods
Oscillometric methods are sometimes used in the long-term measurement and sometimes in general practice. The equipment is functionally similar to that of the auscultatory method, but with an electronic pressure sensor (transducer) fitted in to detect blood flow, instead of using the stethoscope and the expert's ear. In practice, the pressure sensor is a calibrated electronic device with a numerical readout of blood pressure. To maintain accuracy, calibration must be checked periodically, unlike the inherently accurate mercury manometer. In most cases the cuff is inflated and released by an electrically operated pump and valve, which may be fitted on the wrist (elevated to heart height), although the upper arm is preferred. They vary widely in accuracy, and should be checked at specified intervals and if necessary recalibrated.
Oscillometric measurement requires less skill than the auscultatory technique, and may be suitable for use by untrained staff and for automated patient home monitoring.
The cuff is inflated to a pressure initially in excess of the systolic arterial pressure, and then reduces to below diastolic pressure over a period of about 30 seconds. When blood flow is nil (cuff pressure exceeding systolic pressure) or unimpeded (cuff pressure below diastolic pressure), cuff pressure will be essentially constant. It is essential that the cuff size is correct: undersized cuffs may yield too high a pressure, whereas oversized cuffs yield too low a pressure. When blood flow is present, but restricted, the cuff pressure, which is monitored by the pressure sensor, will vary periodically in synchrony with the cyclic expansion and contraction of the brachial artery, i.e., it will oscillate. The values of systolic and diastolic pressure are computed, not actually measured from the raw data, using an algorithm; the computed results are displayed.
Oscillometric monitors may produce inaccurate readings in patients with heart and circulation problems, that include arterial sclerosis, arrhythmia, preeclampsia, pulsus alternans, and pulsus paradoxus.
In practice the different methods do not give identical results; an algorithm and experimentally obtained coefficients are used to adjust the oscillometric results to give readings which match the auscultatory results as well as possible.[4] Some equipment uses computer-aided analysis of the instantaneous arterial pressure waveform to determine the systolic, mean, and diastolic points. Since many oscillometric devices have not been validated, caution must be given as most are not suitable in clinical and acute care settings.
The term NIBP, for Non-Invasive Blood Pressure, is often used to describe oscillometric monitoring equipment.
Invasive measurement
Arterial blood pressure (BP) is most accurately measured invasively through an arterial line. Invasive arterial pressure measurement with intravascular cannulae involves direct measurement of arterial pressure by placing a cannula needle in an artery (usually radial, femoral, dorsalis pedis or brachial). This is usually done by an anesthesiologist or surgeon in a hospital.
The cannula must be connected to a sterile, fluid-filled system, which is connected to an electronic pressure transducer. The advantage of this system is that pressure is constantly monitored beat-by-beat, and a waveform (a graph of pressure against time) can be displayed. This invasive technique is regularly employed in human and veterinary intensive care medicine, anesthesiology, and for research purposes.
Cannulation for invasive vascular pressure monitoring is infrequently associated with complications such as thrombosis, infection, and bleeding. Patients with invasive arterial monitoring require very close supervision, as there is a danger of severe bleeding if the line becomes disconnected. It is generally reserved for patients where rapid variations in arterial pressure are anticipated.
Invasive vascular pressure monitors are pressure monitoring systems designed to acquire pressure information for display and processing. There are a variety of invasive vascular pressure monitors for trauma, critical care, and operating room applications. These include single pressure, dual pressure, and multi-parameter (i.e. pressure / temperature). The monitors can be used for measurement and follow-up of arterial, central venous, pulmonary arterial, left atrial, right atrial, femoral arterial, umbilical venous, umbilical arterial, and intracranial pressures.
Vascular pressure parameters are derived in the monitor's microcomputer system. Usually, systolic, diastolic, and mean pressures are displayed simultaneously for pulsatile waveforms (i.e. arterial and pulmonary arterial). Some monitors also calculate and display CPP (cerebral perfusion pressure). Normally, a zero key on the front of the monitor makes pressure zeroing extremely fast and easy. Alarm limits may be set to assist the medical professional responsible for observing the patient. High and low alarms may be set on displayed temperature parameters.
Home monitoring
For some patients, blood pressure measurements taken in a doctor's office may not correctly characterize their typical blood pressure. In up to 25% of patients, the office visit blood pressure reading is higher than their typical blood pressure. This type of error is called white coat hypertension and can result from anxiety related to an examination by a health care professional.[5] The misdiagnosis of hypertension for these patients can result in needless and possibly harmful medication. On the other hand, in some cases a lower than typical blood pressure reading occurs at the doctor's office and these patients may fail to get needed treatment for hypertension.[6] Ambulatory blood pressure devices that take readings every half hour throughout the day and night have been used for identifying and mitigating these problems. Except for periods during sleep, home monitoring could be used for these purposes instead of ambulatory blood pressure monitoring.[7] Home monitoring may also be used to improve hypertension management and to monitor the effects of lifestyle changes and medication related to blood pressure.[8] Compared to ambulatory blood pressure measurements, home monitoring has been found to be an effective and lower cost alternative.
Aside from the white coat effect, arterial pressure readings outside of a clinical setting are usually slightly lower in the majority of people. The studies that looked into the risks from hypertension and the benefits of lowering the arterial pressure in affected patients were based on readings in a clinical environment.
When measuring blood pressure, an accurate reading requires that one not drink coffee, smoke cigarettes, or engage in strenuous exercise for 30 minutes before taking the reading. A full bladder may have a small effect on blood pressure readings, so if the urge to urinate exists, one should do so before the reading. For 5 minutes before the reading, one should sit upright in a chair with his or her feet flat on the floor and without any limbs crossed. The blood pressure cuff should always be against bare skin, as readings taken over a shirt sleeve are less accurate. During the reading, the arm that is used should be relaxed and kept at heart level, for example by resting it on a table.[11]
Since arterial pressure varies throughout the day, measurements intended to monitor changes over longer time frames should be taken at the same time of day to ensure that the readings taken are comparable. Suitable times are:
* immediately after awakening (before washing/dressing and taking breakfast/drink), while the body is still resting,
* immediately after finishing work.
Automatic self-contained blood pressure monitors are available at reasonable prices, some of which are capable of Korotkoff's measurement in addition to oscillometric methods, enabling irregular heartbeat patients to accurately measure their blood pressure at home, which was not possible using the traditional devices.[citation needed]
Those using home arterial pressure monitoring devices are increasingly also making use of arterial pressure charting software.[12] These charting methods provide print outs for the patients physician and reminders on how often to check arterial pressure.
From Wikipedia, the free encyclopedia
Blood pressure refers to the force exerted by circulating blood on the walls of blood vessels, and constitutes one of the principal vital signs. The pressure of the circulating blood decreases as blood moves through arteries, arterioles, capillaries, and veins; the term blood pressure generally refers to arterial pressure, i.e., the pressure in the larger arteries, the blood vessels that take blood away from the heart. Arterial pressure is most commonly measured via a sphygmomanometer, which historically used the height of a column of mercury to reflect the circulating pressure (see Non-invasive measurement). Today blood pressure values are still reported in millimetres of mercury (mmHg), though aneroid and electronic devices do not use mercury.
