Metronidazole Health Dictionary

A condition caused by a parasitic organism known as Giardia lamblia, which is found in the duodenum (see INTESTINE) and the upper part of the small intestine. This organism is usually harmless, but is sometimes responsible for causing diarrhoea. The illness develops one or two weeks after exposure to infection, and usually starts as an explosive diarrhoea, with the passage of pale fatty stools, abdominal pain and nausea. It responds well to METRONIDAZOLE or MEPACRINE.... giardiasis

Common chronic in?ammation of the facial skin, this condition is seen in middle and late life. Redness, obvious dilatation of venules and crops of ACNE-like papules and pustules affect mainly the central forehead, cheeks, nose and chin. A keratoconjunctivitis (combined in?ammation of the cornea and conjunctiva of the EYE) may be associated. Subjects ?ush easily, especially after alcohol or hot drinks. Eventually the affected areas may become thickened and oedematous, and in men, proliferation of ?brous and sebaceous tissue may lead to gross thickening and enlargement of the nose (RHINOPHYMA).

Treatment Long-term, low-dose, oral tetracycline (see ANTIBIOTICS; TETRACYCLINES) is the treatment of choice. In mild cases, METRONIDAZOLE gel can be helpful. Potent topical CORTICOSTEROIDS are contraindicated and make rosacea worse.... rosacea

A clinical state arising from invasive colo-rectal disease; it is accompanied by abdominal colic, diarrhoea, and passage of blood/mucus in the stool. Although the two major forms are caused by Shigella spp. (bacillary dysentery) and Entamoeba histolytica (amoebic dysentery), other organisms including entero-haemorrhagic Escherichia coli (serotypes 0157:H7 and 026:H11) and Campylobacter spp. are also relevant. Other causes of dysentery include Balantidium coli and that caused by schistosomiasis (bilharzia) – Schistosoma mansoni and S. japonicum infection.

Shigellosis This form is usually caused by Shigella dysenteriae-1 (Shiga’s bacillus), Shigella ?exneri, Shigella boydii, and Shigella sonnei; the latter is the most benign and occurs in temperate climates also. It is transmitted by food and water contamination, by direct contact, and by ?ies; the organisms thrive in the presence of overcrowding and insanitary conditions. The incubation is between one and seven days, and the severity of the illness depends on the strain responsible. Duration of illness varies from a few days to two weeks and can be particularly severe in young, old, and malnourished individuals. Complications include perforation and haemorrhage from the colo-rectum, the haemolytic uraemic syndrome (which includes renal failure), and REITER’S SYNDROME. Diagnosis is dependent on demonstration of Shigella in (a) faecal sample(s) – before or usually after culture.

If dehydration is present, this should be treated accordingly, usually with an oral rehydration technique. Shigella is eradicated by antibiotics such as trimethoprimsulphamethoxazole, trimethoprim, ampicillin, and amoxycillin. Recently, a widespread resistance to many antibiotics has developed, especially in Asia and southern America, where the agent of choice is now a quinolone compound, for example, cipro?oxacin; nalidixic acid is also e?ective. Prevention depends on improved hygiene and sanitation, careful protection of food from ?ies, ?y destruction, and garbage disposal. A Shigella carrier must not be allowed to handle food.

Entamoeba histolytica infection Most cases occur in the tropics and subtropics. Dysentery may be accompanied by weight loss, anaemia, and occasionally DYSPNOEA. E. histolytica contaminates food (e.g. uncooked vegetables) or drinking water. After ingestion of the cyst-stage, and following the action of digestive enzymes, the motile trophozoite emerges in the colon causing local invasive disease (amoebic colitis). On entering the portal system, these organisms may gain access to the liver, causing invasive hepatic disease (amoebic liver ‘abscess’). Other sites of ‘abscess’ formation include the lungs (usually right) and brain. In the colo-rectum an amoeboma may be di?cult to di?erentiate from a carcinoma. Clinical symptoms usually occur within a week, but can be delayed for months, or even years; onset may be acute – as for Shigella spp. infection. Perforation, colo-rectal haemorrhage, and appendicitis are unusual complications. Diagnosis is by demonstration of E. histolytica trophozoites in a fresh faecal sample; other amoebae affecting humans do not invade tissues. Research techniques can be used to di?erentiate between pathogenic (E. dysenteriae) and non-pathogenic strains (E. dispar). Alternatively, several serological tests are of value in diagnosis, but only in the presence of invasive disease.

