CELIAC DISEASE AND GLUTEN

CELIAC DISEASE AND GLUTEN


Other names of this disease : cœliac disease (with œ ligature), gluten intolerance, celiac sprue, nontropical sprue, endemic sprue, gluten enteropathy or gluten-sensitive enteropathy.

Celiac disease is an autoimmune disorder of the small intestine that occurs in genetically predisposed people of all ages from middle infancy onward [1]. For people with celiac disease, a lifelong disorder of the digestive system, these foods aren't always the treats that most people think they are. They usually contain a type of protein called gluten, which causes problems for people with celiac disease. [2]

When people with celiac disease eat foods or use products containing gluten, their immune system responds by damaging or destroying villi—the tiny, fingerlike protrusions lining the small intestine. Villi normally allow nutrients from food to be absorbed through the walls of the small intestine into the bloodstream. Without healthy villi, a person becomes malnourished, no matter how much food one eats. Celiac disease is both a disease of malabsorption—meaning nutrients are not absorbed properly—and an abnormal immune reaction to gluten [3]. Eventually, the decreased absorption of nutrients (malabsorption) that occurs with celiac disease can cause vitamin deficiencies that deprive your brain, peripheral nervous system, bones, liver and other organs of vital nourishment. This can lead to other illnesses and stunted growth in children. [4]

What is gluten ?

Gluten is a composite of the proteins gliadin and glutenin. These exist, conjoined with starch, in the endosperms of some grass-related grains, notably wheat, rye, and barley. Gliadin and glutenin comprise about 80% of the protein contained in wheat seed. Being insoluble in water, they can be purified by washing away the associated starch. Worldwide, gluten is an important source of nutritional protein, both in foods prepared directly from sources containing it, and as an additive to foods otherwise low in protein. [5]

When these proteins are present in the diet of someone with celiac disease, they become toxic and cause damage to the intestine. This damage leads to decreased absorption of essential nutrients and, if left untreated, can lead to nutrient deficiency and subsequent disease (i.e. iron deficiency anemia, decreased bone density, unintentional weight loss, folate and vitamin B12 deficiency). [6]

Gluten is found in most types of cereals and in many types of bread. Not all foods from the grain family, however, contain gluten. Examples of grains that do not have gluten include wild rice, corn, buckwheat, millet, amaranth, quinoa, teff, oats, soybeans, and sunflower seeds.

Gluten can be removed from wheat flour, producing wheat starch. All of the gluten in wheat flour, however, cannot be removed. Gluten helps make bread elastic, providing it with that chewy texture it has when eaten. For this reason, flour that has had most of its gluten removed, produces a sticky dough that feels much like chewing gum. Gluten provides many additional important qualities to bread. For example, gluten keeps the gases that are released during fermentation in the dough, so the bread is able to rise before it is baked. In addition, gluten firms up when it is cooked and, with the help of starch, helps ensure the bread maintains its proper shape.

Gluten also has an absorbent quality, which is why bread is capable of soaking up broth. Because of this feature, gluten is often used by those on a vegetarian diet as an imitation meat. On the downside, gluten is believed to be partly responsible for causing bread to become stale.

According to the Food and Drug Administration (FDA), if a certain amount of the gluten is removed, the food product can be labeled "gluten-free." (This is somewhat similar to food products that can be labeled as 0 Calories even though a serving contains 4 or less Calories) [7]. Standards for "gluten-free" labeling have been set up by the "Codex Alimentarius"; however, these regulations do not apply to "foods which in their normal form do not contain gluten". [1]

The legal definition of the phrase "gluten-free" varies from country to country. Current research suggests that for persons with celiac disease the maximum safe level of gluten in a finished product is probably less than 0.02% (200 parts per million) and possibly as little as 0.002% (20 parts per million).