For each heartbeat, blood pressure varies between systolic and diastolic pressures. Systolic pressure is peak pressure in the arteries, which occurs near the beginning of the cardiac cycle when the ventricles are contracting. Diastolic pressure is minimum pressure in the arteries, which occurs near the end of the cardiac cycle when the ventricles are filled with blood. An example of normal measured values for a resting, healthy adult human is 115 mmHg systolic and 75 mmHg diastolic (written as 115/75 mmHg, and spoken as "one fifteen over seventy-five"). Pulse pressure is the difference between systolic and diastolic pressures.
Systolic and diastolic arterial blood pressures are not static but undergo natural variations from one heartbeat to another and throughout the day (in a circadian rhythm). They also change in response to stress, nutritional factors, drugs, disease, exercise, and momentarily from standing up. Sometimes the variations are large. Hypertension refers to arterial pressure being abnormally high, as opposed to hypotension, when it is abnormally low. Along with body temperature, blood pressure measurements are the most commonly measured physiological parameters.
Measurement
Arterial pressures can be measured invasively (by penetrating the skin and measuring inside the blood vessels) or non-invasively. The former is usually restricted to a hospital setting.
Units
The predominantly used unit for blood pressure measurement is mmHg (millimeter of mercury). Sometimes the unit kPa (kilopascal) is used, where 1 kPa = 7.50 mmHg.
Noninvasive measurement
The noninvasive auscultatory (from the Latin for listening) and oscillometric measurements are simpler and quicker than invasive measurements, require less expertise in fitting, have virtually no complications, and are less unpleasant and painful for the patient. However, non-invasive measures may yield somewhat lower accuracy and small systematic differences in numerical results. Non-invasive measurement methods are more commonly used for routine examinations and monitoring.
Palpation methods
A minimum systolic value can be roughly estimated without any equipment by palpation, most often used in emergency situations. Palpation of a radial pulse indicates a minimum blood pressure of 80 mmHg, a femoral pulse indicates at least 70 mmHg, and a carotid pulse indicates a minimum of 60 mmHg. However, one study indicated that this method was not accurate enough and often overestimated patients' systolic blood pressure.[1] A more accurate value of systolic blood pressure can be obtained with a sphygmomanometer and palpating for when a radial pulse returns.[2] Because a diastolic pressure cannot be obtained by this method, blood pressures obtained by palpation are noted as "
Auscultatory methods
Auscultatory method aneroid sphygmomanometer with stethoscope
Mercury manometer
The auscultatory method uses a stethoscope and a sphygmomanometer. This comprises an inflatable (Riva-Rocci) cuff placed around the upper arm at roughly the same vertical height as the heart, attached to a mercury or aneroid manometer. The mercury manometer, considered to be the gold standard for arterial pressure measurement, measures the height of a column of mercury, giving an absolute result without need for calibration, and consequently not subject to the errors and drift of calibration which affect other methods. The use of mercury manometers is often required in clinical trials and for the clinical measurement of hypertension in high risk patients, such as pregnant women.
A cuff of appropriate size is fitted and inflated manually by repeatedly squeezing a rubber bulb until the artery is completely occluded. Listening with the stethoscope to the brachial artery at the elbow, the examiner slowly releases the pressure in the cuff. When blood just starts to flow in the artery, the turbulent flow creates a "whooshing" or pounding (first Korotkoff sound). The pressure at which this sound is first heard is the systolic blood pressure. The cuff pressure is further released until no sound can be heard (fifth Korotkoff sound), at the diastolic arterial pressure. Sometimes, the pressure is palpated (felt by hand) to get an estimate before auscultation.
Oscillometric methods
Oscillometric methods are sometimes used in the long-term measurement and sometimes in general practice. The equipment is functionally similar to that of the auscultatory method, but with an electronic pressure sensor (transducer) fitted in to detect blood flow, instead of using the stethoscope and the expert's ear. In practice, the pressure sensor is a calibrated electronic device with a numerical readout of blood pressure. To maintain accuracy, calibration must be checked periodically, unlike the inherently accurate mercury manometer. In most cases the cuff is inflated and released by an electrically operated pump and valve, which may be fitted on the wrist (elevated to heart height), although the upper arm is preferred. They vary widely in accuracy, and should be checked at specified intervals and if necessary recalibrated.
Oscillometric measurement requires less skill than the auscultatory technique, and may be suitable for use by untrained staff and for automated patient home monitoring.
The cuff is inflated to a pressure initially in excess of the systolic arterial pressure, and then reduces to below diastolic pressure over a period of about 30 seconds. When blood flow is nil (cuff pressure exceeding systolic pressure) or unimpeded (cuff pressure below diastolic pressure), cuff pressure will be essentially constant. It is essential that the cuff size is correct: undersized cuffs may yield too high a pressure, whereas oversized cuffs yield too low a pressure. When blood flow is present, but restricted, the cuff pressure, which is monitored by the pressure sensor, will vary periodically in synchrony with the cyclic expansion and contraction of the brachial artery, i.e., it will oscillate. The values of systolic and diastolic pressure are computed, not actually measured from the raw data, using an algorithm; the computed results are displayed.
Oscillometric monitors may produce inaccurate readings in patients with heart and circulation problems, that include arterial sclerosis, arrhythmia, preeclampsia, pulsus alternans, and pulsus paradoxus.
In practice the different methods do not give identical results; an algorithm and experimentally obtained coefficients are used to adjust the oscillometric results to give readings which match the auscultatory results as well as possible.[4] Some equipment uses computer-aided analysis of the instantaneous arterial pressure waveform to determine the systolic, mean, and diastolic points. Since many oscillometric devices have not been validated, caution must be given as most are not suitable in clinical and acute care settings.
The term NIBP, for Non-Invasive Blood Pressure, is often used to describe oscillometric monitoring equipment.
Invasive measurement
Arterial blood pressure (BP) is most accurately measured invasively through an arterial line. Invasive arterial pressure measurement with intravascular cannulae involves direct measurement of arterial pressure by placing a cannula needle in an artery (usually radial, femoral, dorsalis pedis or brachial). This is usually done by an anesthesiologist or surgeon in a hospital.
The cannula must be connected to a sterile, fluid-filled system, which is connected to an electronic pressure transducer. The advantage of this system is that pressure is constantly monitored beat-by-beat, and a waveform (a graph of pressure against time) can be displayed. This invasive technique is regularly employed in human and veterinary intensive care medicine, anesthesiology, and for research purposes.
Cannulation for invasive vascular pressure monitoring is infrequently associated with complications such as thrombosis, infection, and bleeding. Patients with invasive arterial monitoring require very close supervision, as there is a danger of severe bleeding if the line becomes disconnected. It is generally reserved for patients where rapid variations in arterial pressure are anticipated.
Invasive vascular pressure monitors are pressure monitoring systems designed to acquire pressure information for display and processing. There are a variety of invasive vascular pressure monitors for trauma, critical care, and operating room applications. These include single pressure, dual pressure, and multi-parameter (i.e. pressure / temperature). The monitors can be used for measurement and follow-up of arterial, central venous, pulmonary arterial, left atrial, right atrial, femoral arterial, umbilical venous, umbilical arterial, and intracranial pressures.
Vascular pressure parameters are derived in the monitor's microcomputer system. Usually, systolic, diastolic, and mean pressures are displayed simultaneously for pulsatile waveforms (i.e. arterial and pulmonary arterial). Some monitors also calculate and display CPP (cerebral perfusion pressure). Normally, a zero key on the front of the monitor makes pressure zeroing extremely fast and easy. Alarm limits may be set to assist the medical professional responsible for observing the patient. High and low alarms may be set on displayed temperature parameters.