Treatment consists of one of the 5nitroimidazole compounds – metronidazole, tinidazole, and ornidazole; alcohol avoidance is important during their administration. A ?ve- to ten-day course should be followed by diloxanide furoate for ten days. Other compounds – emetine, chloroquine, iodoquinol, and paromomycin – are now rarely used. Invasive disease involving the liver or other organ(s) usually responds favourably to a similar regimen; aspiration of a liver ‘abscess’ is now rarely indicated, as controlled trials have indicated a similar resolution rate whether this technique is used or not, provided a 5-nitroimidazole compound is administered.... dysentery

An infection caused by the protozoan TRICHOMONAS VAGINALIS. Trichomoniasis is a common cause of vaginitis. In some cases, the infection is sexually transmitted.

In women, the causative organism may inhabit the vagina for years without causing symptoms. If symptoms occur, they include painful inflammation of the vagina and vulva, and a greenish, frothy, offensive-smelling discharge. Men usually have no symptoms.

The diagnosis is made from examination of a sample of the discharge. Diagnosis usually difficult in men. Treatment is with metronidazole. The sexual partner or partners of an infected person should be treated at the same time to prevent reinfection.... trichomoniasis

A form of dysentery caused by a protozoon known as Balantidium coli – a common parasite in pigs, which are usually the source of infection. It responds to metronidazole.... balantidiasis

(Ale)

Nutritional Profile Energy value (calories per serving): Low Protein: Moderate Fat: None Saturated fat: None Cholesterol: None Carbohydrates: High Fiber: None Sodium: Low Major vitamin contribution: B vitamins Major mineral contribution: Phosphorus

About the Nutrients in This Food Beer and ale are fermented beverages created by yeasts that convert the sugars in malted barley and grain to ethyl alcohol (a.k.a. “alcohol,” “drink- ing alcohol”).* The USDA /Health and Human Services Dietary Guidelines for Americans defines one drink as 12 ounces of beer, five ounces of wine, or 1.25 ounces of distilled spirits. One 12-ounce glass of beer has 140 calo- ries, 86 of them (61 percent) from alcohol. But the beverage—sometimes nicknamed “liquid bread”—is more than empty calories. Like wine, beer retains small amounts of some nutrients present in the food from which it was made. * Because yeasts cannot digest t he starches in grains, t he grains to be used in mak ing beer and ale are allowed to germinate ( “malt” ). When it is t ime to make t he beer or ale, t he malted grain is soaked in water, forming a mash in which t he starches are split into simple sugars t hat can be digested (fermented) by t he yeasts. If undisturbed, t he fermentat ion will cont inue unt il all t he sugars have been digested, but it can be halted at any t ime simply by raising or lowering t he temperature of t he liquid. Beer sold in bott les or cans is pasteurized to k ill t he yeasts and stop t he fermentat ion. Draft beer is not pasteurized and must be refrigerated unt il tapped so t hat it will not cont inue to ferment in t he container. The longer t he shipping t ime, t he more likely it is t hat draft beer will be exposed to temperature variat ions t hat may affect its qualit y—which is why draft beer almost always tastes best when consumed near t he place where it was brewed. The Nutrients in Beer (12-ounce glass)

Nutrients	Beer	%R DA
Calcium	17 mg	1.7
Magnesium	28.51 mg	7–9*
Phosphorus	41.1 mg	6
Potassium	85.7 mg	(na)
Zinc	0.06 mg	0.5– 0.8*
Thiamin	0.02 mg	1.6 –1.8*
R iboflavin	0.09 mg	7– 8*
Niacin	1.55 mg	10
Vitamin B6	0.17 mg	13
Folate	20.57 mcg	5

  * t he first figure is t he %R DA for a man; t he second, for a woman Source: USDA Nut rient Database: w w w.nal.usda.gov/fnic/cgi-bin /nut _search.pl.

Diets That May Restrict or Exclude This Food Bland diet Gluten-free diet Low-purine (antigout) diet

Buying This Food Look for: A popular brand that sells steadily and will be fresh when you buy it. Avoid: Dusty or warm bottles and cans.