Prevalence of Celiac Disease

Celiac disease is a serious health issue and challenge for food scientists, because celiac disease can only be treated by strict adherence to a gluten-free diet. The prevalence of celiac disease, an intolerance of gluten, has been reported to be as high as 1 in 200 of the world population [8 : Shih F.F., Daigle K.W., Truong V.; 2006].

The prevalence of clinically diagnosed disease (symptoms prompting diagnostic testing) is 0.05–0.27% in various studies. However, population studies from parts of Europe, India, South America, Australasia and the USA (using serology and biopsy) indicate that the prevalence may be between 0.33 and 1.06% in children (5.66% in one study of Sahrawi children) and 0.18–1.2% in adults. People of African, Japanese and Chinese descent are rarely diagnosed; this reflects a much lower prevalence of the genetic risk factors. Population studies also indicate that a large proportion of celiacs (coeliacs) remain undiagnosed; this is due to many clinicians being unfamiliar with the condition. [1, accessed Dec. 2009]

Principal Features of This Disorder

It's important to diagnose celiac disease early before it causes damage to the intestine. But because it's easy to confuse the symptoms with other intestinal disorders, such as irritable bowel syndrome or lactose intolerance, teens with celiac disease may not know they have it.

Symptoms of Celiac Disease may include one or more of the following : Recurring bloating; gas or abdominal pain, Chronic diarrhea or constipation or both, Unexplained weight loss or weight gain, Pale; foul-smelling stool, Unexplained anemia, Bone or joint pain, Behavior changes / depression / irritability, Vitamin K Deficiency, Fatigue; weakness or lack of energy, Delayed growth or onset of puberty, Failure to thrive (in infants), Missed menstrual periods, Infertility male and female, Spontaneous miscarriages, Canker sores inside the mouth, Tooth discoloration or loss of enamel.

Symptoms include chronic diarrhea, failure to thrive (in children), and fatigue, but these may be absent, and symptoms in other organ systems have been described. Someone with the disease may feel tired and could be irritable or depressed. Some have skin rashes and mouth sores. Teens with undiagnosed celiac disease may go through puberty late. Someone might not show any symptoms until going through an emotionally or physically stressful event, such as going away to college, illness, or an injury or pregnancy. [1,2]

Sometimes people with celiac disease may have no gastrointestinal symptoms at all. Celiac disease symptoms can also mimic those of other conditions, such as irritable bowel syndrome, gastric ulcers, Crohn's disease, parasite infections, anemia, skin disorders or a nervous condition. [9]

People at higher risk for celiac disease are those that have type 1 diabetes, autoimmune, thyroid disease, dermatitis, herpetiformis, Down syndrome, Turner syndrome, Williams syndrome, or have a relative with celiac disease. You may still have celiac disease even though you are not in a group at higher risk.

Causes

The disease has some genetic background, which means that it may run in families. Just like eye or hair color, people inherit the genes that make them more likely to get celiac disease from their parents and grandparents. If an immediate family member (such as a parent or a sibling) has celiac disease, there's about a 5% to 10% chance that you could have it, too. Celiac disease affects people of all heritages and backgrounds. [2]

A growing portion of diagnoses are being made in asymptomatic persons as a result of increased screening. Celiac disease is caused by a reaction to gliadin, a prolamin (gluten protein) found in wheat, and similar proteins found in the crops of the tribe Triticeae (which includes other cultivars such as barley and rye). Upon exposure to gliadin, and certain other prolamins, the enzyme tissue transglutaminase modifies the protein, and the immune system cross-reacts with the small-bowel tissue, causing an inflammatory reaction. That leads to a truncating of the villi lining the small intestine (called villous atrophy). This interferes with the absorption of nutrients, because the intestinal villi are responsible for absorption. [1]

Treatment

The only known effective treatment is a lifelong gluten-free diet. While the disease is caused by a reaction to wheat proteins, it is not the same as wheat allergy.

If your nutritional deficiencies are severe, you may need to take vitamin and mineral supplements recommended by your doctor or dietitian to help correct these deficiencies. Complete healing and regrowth of the villi may take several months in younger people and as long as two to three years in older people.