Home monitoring
For some patients, blood pressure measurements taken in a doctor's office may not correctly characterize their typical blood pressure. In up to 25% of patients, the office visit blood pressure reading is higher than their typical blood pressure. This type of error is called white coat hypertension and can result from anxiety related to an examination by a health care professional.[5] The misdiagnosis of hypertension for these patients can result in needless and possibly harmful medication. On the other hand, in some cases a lower than typical blood pressure reading occurs at the doctor's office and these patients may fail to get needed treatment for hypertension.[6] Ambulatory blood pressure devices that take readings every half hour throughout the day and night have been used for identifying and mitigating these problems. Except for periods during sleep, home monitoring could be used for these purposes instead of ambulatory blood pressure monitoring.[7] Home monitoring may also be used to improve hypertension management and to monitor the effects of lifestyle changes and medication related to blood pressure.[8] Compared to ambulatory blood pressure measurements, home monitoring has been found to be an effective and lower cost alternative.
Aside from the white coat effect, arterial pressure readings outside of a clinical setting are usually slightly lower in the majority of people. The studies that looked into the risks from hypertension and the benefits of lowering the arterial pressure in affected patients were based on readings in a clinical environment.
When measuring blood pressure, an accurate reading requires that one not drink coffee, smoke cigarettes, or engage in strenuous exercise for 30 minutes before taking the reading. A full bladder may have a small effect on blood pressure readings, so if the urge to urinate exists, one should do so before the reading. For 5 minutes before the reading, one should sit upright in a chair with his or her feet flat on the floor and without any limbs crossed. The blood pressure cuff should always be against bare skin, as readings taken over a shirt sleeve are less accurate. During the reading, the arm that is used should be relaxed and kept at heart level, for example by resting it on a table.[11]
Since arterial pressure varies throughout the day, measurements intended to monitor changes over longer time frames should be taken at the same time of day to ensure that the readings taken are comparable. Suitable times are:
* immediately after awakening (before washing/dressing and taking breakfast/drink), while the body is still resting,
* immediately after finishing work.
Automatic self-contained blood pressure monitors are available at reasonable prices, some of which are capable of Korotkoff's measurement in addition to oscillometric methods, enabling irregular heartbeat patients to accurately measure their blood pressure at home, which was not possible using the traditional devices.[citation needed]
Those using home arterial pressure monitoring devices are increasingly also making use of arterial pressure charting software.[12] These charting methods provide print outs for the patients physician and reminders on how often to check arterial pressure.
giovedì 16 ottobre 2008
cancer (last part): Epidemiology, History and Research
Epidemiology
Cancer epidemiology is the study of the incidence of cancer as a way to infer possible trends and causes. The first such cause of cancer was identified by British surgeon Percivall Pott, who discovered in 1775 that cancer of the scrotum was a common disease among chimney sweeps. The work of other individual physicians led to various insights, but when physicians started working together they could make firmer conclusions.
A founding paper of this discipline was the work of Janet Lane-Claypon, who published a comparative study in 1926 of 500 breast cancer cases and 500 control patients of the same background and lifestyle for the British Ministry of Health. Her ground-breaking work on cancer epidemiology was carried on by Richard Doll and Austin Bradford Hill, who published "Lung Cancer and Other Causes of Death In Relation to Smoking. A Second Report on the Mortality of British Doctors" followed in 1956 (otherwise known as the British doctors study). Richard Doll left the London Medical Research Center (MRC), to start the Oxford unit for Cancer epidemiology in 1968. With the use of computers, the unit was the first to compile large amounts of cancer data. Modern epidemiological methods are closely linked to current concepts of disease and public health policy. Over the past 50 years, great efforts have been spent on gathering data across medical practise, hospital, provincial, state, and even country boundaries, as a way to study the interdependence of environmental and cultural factors on cancer incidence.
Cancer epidemiology must contend with problems of lead time bias and length time bias. Lead time bias is the concept that early diagnosis may artificially inflate the survival statistics of a cancer, without really improving the natural history of the disease. Length bias is the concept that slower growing, more indolent tumors are more likely to be diagnosed by screening tests, but improvements in diagnosing more cases of indolent cancer may not translate into better patient outcomes after the implementation of screening programs. A similar epidemiological concern is overdiagnosis, the tendency of screening tests to diagnose diseases that may not actually impact the patient's longevity. This problem especially applies to prostate cancer and PSA screening.[87]
Some cancer researchers have argued that negative cancer clinical trials lack sufficient statistical power to discover a benefit to treatment. This may be due to fewer patients enrolled in the study than originally planned.[88]
State and regional cancer registries are organizations that abstract clinical data about cancer from patient medical records. These institutions provide information to state and national public health groups to help track trends in cancer diagnosis and treatment. One of the largest and most important cancer registries is SEER, administered by the US Federal government.[89] Health information privacy concerns have led to the restricted use of cancer registry data in the United States Department of Veterans Affairs[90][91][92] and other institutions.[93]
In some Western countries, such as the USA,[4] and the UK[94] cancer is overtaking cardiovascular disease as the leading cause of death. In many Third World countries cancer incidence (insofar as this can be measured) appears much lower, most likely because of the higher death rates due to infectious disease or injury. With the increased control over malaria and tuberculosis in some Third World countries, incidence of cancer is expected to rise; this is termed the epidemiologic transition in epidemiological terminology.
Cancer epidemiology closely mirrors risk factor spread in various countries. Hepatocellular carcinoma (liver cancer) is rare in the West but is the main cancer in China and neighbouring countries, most likely due to the endemic presence of hepatitis B and aflatoxin in that population. Similarly, with tobacco smoking becoming more common in various Third World countries, lung cancer incidence has increased in a parallel fashion.
History
Today, the Greek term carcinoma is the medical term for a malignant tumor derived from epithelial cells. It is Celsus who translated carcinos into the Latin cancer, also meaning crab. Galen used "oncos" to describe all tumours, the root for the modern word oncology.[95]
Hippocrates described several kinds of cancers. He called benign tumours oncos, Greek for swelling, and malignant tumours carcinos, Greek for crab or crayfish. This name comes from the appearance of the cut surface of a solid malignant tumour, with the veins stretched on all sides as the animal the crab has its feet, whence it derives its name[96] (see picture). He later added the suffix -oma, Greek for swelling, giving the name carcinoma. Since it was against Greek tradition to open the body, Hippocrates only described and made drawings of outwardly visible tumors on the skin, nose, and breasts. Treatment was based on the humor theory of four bodily fluids (black and yellow bile, blood, and phlegm). According to the patient's humor, treatment consisted of diet, blood-letting, and/or laxatives. Through the centuries it was discovered that cancer could occur anywhere in the body, but humor-theory based treatment remained popular until the 19th century with the discovery of cells.