Storing This Food Store beer in a cool place. Beer tastes best when consumed within two months of the day it is made. Since you cannot be certain how long it took to ship the beer to the store or how long it has been sitting on the grocery shelves, buy only as much beer as you plan to use within a week or two. Protect bottled beer and open bottles or cans of beer from direct sunlight, which can change sulfur compounds in beer into isopentyl mercaptan, the smelly chemical that gives stale beer its characteristic unpleasant odor.

When You Are Ready to Serve This Food Serve beer only in absolutely clean glasses or mugs. Even the slightest bit of grease on the side of the glass will kill the foam immediately. Wash beer glasses with detergent, not soap, and let them drain dry rather than drying them with a towel that might carry grease from your hands to the glass. If you like a long-lasting head on your beer, serve the brew in tall, tapering glasses to let the foam spread out and stabilize. For full flavor, serve beer and ales cool but not ice-cold. Very low temperatures immo- bilize the molecules that give beer and ale their flavor and aroma.

What Happens When You Cook This Food When beer is heated (in a stew or as a basting liquid), the alcohol evaporates but the flavor- ing agents remain intact. Alcohol, an acid, reacts with metal ions from an aluminum or iron pot to form dark compounds that discolor the pot or the dish you are cooking in. To prevent this, prepare dishes made with beer in glass or enameled pots.

Medical Uses and/or Benefits Reduced risk of heart attack. Data from the American Cancer Society’s Cancer Prevention Study 1, a 12-year survey of more than 1 million Americans in 25 states, shows that men who take one drink a day have a 21 percent lower risk of heart attack and a 22 percent lower risk of stroke than men who do not drink at all. Women who have up to one drink a day also reduce their risk of heart attack. Numerous later studies have confirmed these findings. Lower risk of stroke. In January 1999, the results of a 677-person study published by researchers at New York Presbyterian Hospital-Columbia University showed that moder- ate alcohol consumption reduces the risk of stroke due to a blood clot in the brain among older people (average age: 70). How the alcohol prevents stroke is still unknown, but it is clear that moderate use of alcohol is a key. Heavy drinkers (those who consume more than seven drinks a day) have a higher risk of stroke. People who once drank heavily, but cut their consumption to moderate levels, can also reduce their risk of stroke. Numerous later studies have confirmed these findings. Lower cholesterol levels. Beverage alcohol decreases the body’s production and storage of low-density lipoproteins (LDLs), the protein and fat particles that carr y cholesterol into your arteries. As a result, people who drink moderately tend to have lower cholesterol levels and higher levels of high density lipoproteins (HDLs), the fat and protein particles that carr y cholesterol out of the body. The USDA /Health and Human Services Dietar y Guidelines for Americans defines moderation as two drinks a day for a man, one drink a day for a woman. Stimulating the appetite. Alcoholic beverages stimulate the production of saliva and the gastric acids that cause the stomach contractions we call hunger pangs. Moderate amounts of alcoholic beverages, which may help stimulate appetite, are often prescribed for geriatric patients, convalescents, and people who do not have ulcers or other chronic gastric problems that might be exacerbated by the alcohol. Dilation of blood vessels. Alcohol dilates the capillaries (the tiny blood vessels just under the skin), and moderate amounts of alcoholic beverages produce a pleasant flush that temporar- ily warms the drinker. But drinking is not an effective way to warm up in cold weather since the warm blood that flows up to the capillaries will cool down on the surface of your skin and make you even colder when it circulates back into the center of your body. Then an alco- hol flush will make you perspire, so that you lose more heat. Excessive amounts of beverage alcohol may depress the mechanism that regulates body temperature.