If you notice or experience any of the signs or symptoms common to celiac disease, see your doctor. If someone in your family is known to have celiac disease, you may need to be tested.

ALZHEIMER’S DISEASE

ALZHEIMER’S DISEASE


General Description of Alzheimer’s Disease

Other names : Alzheimer’s presenile and senile dementia, senile dementia (Alzheimer type)
Alzheimer’s disease is a brain disorder named for German physician Alois Alzheimer, who first described it in 1906. Scientists have learned a great deal about Alzheimer’s disease in the century since Dr. Alois Alzheimer first drew attention to it.

Alzheimer's disease is the most common cause of dementia — the loss of intellectual and social abilities severe enough to interfere with daily functioning. In Alzheimer's disease, healthy brain tissue degenerates, causing a steady decline in memory and mental abilities. Alzheimer's disease is not a part of normal aging, but the risk of the disorder increases with age. About 5 percent of people between the ages of 65 and 74 have Alzheimer's disease, while nearly half the people over the age of 85 have Alzheimer's. Although there's no cure, treatments may improve the quality of life for people with Alzheimer's disease. Those with Alzheimer's — as well as those who care for them — need support and affe. [definition by Mayo Clinic]

Alzheimer's disease (AD) is a slowly progressive disease of the brain that is characterized by impairment of memory and eventually by disturbances in reasoning, planning, language, and perception. Many scientists believe that Alzheimer's disease results from an increase in the production or accumulation of a specific protein (beta-amyloid protein) in the brain that leads to nerve cell death; called amyloid plaque.

Other major hallmarks in the brain that are associated with the disease processes of AD are Neurofibrillary tangles (NFTs) and Loss of connections between neurons responsible for memory and learning.

Neurofibrillary tangles (NFTs), found inside neurons, are abnormal collections of a protein called tau. Normal tau is required for healthy neurons. However, in AD, tau clumps together. As a result, neurons fail to function normally and eventually die.
Loss of connections between neurons responsible for memory and learning. Neurons can't survive when they lose their connections to other neurons. As neurons die throughout the brain, the affected regions begin to atrophy, or shrink. By the final stage of AD, damage is widespread and brain tissue has shrunk significantly.

Prevalence

Prevalence of AD in populations is dependent upon different factors including incidence and survival. Since the incidence of AD increases with age, it is particularly important to include the mean age of the population of interest. In the United States, Alzheimer prevalence was estimated to be 1.6% in the year 2000 both overall and in the 65–74 age group, with the rate increasing to 19% in the 75–84 group and to 42% in the greater than 84 group. Prevalence rates in less developed regions are lower. The World Health Organization estimated that in 2005, 0.379% of people worldwide had dementia, and that the prevalence would increase to 0.441% in 2015 and to 0.556% in 2030. Other studies have reached similar conclusions. Another study estimated that in 2006, 0.40% of the world population (range 0.17–0.89%; absolute number 26.6 million, range 11.4–59.4 million) were afflicted by AD, and that the prevalence rate would triple and the absolute number would quadruple by the year 2050. As of September 2009, this number is reported to be 35 million-plus worldwide. The prevalence of Alzheimer's is thought to reach approximately 107 million people by 2050. [Wikipedia, December 24, 2009]

Principal Features

Insidious onset leading to progressive and permanent decline of all intellectual functions. Mood changes apathy, depression, irritability, anxiety, paranoia. Loss of recent memory, inability to recall facts of common knowledge, disorientation, confusion, all worse at night. Impaired attention, understanding, judgment. Loss of ability to think abstractly, to use language correctly, to calculate. Eventual gait disturbances, incoordination of movements. Social skills may be retained until late in course of disease. Course is from 3 to 20 years, with mean duration of 7 years.