Our oldest description and surgical treatment of cancer was discovered in Egypt and dates back to approximately 1600 B.C. The Papyrus describes 8 cases of ulcers of the breast that were treated by cauterization, with a tool called "the fire drill." The writing says about the disease, "There is no treatment."[97]
Another very early surgical treatment for cancer was described in the 1020s by Avicenna (Ibn Sina) in The Canon of Medicine. He stated that the excision should be radical and that all diseased tissue should be removed, which included the use of amputation or the removal of veins running in the direction of the tumor. He also recommended the use of cauterization for the area being treated if necessary.[98]
In the 16th and 17th centuries, it became more acceptable for doctors to dissect bodies to discover the cause of death. The German professor Wilhelm Fabry believed that breast cancer was caused by a milk clot in a mammary duct. The Dutch professor Francois de la Boe Sylvius, a follower of Descartes, believed that all disease was the outcome of chemical processes, and that acidic lymph fluid was the cause of cancer. His contemporary Nicolaes Tulp believed that cancer was a poison that slowly spreads, and concluded that it was contagious.[99]
With the widespread use of the microscope in the 18th century, it was discovered that the 'cancer poison' spread from the primary tumor through the lymph nodes to other sites ("metastasis"). This view of the disease was first formulated by the English surgeon Campbell De Morgan between 1871 and 1874.[100] The use of surgery to treat cancer had poor results due to problems with hygiene. The renowned Scottish surgeon Alexander Monro saw only 2 breast tumor patients out of 60 surviving surgery for two years. In the 19th century, asepsis improved surgical hygiene and as the survival statistics went up, surgical removal of the tumor became the primary treatment for cancer. With the exception of William Coley who in the late 1800s felt that the rate of cure after surgery had been higher before asepsis (and who injected bacteria into tumors with mixed results), cancer treatment became dependent on the individual art of the surgeon at removing a tumor. During the same period, the idea that the body was made up of varous tissues, that in turn were made up of millions of cells, laid rest the humor-theories about chemical imbalances in the body. The age of cellular pathology was born.
When Marie Curie and Pierre Curie discovered radiation at the end of the 19th century, they stumbled upon the first effective non-surgical cancer treatment. With radiation came also the first signs of multi-disciplinary approaches to cancer treatment. The surgeon was no longer operating in isolation, but worked together with hospital radiologists to help patients. The complications in communication this brought, along with the necessity of the patient's treatment in a hospital facility rather than at home, also created a parallel process of compiling patient data into hospital files, which in turn led to the first statistical patient studies.
Cancer patient treatment and studies were restricted to individual physicians' practices until World War II, when medical research centers discovered that there were large international differences in disease incidence. This insight drove national public health bodies to make it possible to compile health data across practises and hospitals, a process that many countries do today. The Japanese medical community observed that the bone marrow of bomb victims in Hiroshima and Nagasaki was completely destroyed. They concluded that diseased bone marrow could also be destroyed with radiation, and this led to the discovery of bone marrow transplants for leukemia. Since WWII, trends in cancer treatment are to improve on a micro-level the existing treatment methods, standardize them, and globalize them as a way to find cures through epidemiology and international partnerships.
Research
Cancer research is the intense scientific effort to understand disease processes and discover possible therapies. The improved understanding of molecular biology and cellular biology due to cancer research has led to a number of new, effective treatments for cancer since President Nixon declared "War on Cancer" in 1971. Since 1971 the United States has invested over $200 billion on cancer research, that total includes money invested by public and private sectors and foundations.[101]
from wikipedia.org
Cancer epidemiology is the study of the incidence of cancer as a way to infer possible trends and causes. The first such cause of cancer was identified by British surgeon Percivall Pott, who discovered in 1775 that cancer of the scrotum was a common disease among chimney sweeps. The work of other individual physicians led to various insights, but when physicians started working together they could make firmer conclusions.
A founding paper of this discipline was the work of Janet Lane-Claypon, who published a comparative study in 1926 of 500 breast cancer cases and 500 control patients of the same background and lifestyle for the British Ministry of Health. Her ground-breaking work on cancer epidemiology was carried on by Richard Doll and Austin Bradford Hill, who published "Lung Cancer and Other Causes of Death In Relation to Smoking. A Second Report on the Mortality of British Doctors" followed in 1956 (otherwise known as the British doctors study). Richard Doll left the London Medical Research Center (MRC), to start the Oxford unit for Cancer epidemiology in 1968. With the use of computers, the unit was the first to compile large amounts of cancer data. Modern epidemiological methods are closely linked to current concepts of disease and public health policy. Over the past 50 years, great efforts have been spent on gathering data across medical practise, hospital, provincial, state, and even country boundaries, as a way to study the interdependence of environmental and cultural factors on cancer incidence.
Cancer epidemiology must contend with problems of lead time bias and length time bias. Lead time bias is the concept that early diagnosis may artificially inflate the survival statistics of a cancer, without really improving the natural history of the disease. Length bias is the concept that slower growing, more indolent tumors are more likely to be diagnosed by screening tests, but improvements in diagnosing more cases of indolent cancer may not translate into better patient outcomes after the implementation of screening programs. A similar epidemiological concern is overdiagnosis, the tendency of screening tests to diagnose diseases that may not actually impact the patient's longevity. This problem especially applies to prostate cancer and PSA screening.[87]
Some cancer researchers have argued that negative cancer clinical trials lack sufficient statistical power to discover a benefit to treatment. This may be due to fewer patients enrolled in the study than originally planned.[88]
State and regional cancer registries are organizations that abstract clinical data about cancer from patient medical records. These institutions provide information to state and national public health groups to help track trends in cancer diagnosis and treatment. One of the largest and most important cancer registries is SEER, administered by the US Federal government.[89] Health information privacy concerns have led to the restricted use of cancer registry data in the United States Department of Veterans Affairs[90][91][92] and other institutions.[93]
In some Western countries, such as the USA,[4] and the UK[94] cancer is overtaking cardiovascular disease as the leading cause of death. In many Third World countries cancer incidence (insofar as this can be measured) appears much lower, most likely because of the higher death rates due to infectious disease or injury. With the increased control over malaria and tuberculosis in some Third World countries, incidence of cancer is expected to rise; this is termed the epidemiologic transition in epidemiological terminology.
Cancer epidemiology closely mirrors risk factor spread in various countries. Hepatocellular carcinoma (liver cancer) is rare in the West but is the main cancer in China and neighbouring countries, most likely due to the endemic presence of hepatitis B and aflatoxin in that population. Similarly, with tobacco smoking becoming more common in various Third World countries, lung cancer incidence has increased in a parallel fashion.
History
Today, the Greek term carcinoma is the medical term for a malignant tumor derived from epithelial cells. It is Celsus who translated carcinos into the Latin cancer, also meaning crab. Galen used "oncos" to describe all tumours, the root for the modern word oncology.[95]
Hippocrates described several kinds of cancers. He called benign tumours oncos, Greek for swelling, and malignant tumours carcinos, Greek for crab or crayfish. This name comes from the appearance of the cut surface of a solid malignant tumour, with the veins stretched on all sides as the animal the crab has its feet, whence it derives its name[96] (see picture). He later added the suffix -oma, Greek for swelling, giving the name carcinoma. Since it was against Greek tradition to open the body, Hippocrates only described and made drawings of outwardly visible tumors on the skin, nose, and breasts. Treatment was based on the humor theory of four bodily fluids (black and yellow bile, blood, and phlegm). According to the patient's humor, treatment consisted of diet, blood-letting, and/or laxatives. Through the centuries it was discovered that cancer could occur anywhere in the body, but humor-theory based treatment remained popular until the 19th century with the discovery of cells.