Adverse Effects Associated with This Food Increased risk of breast cancer. In 2008, scientists at the National Cancer Institute released data from a seven-year survey of more than 100,000 postmenopausal women showing that even moderate drinking (one to two drinks a day) may increase by 32 percent a woman’s risk of developing estrogen-receptor positive (ER+) and progesterone-receptor positive (PR+) breast cancer, tumors whose growth is stimulated by hormones. No such link was found between consuming alcohol and the risk of developing ER-/PR- tumors (not fueled by hor- mones). The finding applies to all types of alcohol: beer, wine, and spirits. Increased risk of oral cancer (cancer of the mouth and throat). Numerous studies confirm the American Cancer Society’s warning that men and women who consume more than two drinks a day are at higher risk of oral cancer than are nondrinkers or people who drink less. Note: The Dietary Guidelines for Americans describes one drink as 12 ounces of beer, five ounces of wine, or 1.5 ounces of distilled spirits. Increased risk of cancer of the colon and rectum. In the mid-1990s, studies at the University of Oklahoma suggested that men who drink more than five beers a day are at increased risk of rectal cancer. Later studies suggested that men and women who are heavy beer or spirits drinkers (but not those who are heavy wine drinkers) have a higher risk of colorectal cancers. Further studies are required to confirm these findings. Fetal alcohol syndrome. Fetal alcohol syndrome is a specific pattern of birth defects—low birth weight, heart defects, facial malformations, and mental retardation—first recognized in a study of babies born to alcoholic women who consumed more than six drinks a day while pregnant. Subsequent research has found a consistent pattern of milder defects in babies born to women who consume three to four drinks a day or five drinks on any one occasion while pregnant. To date, there is no evidence of a consistent pattern of birth defects in babies born to women who consume less than one drink a day while pregnant, but two studies at Columbia University have suggested that as few as two drinks a week while preg- nant may raise a woman’s risk of miscarriage. (“One drink” means 12 ounces of beer, five ounces of wine, or 1.25 ounces of distilled spirits.) Alcoholism. Alcoholism is an addiction disease, the inability to control one’s alcohol consumption. It is a potentially life-threatening condition, with a higher risk of death by accident, suicide, malnutrition, or acute alcohol poisoning, a toxic reaction that kills by para- lyzing body organs, including the heart. Malnutrition. While moderate alcohol consumption stimulates appetite, alcohol abuse depresses it. In addition, an alcoholic may drink instead of eating. When an alcoholic does eat, excess alcohol in his/her body prevents absorption of nutrients and reduces the ability to synthesize new tissue. Hangover. Alcohol is absorbed from the stomach and small intestine and carried by the bloodstream to the liver, where it is oxidized to acetaldehyde by alcohol dehydrogenase (ADH), the enzyme our bodies use to metabolize the alcohol we produce when we digest carbohydrates. The acetaldehyde is converted to acetyl coenzyme A and either eliminated from the body or used in the synthesis of cholesterol, fatty acids, and body tissues. Although individuals vary widely in their capacity to metabolize alcohol, on average, normal healthy adults can metabolize the alcohol in one quart of beer in approximately five to six hours. If they drink more than that, they will have more alcohol than the body’s natural supply of ADH can handle. The unmetabolized alcohol will pile up in the bloodstream, interfering with the liver’s metabolic functions. Since alcohol decreases the reabsorption of water from the kidneys and may inhibit the secretion of an antidiuretic hormone, they will begin to urinate copiously, losing magnesium, calcium, and zinc but retaining more irritating uric acid. The level of lactic acid in the body will increase, making them feel tired and out of sorts; their acid-base balance will be out of kilter; the blood vessels in their heads will swell and throb; and their stomachs, with linings irritated by the alcohol, will ache. The ultimate result is a “hangover” whose symptoms will disappear only when enough time has passed to allow their bodies to marshal the ADH needed to metabolize the extra alcohol in their blood. Changes in body temperature. Alcohol dilates capillaries, tiny blood vessels just under the skin, producing a “flush” that temporarily warms the drinker. But drinking is not an effective way to stay warm in cold weather. Warm blood flowing up from the body core to the surface capillaries is quickly chilled, making you even colder when it circulates back into your organs. In addition, an alcohol flush triggers perspiration, further cooling your skin. Finally, very large amounts of alcohol may actually depress the mechanism that regulates body temperature. Impotence. Excessive drinking decreases libido (sexual desire) and interferes with the ability to achieve or sustain an erection. “Beer belly.” Data from a 1995, 12,000 person study at the University of North Carolina in Chapel Hill show that people who consume at least six beers a week have more rounded abdomens than people who do not drink beer. The question left to be answered is which came first: the tummy or the drinking.