Causes

Degeneration of nerve cell in the areas of the brain that control intellectual functions. Actual cause of degeneration in unknown. Scientists are not absolutely sure what role plaques and tangles play in Alzheimer’s disease. Most experts believe they somehow block communication among nerve cells and disrupt activities that cells need to survive.

Genetic predisposition appears probable; Alzheimer type dementia is four times more frequent among family members than in the general population. There is a history of previous head injury in 15% to 20% of cases. One common feature is a marked deficiency of the nerve transmitter acetyl-choline.

Drugs That Can Cause This Disease

No drugs cause true Alzheimer’s dementia. However, 3% of all dementias are drug induced. The following drugs can cause symptoms in the elderly that resemble Alzheimer’s disease : antidepressants, atropinelike drugs, barbiturates, benzodiazepines, butyrophenones, cortisonelike drugs, digitalis preparations, MAO inhibitors.

Drugs Used to Treat This Disease

No specific or truly effective drug treatment is available at this time. Ergoloid mesylates (Deapril-ST, Hydergine) are tried during the early stages to relieve symptoms; benefits are infrequent, negligible and fleeting.
Experimental drugs : choline, lecithin, physostigmine (none re curative or significantly beneficial). Nimodipine, a calcium channel blocking drug, is currently under study for human use. It has been shown to accelerate learning in aged rabbits.

Goals of Drug Treatment

Temporary improvement of alertness and memory. Relief of confusion, depression and behavioral disturbances.

CROHN’S DISEASE

CROHN’S DISEASE

Other Names of This Disease
Regional enteritis, regional ileitis, granulomatous colitis, inflammatory bowel disease.

Incidence of Crohn’s Disease

The incidence of Crohn's disease has been ascertained from population studies in Norway and the United States and is similar at 6 to 7.1:100,000. Crohn's disease is more common in northern countries, and shows a higher preponderance in northern areas of the same country. The incidence of Crohn's disease is thought to be similar in Europe but lower in Asia and Africa. It also has a higher incidence in Ashkenazi Jews.

The incidences of Crohn’s disease based on age group; onset from infacy to 25 years of age, 15% to 30% have onset before puberty. Peak incidence is from 10 to 25 years of age. It slightly more common in females. [Long J W, 1993]

What is Crohn's Disease ?

Crohn's disease is a chronic inflammatory disease of the intestines. Crohn's disease is one type of inflammatory bowel disease (IBD). Inflammatory bowel diseases were described by Giovanni Battista Morgagni (1682-1771), by Polish surgeon Antoni Leśniowski in 1904 (leading to the use of the eponym "Leśniowski-Crohn disease" in Poland) and by Scottish physician T. Kennedy Dalziel in 1913.

Burrill Bernard Crohn, an American gastroenterologist at New York City's Mount Sinai Hospital, described fourteen cases in 1932, and submitted them to the American Medical Association under the rubric of "Terminal ileitis: A new clinical entity". Later that year, he, along with colleagues Leon Ginzburg and Gordon Oppenheimer published the case series as "Regional ileitis: a pathologic and clinical entity".

Crohn's disease invariably affects the gastrointestinal tract, and most gastroenterologists categorize the presenting disease by the affected areas.
Ileocolic Crohn's disease, which affects both the ileum (the last part of the small intestine that connects to the large intestine) and the large intestine, accounts for fifty percent of cases. Crohn's ileitis, affecting the ileum only, accounts for thirty percent of cases, and Crohn's colitis, affecting the large intestine, accounts for the remaining twenty percent of cases and may be particularly difficult to distinguish from ulcerative colitis. The disease can attack any part of the digestive tract, from mouth to anus. However, individuals affected by the disease rarely fall outside these three classifications, being affected in other parts of the gastrointestinal tract such as the stomach and esophagus.

IBD and Colon Cancer

Having Crohn's disease increases your risk of colon cancer. Despite this increased risk, more than 90 percent of people with inflammatory bowel disease (IBD) never develop cancer. Your risk is greatest if you've had inflammatory bowel disease for at least eight years and if it has spread through your entire colon. The longer you've had the disease and the larger the area affected, the greater your risk of colon cancer. The risk of other cancers also is increased, including cancer of the anus.