Our oldest description and surgical treatment of cancer was discovered in Egypt and dates back to approximately 1600 B.C. The Papyrus describes 8 cases of ulcers of the breast that were treated by cauterization, with a tool called "the fire drill." The writing says about the disease, "There is no treatment."[97]
Another very early surgical treatment for cancer was described in the 1020s by Avicenna (Ibn Sina) in The Canon of Medicine. He stated that the excision should be radical and that all diseased tissue should be removed, which included the use of amputation or the removal of veins running in the direction of the tumor. He also recommended the use of cauterization for the area being treated if necessary.[98]
In the 16th and 17th centuries, it became more acceptable for doctors to dissect bodies to discover the cause of death. The German professor Wilhelm Fabry believed that breast cancer was caused by a milk clot in a mammary duct. The Dutch professor Francois de la Boe Sylvius, a follower of Descartes, believed that all disease was the outcome of chemical processes, and that acidic lymph fluid was the cause of cancer. His contemporary Nicolaes Tulp believed that cancer was a poison that slowly spreads, and concluded that it was contagious.[99]
With the widespread use of the microscope in the 18th century, it was discovered that the 'cancer poison' spread from the primary tumor through the lymph nodes to other sites ("metastasis"). This view of the disease was first formulated by the English surgeon Campbell De Morgan between 1871 and 1874.[100] The use of surgery to treat cancer had poor results due to problems with hygiene. The renowned Scottish surgeon Alexander Monro saw only 2 breast tumor patients out of 60 surviving surgery for two years. In the 19th century, asepsis improved surgical hygiene and as the survival statistics went up, surgical removal of the tumor became the primary treatment for cancer. With the exception of William Coley who in the late 1800s felt that the rate of cure after surgery had been higher before asepsis (and who injected bacteria into tumors with mixed results), cancer treatment became dependent on the individual art of the surgeon at removing a tumor. During the same period, the idea that the body was made up of varous tissues, that in turn were made up of millions of cells, laid rest the humor-theories about chemical imbalances in the body. The age of cellular pathology was born.
When Marie Curie and Pierre Curie discovered radiation at the end of the 19th century, they stumbled upon the first effective non-surgical cancer treatment. With radiation came also the first signs of multi-disciplinary approaches to cancer treatment. The surgeon was no longer operating in isolation, but worked together with hospital radiologists to help patients. The complications in communication this brought, along with the necessity of the patient's treatment in a hospital facility rather than at home, also created a parallel process of compiling patient data into hospital files, which in turn led to the first statistical patient studies.
Cancer patient treatment and studies were restricted to individual physicians' practices until World War II, when medical research centers discovered that there were large international differences in disease incidence. This insight drove national public health bodies to make it possible to compile health data across practises and hospitals, a process that many countries do today. The Japanese medical community observed that the bone marrow of bomb victims in Hiroshima and Nagasaki was completely destroyed. They concluded that diseased bone marrow could also be destroyed with radiation, and this led to the discovery of bone marrow transplants for leukemia. Since WWII, trends in cancer treatment are to improve on a micro-level the existing treatment methods, standardize them, and globalize them as a way to find cures through epidemiology and international partnerships.
Research
Cancer research is the intense scientific effort to understand disease processes and discover possible therapies. The improved understanding of molecular biology and cellular biology due to cancer research has led to a number of new, effective treatments for cancer since President Nixon declared "War on Cancer" in 1971. Since 1971 the United States has invested over $200 billion on cancer research, that total includes money invested by public and private sectors and foundations.[101]
from wikipedia.org
martedì 16 settembre 2008
cancer (five part):vaccination and screening
Prevention
Cancer prevention is defined as active measures to decrease the incidence of cancer. This can be accomplished by avoiding carcinogens or altering their metabolism, pursuing a lifestyle or diet that modifies cancer-causing factors and/or medical intervention (chemoprevention, treatment of pre-malignant lesions). The epidemiological concept of "prevention" is usually defined as either primary prevention, for people who have not been diagnosed with a particular disease, or secondary prevention, aimed at reducing recurrence or complications of a previously diagnosed illness.
Observational epidemiological studies that show associations between risk factors and specific cancers mostly serve to generate hypotheses about potential interventions that could reduce cancer incidence or morbidity. Randomized controlled trials then test whether hypotheses generated by epidemiological trials and laboratory research actually result in reduced cancer incidence and mortality. In many cases, findings from observational epidemiological studies are not confirmed by randomized controlled trials.
About a third of the twelve most common cancers worldwide are due to nine potentially modifiable risk factors. Men with cancer are twice as likely as women to have a modifiable risk factor for their disease. The nine risk factors are tobacco smoking, excessive alcohol use, diet low in fruit and vegetables, limited physical exercise, human papillomavirus infection (unsafe sex), urban air pollution, domestic use of solid fuels, and contaminated injections (hepatitis B and C).[34]
Modifiable ("lifestyle") risk factors
Examples of modifiable cancer risk factors include alcohol consumption (associated with increased risk of oral, esophageal, breast, and other cancers), smoking (although 20% of women with lung cancer have never smoked, versus 10% of men[35]), physical inactivity (associated with increased risk of colon, breast, and possibly other cancers), and being overweight (associated with colon, breast, endometrial, and possibly other cancers). Based on epidemiologic evidence, it is now thought that avoiding excessive alcohol consumption may contribute to reductions in risk of certain cancers; however, compared with tobacco exposure, the magnitude of effect is modest or small and the strength of evidence is often weaker. Other lifestyle and environmental factors known to affect cancer risk (either beneficially or detrimentally) include certain sexually transmitted diseases, the use of exogenous hormones, exposure to ionizing radiation and ultraviolet radiation, and certain occupational and chemical exposures.
Every year, at least 200,000 people die worldwide from cancer related to their workplace.[36] Millions of workers run the risk of developing cancers such as lung cancer and mesothelioma from inhaling asbestos fibers and tobacco smoke, or leukemia from exposure to benzene at their workplaces.[36] Currently, most cancer deaths caused by occupational risk factors occur in the developed world.[36] It is estimated that approximately 20,000 cancer deaths and 40,000 new cases of cancer each year in the U.S. are attributable to occupation.[37]
See alcohol and cancer for more on that topic.
Diet
The consensus on diet and cancer is that obesity increases the risk of developing cancer. Particular dietary practices often explain differences in cancer incidence in different countries (e.g. gastric cancer is more common in Japan, while colon cancer is more common in the United States). Studies have shown that immigrants develop the risk of their new country, often within one generation, suggesting a substantial link between diet and cancer.[38] Whether reducing obesity in a population also reduces cancer incidence is unknown.
Despite frequent reports of particular substances (including foods) having a beneficial or detrimental effect on cancer risk, few of these have an established link to cancer. These reports are often based on studies in cultured cell media or animals. Public health recommendations cannot be made on the basis of these studies until they have been validated in an observational (or occasionally a prospective interventional) trial in humans.
Proposed dietary interventions for primary cancer risk reduction generally gain support from epidemiological association studies. Examples of such studies include reports that reduced meat consumption is associated with decreased risk of colon cancer,[39] and reports that consumption of coffee is associated with a reduced risk of liver cancer.[40] Studies have linked consumption of grilled meat to an increased risk of stomach cancer,[41] colon cancer,[42] breast cancer,[43] and pancreatic cancer,[44] a phenomenon which could be due to the presence of carcinogens such as benzopyrene in foods cooked at high temperatures.