Food/Drug Interactions Acetaminophen (Tylenol, etc.). The FDA recommends that people who regularly have three or more drinks a day consult a doctor before using acetaminophen. The alcohol/acetamino- phen combination may cause liver failure. Disulfiram (Antabuse). Taken with alcohol, disulfiram causes flushing, nausea, low blood pressure, faintness, respiratory problems, and confusion. The severity of the reaction gener- ally depends on how much alcohol you drink, how much disulfiram is in your body, and how long ago you took it. Disulfiram is used to help recovering alcoholics avoid alcohol. (If taken with alcohol, metronidazole [Flagyl], procarbazine [Matulane], quinacrine [Atabrine], chlorpropamide (Diabinase), and some species of mushrooms may produce a mild disulfi- ramlike reaction.) Anticoagulants. Alcohol slows the body’s metabolism of anticoagulants (blood thinners) such as warfarin (Coumadin), intensif ying the effect of the drugs and increasing the risk of side effects such as spontaneous nosebleeds. Antidepressants. Alcohol may increase the sedative effects of antidepressants. Drinking alcohol while you are taking a monoamine oxidase (M AO) inhibitor is especially hazard- ous. M AO inhibitors inactivate naturally occurring enzymes in your body that metabolize tyramine, a substance found in many fermented or aged foods. Tyramine constricts blood vessels and increases blood pressure. If you eat a food containing tyramine while you are taking an M AO inhibitor, you cannot effectively eliminate the tyramine from your body. The result may be a hypertensive crisis. Ordinarily, fermentation of beer and ale does not produce tyramine, but some patients have reported tyramine reactions after drinking some imported beers. Beer and ale are usually prohibited to those using M AO inhibitors. Aspirin, ibuprofen, ketoprofen, naproxen, and nonsteroidal anti-inflammatory drugs. Like alcohol, these analgesics irritate the lining of the stomach and may cause gastric bleeding. Combining the two intensifies the effect. Insulin and oral hypoglycemics. Alcohol lowers blood sugar and interferes with the metabo- lism of oral antidiabetics; the combination may cause severe hypoglycemia. Sedatives and other central nervous system depressants (tranquilizers, sleeping pills, antidepres- sants, sinus and cold remedies, analgesics, and medication for motion sickness). Alcohol inten- sifies sedation and, depending on the dose, may cause drowsiness, respiratory depression, coma, or death.... beer

The prevention or treatment of disease by chemical substances. The term is generally used in two senses: the use of antibacterial and other drugs to treat infections; and the administration of ANTIMETABOLITES and other drugs to treat cancer. The discovery by Paul Ehrlich in 1910 of the action of Salvarsan in treating syphilis led to the introduction of sulphonamides in 1935, followed by PENICILLIN during World War II, which revolutionised the treatment of common infections. Many ANTIBACTERIAL DRUGS have been developed since then: these include CEPHALOSPORINS, cephamycins, TETRACYCLINES, AMINOGLYCOSIDES, MACROLIDES and CLINDAMYCIN as well as antituberculous drugs such as STREPTOMYCIN and METRONIDAZOLE. Unfortunately, overuse of chemotherapeutic drugs in medicine and in animal husbandry has stimulated widespread resistance among previously susceptible pathogenic microorganisms. Chemotherapy also plays an important role in treating tropical diseases, especially MALARIA, SLEEPING SICKNESS and LEPROSY.

Recently chemotherapy has become increasingly e?ective in the treatment of cancer. Numerous drugs, generally CYTOTOXIC, are available; great care is required in their selection and to minimise side-effects. Certain tumours are highly sensitive to chemotherapy

– especially testicular tumours, LEUKAEMIA, LYMPHOMA and various tumours occurring in childhood (e.g. Wilm’s tumour – see NEPHROBLASTOMA) – and may even be cured.... chemotherapy

This disorder is related to gastric ulcer (see STOMACH, DISEASES OF), both being a form of chronic peptic ulcer. Although becoming less frequent in western communities, peptic ulcers still affect around 10 per cent of the UK population at some time. Duodenal ulcers are 10–15 times more common than gastric ulcers, and occur in people aged from 20 years onwards. The male to female ratio for duodenal ulcer varies between 4:1 and 2:1 in di?erent communities. Social class and blood groups are also in?uential, with duodenal ulcer being more common among the upper social classes, and those of blood group O.

Causes It is likely that there is some abrasion, or break, in the lining membrane (or mucosa) of the stomach and/or duodenum, and that it is gradually eroded and deepened by the acidic gastric juice. The bacterium helicobacter pylori is present in the antrum of the stomach of people with peptic ulcers; 15 per cent of people infected with the bacterium develop an ulcer, and the ulcers heal if H. pylori is eradicated. Thus, this organism has an important role in creating ulcers. Mental stress may possibly be a provocative factor. Smoking seems to accentuate, if not cause, duodenal ulcer, and the drinking of alcohol is probably harmful. The apparent association with a given blood group, and the fact that relatives of a patient with a peptic ulcer are unduly likely to develop such an ulcer, suggest that there is some constitutional factor.