Principal Features of Crohn’s Disease

An intermittent to chronic disorders of the small intestine and colon; one third of cases occur in the lower segment of the small intestine (the ileum), one third in the colon and one third in both. Less than 50% of cases involve the rectum. The onset is usually insidious, but may be rapid and resemble acute appendicitis. Symptoms include loss of appetite, fatigue, fever, loss of weight, abdominal cramps and pain after eating, nausea, vomiting, diarrhea (occasionally bloody), anal sores and retarded growth in children. There may also be inflammatory disorders in the skin, eyes, mouth and large joints. Children may experience fever and joint pains before any indications of disease in the intestine or colon. Adults may have a higher incidence of gallstones or kidney stones. This disorders often recurs throughout life.
Caution: The early manifestations of Crohn’s disease may vary. Loss of appetite and weight may lead to the mistaken diagnosis of anorexia nervosa.

Causes of Crohn’s Disease

The primary cause in unknown. There is a familial clustering in 15% to 20% of cases. It is thought that an inherited susceptibility may predispose to unknown environmental factors capable of inducing the disorder.

Drugs That Can Cause This Disease

By altering the normal balance of bacteria in the intestine, several antibiotics can cause a form of enteritis that might resemble crohn’s disease. These include some of the tetracyclines, penicillin and chloramphenicol. Antibiotic-induced enteritis is transient and easily corrected; no permanent damage occurs. The vitamin A derivative etretinate (Tegison) has been reported to cause Crohn’s disease.

Drugs Used to Treat This Disease

Sulfasalazine, cortisonelike streroids, principally prednisone, azathioprine; 6-mercaptopurine, metronidazole, antidiarrheals (diphenoxylate, loperamide), antispasmodics (belladonna, dicyclomine), antibiotics (ampicillin, tetracycline; used when appropriate for bacterial infections of intestine).

Alternative Medicine

Many people with either Crohn's disease or ulcerative colitis have used some form of complementary or alternative therapy. Some commonly used therapies include:
• Herbal and nutritional supplements
• Probiotics
• Fish oil
• Acupuncture

Treatment Goals of Crohn’s Disease

1. Induction of remission (return to normal) during the active phase of the disease.
2. Relief of symptoms.
3. Protection of bowel, avoidance of complications.
4. Maintenance of general nutrition.

Classification and external resources


The three most common sites of intestinal involvement in Crohn's disease are ileal, ileocolic and colonic

KAWASAKI SYNDROME

KAWASAKI SYNDROME


Introduction
Kawasaki syndrome (KS) was first described by Tomisaku Kawasaki in the Japanese-language medical literature in 1967. At that time, he reported his experience with 50 children who presented from 1961 to 1967 with symptoms distinct from other known childhood illnesses. He termed the condition “mucocutaneous lymph node syndrome” and originally thought that the syndrome represented a benign childhood illness. [Rowley A H and Shulman S T, 1998]

Kawasaki syndrome (KS) is the most common cause of acquired heart disease in children. This acute, self-limited vasculitis results in permanent coronary artery damage in up to 25% of untreated children. High dose intravenous gamma globulin reduces the risk of coronary artery aneurysm to 3-5% if administered early in the course of disease. However, without a specific diagnostic test, affected children may be difficult to recognize, and delayed diagnosis and treatment continue to result in potentially preventable morbidity and mortality. The etiology of Kawasaki syndrome (KS) remains unknown despite 30 years of intensive search for an agent. [Pediatr Infect Dis J. 2008;27(11):981-985)]

Incidences of Kawasaki Syndrome
In the continental United States, population-based and hospitalization studies have estimated an incidence of KS ranging from 9 to 19 per 100,000 children younger than 5 years of age. Approximately 4248 hospitalizations with KS, of which 3277 (77%) were for children under 5 years of age, were estimated among children younger than 18 years of age in the United States in the year 2000. In 2006, the number of hospitalizations with KS was 5523 (standard error [SE] 289) and the percentage of children under 5 years of age remained the same (unpublished data).