A 2005 secondary prevention study showed that consumption of a plant-based diet and lifestyle changes resulted in a reduction in cancer markers in a group of men with prostate cancer who were using no conventional treatments at the time.[45] These results were amplified by a 2006 study in which over 2,400 women were studied, half randomly assigned to a normal diet, the other half assigned to a diet containing less than 20% calories from fat. The women on the low fat diet were found to have a markedly lower risk of breast cancer recurrence, in the interim report of December, 2006.[46]
Recent studies have also demonstrated potential links between some forms of cancer and high consumption of refined sugars and other simple carbohydrates.[47][48][49][50][51] Although the degree of correlation and the degree of causality is still debated,[52][53][54] some organizations have in fact begun to recommend reducing intake of refined sugars and starches as part of their cancer prevention regimens.
In November 2007, the American Institute for Cancer Research (AICR), in conjunction with the World Cancer Research Fund (WCRF), published Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective', "the most current and comprehensive analysis of the literature on diet, physical activity and cancer".[59] The WCRF/AICR Expert Report lists 10 recommendations that people can follow to help reduce their risk of developing cancer, including the following dietary guidelines: (1) reducing intake of foods and drinks that promote weight gain, namely energy-dense foods and sugary drinks, (2) eating mostly foods of plant origin, (3) limiting intake of red meat and avoiding processed meat, (4) limiting consumption of alcoholic beverages, and (5) reducing intake of salt and avoiding mouldy cereals (grains) or pulses (legumes).[60][61]
Vitamins
The idea that cancer can be prevented through vitamin supplementation stems from early observations correlating human disease with vitamin deficiency, such as pernicious anemia with vitamin B12 deficiency, and scurvy with Vitamin C deficiency. This has largely not been proven to be the case with cancer, and vitamin supplementation is largely not proving effective in preventing cancer. The cancer-fighting components of food are also proving to be more numerous and varied than previously understood, so patients are increasingly being advised to consume fresh, unprocessed fruits and vegetables for maximal health benefits.[62]
Epidemiological studies have shown that low vitamin D status is correlated to increased cancer risk.[63][64] However, the results of such studies need to be treated with caution, as they cannot show whether a correlation between two factors means that one causes the other (i.e. correlation does not imply causation).[65] The possibility that Vitamin D might protect against cancer has been contrasted with the risk of malignancy from sun exposure. Since exposure to the sun enhances natural human production of vitamin D, some cancer researchers have argued that the potential deleterious malignant effects of sun exposure are far outweighed by the cancer-preventing effects of extra vitamin D synthesis in sun-exposed skin. In 2002, Dr. William B. Grant claimed that 23,800 premature cancer deaths occur in the US annually due to insufficient UVB exposure (apparently via vitamin D deficiency).[66] This is higher than 8,800 deaths occurred from melanoma or squamous cell carcinoma, so the overall effect of sun exposure might be beneficial. Another research group[67][68] estimates that 50,000–63,000 individuals in the United States and 19,000 - 25,000 in the UK die prematurely from cancer annually due to insufficient vitamin D.
The case of beta-carotene provides an example of the importance of randomized clinical trials. Epidemiologists studying both diet and serum levels observed that high levels of beta-carotene, a precursor to vitamin A, were associated with a protective effect, reducing the risk of cancer. This effect was particularly strong in lung cancer. This hypothesis led to a series of large randomized clinical trials conducted in both Finland and the United States (CARET study) during the 1980s and 1990s. This study provided about 80,000 smokers or former smokers with daily supplements of beta-carotene or placebos. Contrary to expectation, these tests found no benefit of beta-carotene supplementation in reducing lung cancer incidence and mortality. In fact, the risk of lung cancer was slightly, but not significantly, increased by beta-carotene, leading to an early termination of the study.[69]
Results reported in the Journal of the American Medical Association (JAMA) in 2007 indicate that folic acid supplementation is not effective in preventing colon cancer, and folate consumers may be more likely to form colon polyps.[70]
Chemoprevention
The neutrality of this section is disputed.
Please see the discussion on the talk page. (June 2008)
Please do not remove this message until the dispute is resolved.
The concept that medications could be used to prevent cancer is an attractive one, and many high-quality clinical trials support the use of such chemoprevention in defined circumstances.
Daily use of tamoxifen, a selective estrogen receptor modulator (SERM), typically for 5 years, has been demonstrated to reduce the risk of developing breast cancer in high-risk women by about 50%. A recent study reported that the selective estrogen receptor modulator raloxifene has similar benefits to tamoxifen in preventing breast cancer in high-risk women, with a more favorable side effect profile.[71]
Raloxifene is a SERM like tamoxifen; it has been shown (in the STAR trial) to reduce the risk of breast cancer in high-risk women equally as well as tamoxifen. In this trial, which studied almost 20,000 women, raloxifene had fewer side effects than tamoxifen, though it did permit more DCIS to form.[71]
Finasteride, a 5-alpha-reductase inhibitor, has been shown to lower the risk of prostate cancer, though it seems to mostly prevent low-grade tumors.[72] The effect of COX-2 inhibitors such as rofecoxib and celecoxib upon the risk of colon polyps have been studied in familial adenomatous polyposis patients[73] and in the general population.[74][75] In both groups, there were significant reductions in colon polyp incidence, but this came at the price of increased cardiovascular toxicity.
Vaccination
Considerable[weasel words] research effort is now devoted to the development of vaccines to prevent infection by oncogenic infectious agents, as well as to mount an immune response against cancer-specific epitopes) and to potential venues for gene therapy for individuals with genetic mutations or polymorphisms that put them at high risk of cancer.
As reported above, a preventive human papillomavirus vaccine exists that targets certain sexually transmitted strains of human papillomavirus that are associated with the development of cervical cancer and genital warts. The only two HPV vaccines on the market as of October 2007 are Gardasil and Cervarix.
Screening
Cancer screening is an attempt to detect unsuspected cancers in an asymptomatic population. Screening tests suitable for large numbers of healthy people must be relatively affordable, safe, noninvasive procedures with acceptably low rates of false positive results. If signs of cancer are detected, more definitive and invasive follow up tests are performed to confirm the diagnosis.
Screening for cancer can lead to earlier diagnosis in specific cases. Early diagnosis may lead to extended life, but may also falsely prolong the lead time to death through lead time bias or length time bias.
A number of different screening tests have been developed for different malignancies. Breast cancer screening can be done by breast self-examination, though this approach was discredited by a 2005 study in over 300,000 Chinese women. Screening for breast cancer with mammograms has been shown to reduce the average stage of diagnosis of breast cancer in a population. Stage of diagnosis in a country has been shown to decrease within ten years of introduction of mammographic screening programs. Colorectal cancer can be detected through fecal occult blood testing and colonoscopy, which reduces both colon cancer incidence and mortality, presumably through the detection and removal of pre-malignant polyps. Similarly, cervical cytology testing (using the Pap smear) leads to the identification and excision of precancerous lesions. Over time, such testing has been followed by a dramatic reduction of cervical cancer incidence and mortality. Testicular self-examination is recommended for men beginning at the age of 15 years to detect testicular cancer. Prostate cancer can be screened using a digital rectal exam along with prostate specific antigen (PSA) blood testing, though some authorities (such as the US Preventive Services Task Force) recommend against routinely screening all men.
Screening for cancer is controversial in cases when it is not yet known if the test actually saves lives. The controversy arises when it is not clear if the benefits of screening outweigh the risks of follow-up diagnostic tests and cancer treatments. For example: when screening for prostate cancer, the PSA test may detect small cancers that would never become life threatening, but once detected will lead to treatment. This situation, called overdiagnosis, puts men at risk for complications from unnecessary treatment such as surgery or radiation. Follow up procedures used to diagnose prostate cancer (prostate biopsy) may cause side effects, including bleeding and infection. Prostate cancer treatment may cause incontinence (inability to control urine flow) and erectile dysfunction (erections inadequate for intercourse). Similarly, for breast cancer, there have recently been criticisms that breast screening programs in some countries cause more problems than they solve. This is because screening of women in the general population will result in a large number of women with false positive results which require extensive follow-up investigations to exclude cancer, leading to having a high number-to-treat (or number-to-screen) to prevent or catch a single case of breast cancer early.
Cervical cancer screening via the Pap smear has the best cost-benefit profile of all the forms of cancer screening from a public health perspective as, being largely caused by a virus, it has clear risk factors (sexual contact), and the natural progression of cervical cancer is that it normally spreads slowly over a number of years therefore giving more time for the screening program to catch it early. Moreover, the test itself is easy to perform and relatively cheap.
For these reasons, it is important that the benefits and risks of diagnostic procedures and treatment be taken into account when considering whether to undertake cancer screening.
Use of medical imaging to search for cancer in people without clear symptoms is similarly marred with problems. There is a significant risk of detection of what has been recently called an incidentaloma - a benign lesion that may be interpreted as a malignancy and be subjected to potentially dangerous investigations. Recent studies of CT scan-based screening for lung cancer in smokers have had equivocal results, and systematic screening is not recommended as of July 2007. Randomized clinical trials of plain-film chest X-rays to screen for lung cancer in smokers have shown no benefit for this approach.
Canine cancer detection has shown promise, but is still in the early stages of research.
Cancer prevention is defined as active measures to decrease the incidence of cancer. This can be accomplished by avoiding carcinogens or altering their metabolism, pursuing a lifestyle or diet that modifies cancer-causing factors and/or medical intervention (chemoprevention, treatment of pre-malignant lesions). The epidemiological concept of "prevention" is usually defined as either primary prevention, for people who have not been diagnosed with a particular disease, or secondary prevention, aimed at reducing recurrence or complications of a previously diagnosed illness.
Observational epidemiological studies that show associations between risk factors and specific cancers mostly serve to generate hypotheses about potential interventions that could reduce cancer incidence or morbidity. Randomized controlled trials then test whether hypotheses generated by epidemiological trials and laboratory research actually result in reduced cancer incidence and mortality. In many cases, findings from observational epidemiological studies are not confirmed by randomized controlled trials.
About a third of the twelve most common cancers worldwide are due to nine potentially modifiable risk factors. Men with cancer are twice as likely as women to have a modifiable risk factor for their disease. The nine risk factors are tobacco smoking, excessive alcohol use, diet low in fruit and vegetables, limited physical exercise, human papillomavirus infection (unsafe sex), urban air pollution, domestic use of solid fuels, and contaminated injections (hepatitis B and C).[34]
Modifiable ("lifestyle") risk factors
Examples of modifiable cancer risk factors include alcohol consumption (associated with increased risk of oral, esophageal, breast, and other cancers), smoking (although 20% of women with lung cancer have never smoked, versus 10% of men[35]), physical inactivity (associated with increased risk of colon, breast, and possibly other cancers), and being overweight (associated with colon, breast, endometrial, and possibly other cancers). Based on epidemiologic evidence, it is now thought that avoiding excessive alcohol consumption may contribute to reductions in risk of certain cancers; however, compared with tobacco exposure, the magnitude of effect is modest or small and the strength of evidence is often weaker. Other lifestyle and environmental factors known to affect cancer risk (either beneficially or detrimentally) include certain sexually transmitted diseases, the use of exogenous hormones, exposure to ionizing radiation and ultraviolet radiation, and certain occupational and chemical exposures.
Every year, at least 200,000 people die worldwide from cancer related to their workplace.[36] Millions of workers run the risk of developing cancers such as lung cancer and mesothelioma from inhaling asbestos fibers and tobacco smoke, or leukemia from exposure to benzene at their workplaces.[36] Currently, most cancer deaths caused by occupational risk factors occur in the developed world.[36] It is estimated that approximately 20,000 cancer deaths and 40,000 new cases of cancer each year in the U.S. are attributable to occupation.[37]
See alcohol and cancer for more on that topic.
Diet
The consensus on diet and cancer is that obesity increases the risk of developing cancer. Particular dietary practices often explain differences in cancer incidence in different countries (e.g. gastric cancer is more common in Japan, while colon cancer is more common in the United States). Studies have shown that immigrants develop the risk of their new country, often within one generation, suggesting a substantial link between diet and cancer.[38] Whether reducing obesity in a population also reduces cancer incidence is unknown.
Despite frequent reports of particular substances (including foods) having a beneficial or detrimental effect on cancer risk, few of these have an established link to cancer. These reports are often based on studies in cultured cell media or animals. Public health recommendations cannot be made on the basis of these studies until they have been validated in an observational (or occasionally a prospective interventional) trial in humans.
Proposed dietary interventions for primary cancer risk reduction generally gain support from epidemiological association studies. Examples of such studies include reports that reduced meat consumption is associated with decreased risk of colon cancer,[39] and reports that consumption of coffee is associated with a reduced risk of liver cancer.[40] Studies have linked consumption of grilled meat to an increased risk of stomach cancer,[41] colon cancer,[42] breast cancer,[43] and pancreatic cancer,[44] a phenomenon which could be due to the presence of carcinogens such as benzopyrene in foods cooked at high temperatures.
A 2005 secondary prevention study showed that consumption of a plant-based diet and lifestyle changes resulted in a reduction in cancer markers in a group of men with prostate cancer who were using no conventional treatments at the time.[45] These results were amplified by a 2006 study in which over 2,400 women were studied, half randomly assigned to a normal diet, the other half assigned to a diet containing less than 20% calories from fat. The women on the low fat diet were found to have a markedly lower risk of breast cancer recurrence, in the interim report of December, 2006.[46]
Recent studies have also demonstrated potential links between some forms of cancer and high consumption of refined sugars and other simple carbohydrates.[47][48][49][50][51] Although the degree of correlation and the degree of causality is still debated,[52][53][54] some organizations have in fact begun to recommend reducing intake of refined sugars and starches as part of their cancer prevention regimens.