Outside the United States, the disease is most frequently observed in Japan, Taiwan, and Korea. The prevalence of Kawasaki disease increased from 1967 to the mid 1980s and has leveled out at 5000-6000 cases per year. Several epidemics occurred in Japan during the years 1979, 1982, and 1985. The current Japanese incidence is approximately 112 cases per 100,000 population.

In Indonesia, an investigation of KS on January 2005 found 100 cases, generally in children 3 months of age to 4 years of age. In the report, that wasn’t much of an accidence in children under 3 months of age or in children older than 8 years of age. Statistic-based; estimated that in Indonesia will be found 6000 – 7000 cases per year.

Causes

Kawasaki disease is a poorly understood illness. The cause has not been determined. Although, some now believe that many factors (viruses, staphylococci "super antigens") are capable of triggering a final common pathway that results in immune activation. It may be an autoimmune disorder. The disorder affects the mucus membranes, lymph nodes, walls of the blood vessels, and the heart.
Kawasaki disease can cause inflammation of blood vessels in the arteries, especially the coronary arteries. This inflammation can lead to aneurysms. An aneurysm can lead to a heart attack, even in young children, although this is rare.

Symptoms

1. High-grade fever (greater than 39 °C or 102 °F; often as high as 40 °C or 104 °F) that normally lasts for more than 5 days if left untreated.
2. Red eyes (conjunctivitis) without pus or drainage, also known as "conjunctival injection"
3. Bright red, chapped, or cracked lips
4. Red mucous membranes in the mouth
5. Strawberry tongue, white coating on the tongue or prominent red bumps (papillae) on the back of the tongue
6. Red palms of the hands and the soles of the feet
7. Rash which may take many forms, but not vesicular (blister-like), on the trunk
8. Swollen lymph nodes (frequently only one lymph node is swollen), particularly in the neck area
9. Joint pain (arthralgia) and swelling, frequently symmetrical
10. Irritability
11. Tachycardia (rapid heart beat)
12. Peeling (desquamation) palms and soles (later in the illness); peeling may begin around the nails
13. Beau's lines (transverse grooves on nails)
14. Increased peeling on palms of the hand
15. May find breathing difficult.

Additional symptoms may include: diarrhea, vomiting, abdominal pain, cough and runny nose.

Complications

The main complication of Kawasaki disease is development and rupture of coronary artery aneurysms. These aneurysms may also cause heart problems in later life. Other complications include dehydration and limited mobility from joint inflammation.

Prevention

There are no known measures that will prevent this disorder.

Treatment

Children with Kawasaki disease are admitted to the hospital. Treatment must be started as soon as the diagnosis is made to prevent damage to the coronary arteries and heart.
Intravenous gamma globulin is the standard treatment. It is given in high doses. The child's condition usually greatly improves within 24 hours of treatment with IV gamma globulin.
High-dose aspirin is often given along with IV gamma globulin.
Even when they're treated with aspirin and IVIG, up to 25% of children may still develop problems in their coronary arteries. Some research has suggested that adding steroids to the usual treatment routine may improve a child's outcome, but more research is needed.


See more informations : kidshealth, americanheart, emedicine, cdc

MEASUREMENT OF BLOOD PRESSURE WITH SPHYGMOMANOMETERS

MEASUREMENT OF BLOOD PRESSURE WITH SPHYGMOMANOMETERS


Brief History of Sphygmomanometer

Hypertension is a 20th century diseases only, because measurement of the arterial blood pressure became conveniently possible when Scipione Rivarocci (1863-1973) perfected an early version of the modern sphygmomanometer in 1896. Stephen Hales, an English clergymen, was the first to measure blood pressure directly – in a mare, in 1733 - and investigators utilizing mercury manometers had measured blood pressure in various ways in the 19th century. Richard Bright ((1789-1858), during the course of his classic studies of the diseases that bears his name, concluded that the thick left ventricle, dilated aorta, and arterial disease could be due to increased resistance to the flow of blood in the blood vessels, but Bright had no method of measuring blood pressure.