In November 2007, the American Institute for Cancer Research (AICR), in conjunction with the World Cancer Research Fund (WCRF), published Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective', "the most current and comprehensive analysis of the literature on diet, physical activity and cancer".[59] The WCRF/AICR Expert Report lists 10 recommendations that people can follow to help reduce their risk of developing cancer, including the following dietary guidelines: (1) reducing intake of foods and drinks that promote weight gain, namely energy-dense foods and sugary drinks, (2) eating mostly foods of plant origin, (3) limiting intake of red meat and avoiding processed meat, (4) limiting consumption of alcoholic beverages, and (5) reducing intake of salt and avoiding mouldy cereals (grains) or pulses (legumes).[60][61]
Vitamins
The idea that cancer can be prevented through vitamin supplementation stems from early observations correlating human disease with vitamin deficiency, such as pernicious anemia with vitamin B12 deficiency, and scurvy with Vitamin C deficiency. This has largely not been proven to be the case with cancer, and vitamin supplementation is largely not proving effective in preventing cancer. The cancer-fighting components of food are also proving to be more numerous and varied than previously understood, so patients are increasingly being advised to consume fresh, unprocessed fruits and vegetables for maximal health benefits.[62]
Epidemiological studies have shown that low vitamin D status is correlated to increased cancer risk.[63][64] However, the results of such studies need to be treated with caution, as they cannot show whether a correlation between two factors means that one causes the other (i.e. correlation does not imply causation).[65] The possibility that Vitamin D might protect against cancer has been contrasted with the risk of malignancy from sun exposure. Since exposure to the sun enhances natural human production of vitamin D, some cancer researchers have argued that the potential deleterious malignant effects of sun exposure are far outweighed by the cancer-preventing effects of extra vitamin D synthesis in sun-exposed skin. In 2002, Dr. William B. Grant claimed that 23,800 premature cancer deaths occur in the US annually due to insufficient UVB exposure (apparently via vitamin D deficiency).[66] This is higher than 8,800 deaths occurred from melanoma or squamous cell carcinoma, so the overall effect of sun exposure might be beneficial. Another research group[67][68] estimates that 50,000–63,000 individuals in the United States and 19,000 - 25,000 in the UK die prematurely from cancer annually due to insufficient vitamin D.
The case of beta-carotene provides an example of the importance of randomized clinical trials. Epidemiologists studying both diet and serum levels observed that high levels of beta-carotene, a precursor to vitamin A, were associated with a protective effect, reducing the risk of cancer. This effect was particularly strong in lung cancer. This hypothesis led to a series of large randomized clinical trials conducted in both Finland and the United States (CARET study) during the 1980s and 1990s. This study provided about 80,000 smokers or former smokers with daily supplements of beta-carotene or placebos. Contrary to expectation, these tests found no benefit of beta-carotene supplementation in reducing lung cancer incidence and mortality. In fact, the risk of lung cancer was slightly, but not significantly, increased by beta-carotene, leading to an early termination of the study.[69]
Results reported in the Journal of the American Medical Association (JAMA) in 2007 indicate that folic acid supplementation is not effective in preventing colon cancer, and folate consumers may be more likely to form colon polyps.[70]
Chemoprevention
The neutrality of this section is disputed.
Please see the discussion on the talk page. (June 2008)
Please do not remove this message until the dispute is resolved.
The concept that medications could be used to prevent cancer is an attractive one, and many high-quality clinical trials support the use of such chemoprevention in defined circumstances.
Daily use of tamoxifen, a selective estrogen receptor modulator (SERM), typically for 5 years, has been demonstrated to reduce the risk of developing breast cancer in high-risk women by about 50%. A recent study reported that the selective estrogen receptor modulator raloxifene has similar benefits to tamoxifen in preventing breast cancer in high-risk women, with a more favorable side effect profile.[71]
Raloxifene is a SERM like tamoxifen; it has been shown (in the STAR trial) to reduce the risk of breast cancer in high-risk women equally as well as tamoxifen. In this trial, which studied almost 20,000 women, raloxifene had fewer side effects than tamoxifen, though it did permit more DCIS to form.[71]
Finasteride, a 5-alpha-reductase inhibitor, has been shown to lower the risk of prostate cancer, though it seems to mostly prevent low-grade tumors.[72] The effect of COX-2 inhibitors such as rofecoxib and celecoxib upon the risk of colon polyps have been studied in familial adenomatous polyposis patients[73] and in the general population.[74][75] In both groups, there were significant reductions in colon polyp incidence, but this came at the price of increased cardiovascular toxicity.
Vaccination
Considerable[weasel words] research effort is now devoted to the development of vaccines to prevent infection by oncogenic infectious agents, as well as to mount an immune response against cancer-specific epitopes) and to potential venues for gene therapy for individuals with genetic mutations or polymorphisms that put them at high risk of cancer.
As reported above, a preventive human papillomavirus vaccine exists that targets certain sexually transmitted strains of human papillomavirus that are associated with the development of cervical cancer and genital warts. The only two HPV vaccines on the market as of October 2007 are Gardasil and Cervarix.
Screening
Cancer screening is an attempt to detect unsuspected cancers in an asymptomatic population. Screening tests suitable for large numbers of healthy people must be relatively affordable, safe, noninvasive procedures with acceptably low rates of false positive results. If signs of cancer are detected, more definitive and invasive follow up tests are performed to confirm the diagnosis.
Screening for cancer can lead to earlier diagnosis in specific cases. Early diagnosis may lead to extended life, but may also falsely prolong the lead time to death through lead time bias or length time bias.
A number of different screening tests have been developed for different malignancies. Breast cancer screening can be done by breast self-examination, though this approach was discredited by a 2005 study in over 300,000 Chinese women. Screening for breast cancer with mammograms has been shown to reduce the average stage of diagnosis of breast cancer in a population. Stage of diagnosis in a country has been shown to decrease within ten years of introduction of mammographic screening programs. Colorectal cancer can be detected through fecal occult blood testing and colonoscopy, which reduces both colon cancer incidence and mortality, presumably through the detection and removal of pre-malignant polyps. Similarly, cervical cytology testing (using the Pap smear) leads to the identification and excision of precancerous lesions. Over time, such testing has been followed by a dramatic reduction of cervical cancer incidence and mortality. Testicular self-examination is recommended for men beginning at the age of 15 years to detect testicular cancer. Prostate cancer can be screened using a digital rectal exam along with prostate specific antigen (PSA) blood testing, though some authorities (such as the US Preventive Services Task Force) recommend against routinely screening all men.
Screening for cancer is controversial in cases when it is not yet known if the test actually saves lives. The controversy arises when it is not clear if the benefits of screening outweigh the risks of follow-up diagnostic tests and cancer treatments. For example: when screening for prostate cancer, the PSA test may detect small cancers that would never become life threatening, but once detected will lead to treatment. This situation, called overdiagnosis, puts men at risk for complications from unnecessary treatment such as surgery or radiation. Follow up procedures used to diagnose prostate cancer (prostate biopsy) may cause side effects, including bleeding and infection. Prostate cancer treatment may cause incontinence (inability to control urine flow) and erectile dysfunction (erections inadequate for intercourse). Similarly, for breast cancer, there have recently been criticisms that breast screening programs in some countries cause more problems than they solve. This is because screening of women in the general population will result in a large number of women with false positive results which require extensive follow-up investigations to exclude cancer, leading to having a high number-to-treat (or number-to-screen) to prevent or catch a single case of breast cancer early.
Cervical cancer screening via the Pap smear has the best cost-benefit profile of all the forms of cancer screening from a public health perspective as, being largely caused by a virus, it has clear risk factors (sexual contact), and the natural progression of cervical cancer is that it normally spreads slowly over a number of years therefore giving more time for the screening program to catch it early. Moreover, the test itself is easy to perform and relatively cheap.
For these reasons, it is important that the benefits and risks of diagnostic procedures and treatment be taken into account when considering whether to undertake cancer screening.
Use of medical imaging to search for cancer in people without clear symptoms is similarly marred with problems. There is a significant risk of detection of what has been recently called an incidentaloma - a benign lesion that may be interpreted as a malignancy and be subjected to potentially dangerous investigations. Recent studies of CT scan-based screening for lung cancer in smokers have had equivocal results, and systematic screening is not recommended as of July 2007. Randomized clinical trials of plain-film chest X-rays to screen for lung cancer in smokers have shown no benefit for this approach.
Canine cancer detection has shown promise, but is still in the early stages of research.
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