At the turn of the century, Rechklinghausen noted the falsely high levels of blood pressure (especially in the obese) that could be obtained with narrow cuffs such as those used by Riva-Rocci; the standard 12.5 cm cuff used today owes its origin to Recklinghausen’s research. Korotkoff in 1905 described the 5 sounds heard over the brachial artery, distal to the cuff, as the pressure in the sphygmomanometer is reduced: Phase I, the abrupt sharp sound as the pressure is reduced just below systolic pressure. Phase II, a prolonged, louder murmuring sound. Phase III, a load clear with only a slight murmur. Phase IV, an abrupt muffling of sounds, thought by some to represent the diastolic pressure. Phase V, the total disappearance of sounds, used usually in the USA to reflect the diastolic pressure.
Mahomed (about 1879) was the first to demonstrate that renal and cardiac disease were complications of hypertension in some patients (and not the reverse, as had been suggested by Bright and by Allbutt).

Types of Sphygmomanometers

At the modern era, there are three types of sphygmomanometers:

1. Digital with manual or automatic inflation. These are electronic, easy to operate, and practical in noisy environments. Many have not been validated for all patient groups, and they can give very inaccurate readings. They measure mean arterial pressure (MAP) and use algorithm to calculate systolic and diastolic values. In this sense, they do not actually measure the blood pressure, but rather derive the readings. Digital oscillometric monitors are also confronted with "special conditions" for which they are not designed to be used: arteriosclerosis; arrhythmia; preeclampsia; pulsus alternans; and pulsus paradoxus. Some wrist cuff blood pressure monitors have been found to be quite accurate, but the monitor has to be at the level of the heart when the reading is taken.
2. Digital portable finger blood pressure monitors with automatic inflation. These are more portable and easy to operate, although less accurate. They are the smallest blood pressure monitors.
3. Manual. Should be operated by a trained person. Mercury manometers are considered to be the "gold standard" of measurement because their measurement is absolute and does not require re-calibration. For this reason they are often required in clinical trials of pharmaceuticals and for clinical evaluations of determining blood pressure for high risk patients including pregnant women. Aneroid, mechanical types are in common use, but they should be calibrated against a mercury manometer. The unit of measurement of blood pressure is millimeters of mercury (mmHg). Blood pressures are usually given as an even number. Manual sphygmomanometers require a stethoscope for auscultation.

Regular Maintenance and Calibration of Sphygmomanometers

The Sphygmomanometer is an essential piece of equipment used daily in general medical practice, and plays a role in many routine consultations. Without regular maintenance and calibration, however, both mercury and aneroid sphygmomanometers are at risk of becoming inaccurate over time. A significant level of inaccuracy may lead to misdiagnosis of hypertension and inhibit its control, thus placing patients at unnecessary risk.

Raouse A and Marshal T (2001) in their study [1]; a researcher trained in the calibration of sphygmomanometers visited 231 general practices in the Birmingham area and calibrated 1462 mercury and aneroid sphygmomanometers. The Practices in Birmingham were asked about what arrangement had been made for maintenance and calibration of their instruments, and, in a small telephone survey, 54 practices across the country were asked the same question. Almost one in 10 of the sphygmomanometers checked gave readings that were inaccurate by more than 5 mmHg (9.2%). None of the practices visited had arrangements in place for the maintenance and calibration of their Sphygmomanometers. Of the 54 practices questioned by telephone, only one had such arrangements in place. The finding has implication for public health, primary care, and medical ethics. Inaccurate sphygmomanometers may result in the prescription of treatment to patient who do not require it.

In the other study by Mion D and Pierin AMG, 1998 [2]; was to assess the accuracy and reliability of mercury and aneroid sphygmomanometers. Measurement of accuracy of calibration and evaluation of physical conditions were carried out in 524 sphygmomanometers, 351 from a hospital setting, and 173 from private medical offices. Mercury sphygmomanometers were considered inaccurate if the meniscus was not ‘0’ at rest. Aneroid sphygmomanometers were tested against a properly calibrated mercury manometer, and were considered calibrated when the error was <3 mm Hg. Both types of sphygmomamometers were evaluated for conditions of cuff/bladder, bulb, pump and valve.

In this study; of the mercury sphygmomanometers tested 21% were found to be inaccurate. Of this group, unreliability was noted due to: excessive bouncing (14%), illegibility of the gauge (7%), blockage of the filter (6%), and lack of mercury in the reservoir (3%). Bladder damage was noted in 10% of the hospital devices and in 6% of private medical practices. Rubber aging occurred in 34% and 25%, leaks/holes in 19% and 18%, and leaks in the pump bulb in 16% and 30% of hospital devices and private practice devices, respectively. Of the aneroid sphygmomanometers tested, 44% in the hospital setting and 61% in private medical practices were found to be inaccurate. Of these, the magnitude of inaccuracy was 4–6 mm Hg in 32%, 7–12 mm Hg in 19% and . 13 mm Hg in 7%. In summary, most of the mercury and aneroid sphygmomanometers showed inaccuracy (21% vs 58%) and unreliability (64% vs 70%).

Additionally, home blood pressure readings may be more representative than those obtained in the clinicians's office. The prevalence of home sphygmomanometers in the general population is currently undocumented. The prevalence of ownership (7.5 per cent) and the accuracy of home sphygmomanometers were determined in a population-based survey in the Minneapolis-St. Paul metropolitan area. A study by Hahn LP and Folsom AR (1987) [3]; Prevalence and Accuracy of Home Sphygmomanometers
in an Urban Population. Sixty-four per cent of home sphygmomanometers were accurate within ±2 mm Hg of a calibrating sphygmomanometer; another 26 per cent were within ±3-6 mm Hg. These results suggest that although many home sphygmomanometers are accurate, some are very inaccurate. Health care providers should advise regular calibration when home sphygmomanometers are used for therapeutic self-management of hypertension.

As conclusion, the present studies showed a high incidence of inaccuracy in both aneroid and mercury sphygmomanometers, and in both hospital and private medical practice based settings. These results reinforce the recommendations made by The American Heart Association and The British Hypertension Society that aneroid and mercury sphygmomanometers must be checked regularly in order to avoid errors in blood pressure measurement and consequently the diagnosis and treatment of hypertension.

Andi Surya Amal
email : suryaamal88@gmail.com

Reference :

1. Rouse A, Marshal T (2001), The Extent and Implication of Sphygmomanometer Calibration Error in Primary Care, Journal of Human Hypertension; 15[9]:587-591
2. Mion D and Pierin AMG (1998), How accurate are sphygmomanometers?, Journal of Human Hypertension; 12, 245–248
3. Hahn LP and Folsom AR et al (1987), Prevalence and Accuracy of Home Sphygmomanometers in an Urban Population, American Journal of Public Health, Vol. 77, No. 11, 77:1459-1461
4. Markandu NK, Whitcher F, Arnold A, Carney C (2000), The Mercury sphygmomanometer should be abandoned before it is prescribed. Journal of Human Hypertension 14(1): 31-6.
5. Sokolow M and Mcllroy MB (1979), Clinical Cardiology, 2nd Ed., Lange Medical Publications, 208-209
6. Jones DW, Frohlich ED (2001), Mercury Sphygmomanometers Should Not be Abandoned: An Advisory Statement From the Council for High Blood Pressure Research, American Heart Association, Hypertension;37:185