Symptoms and signs Peptic ulcers may present in di?erent ways, but chronic, episodic pain lasting several months or years is most common. Occasionally, however, there may be an acute episode of bleeding or perforation, or obstruction of the gastric outlet, with little previous history. Most commonly there is pain of varying intensity in the middle or upper right part of the abdomen. It tends to occur 2–3 hours after a meal, most commonly at night, and is relieved by some food such as a glass of milk; untreated it may last up to an hour. Vomiting is unusual, but there is often tenderness and sti?ness (‘guarding’) of the abdominal muscles. Con?rmation of the diagnosis is made by radiological examination (‘barium meal’), the ulcer appearing as a niche on the ?lm, or by looking at the ulcer directly with an endoscope (see FIBREOPTIC ENDOSCOPY). Chief complications are perforation of the ulcer, leading to the vomiting of blood, or HAEMATEMESIS; or less severe bleeding from the ulcer, the blood passing down the gut, resulting in dark, tarry stools (see MELAENA).

Treatment of a perforation involves initial management of any complications, such as shock, haemorrhage, perforation, or gastric outlet obstruction, usually involving surgery and blood replacement. Medical treatment of a chronic ulcer should include regular meals, and the avoidance of fatty foods, strong tea or co?ee and alcohol. Patients should also stop smoking and try to reduce the stress in their lives. ANTACIDS may provide symptomatic relief. However, the mainstay of treatment involves four- to six-week courses with drugs such as CIMETIDINE and RANITIDINE. These are H2 RECEPTOR ANTAGONISTS which heal peptic ulcers by reducing gastric-acid output. Of those relapsing after stopping this treatment, 60–95 per cent have infection with H. pylori. A combination of BISMUTH chelate, amoxycillin (see PENICILLIN; ANTIBIOTICS) and METRONIDAZOLE – ‘triple regime’ – should eliminate the infection: most physicians advise the triple regime as ?rst-choice treatment because it is more likely to eradicate Helicobacter and this, in turn, enhances healing of the ulcer or prevents recurrence. Surgery may be necessary if medical measures fail, but its use is much rarer than before e?ective medical treatments were developed.... duodenal ulcer

A rare chronic in?ammatory disease in the ileal pouch, which remains after a patient has had intestinal resection because of INFLAMMATORY BOWEL DISEASE (IBD). Metronidazole and oral PROBIOTICS are e?ective treatments.... pouchitis

Gastritis is the description for several unrelated diseases of the gastric mucosa.

Acute gastritis is an in?ammatory reaction of the gastric mucosa to various precipitating factors, ranging from physical and chemical injury to infections. Acute gastritis (especially of the antral mucosas) may well represent a reaction to infection by a bacterium called Helicobacter pylori. The in?ammatory changes usually go after appropriate antibiotic treatment for the H. pylori infection. Acute and chronic in?ammation occurs in response to chemical damage of the gastric mucosa. For example, REFLUX of duodenal contents may predispose to in?ammatory acute and chronic gastritis. Similarly, multiple small erosions or single or multiple ulcers have resulted from consumption of chemicals, especialy aspirin and antirheumatic NONSTEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS).

Acute gastritis may cause anorexia, nausea, upper abdominal pain and, if erosive, haemorrhage. Treatment involves removal of the o?ending cause.

Chronic gastritis Accumulation of cells called round cells in the gastric mucosal characterises chronic gastritis. Most patients with chronic gastritis have no symptoms, and treatment of H. pylori infection usually cures the condition.

Atrophic gastritis A few patients with chronic gastritis may develop atrophic gastritis. With or without in?ammatory change, this disorder is common in western countries. The incidence increases with age, and more than 50 per cent of people over 50 may have it. A more complete and uniform type of ATROPHY, called ‘gastric atrophy’, characterises a familial disease called PERNICIOUS ANAEMIA. The cause of the latter disease is not known but it may be an autoimmune disorder.

Since atrophy of the corpus mucosa results in loss of acid- and pepsin-secreting cells, gastric secretion is reduced or absent. Patients with pernicious anaemia or severe atrophic gastritis of the corpus mucosa may secrete too little intrinsic factor for absorption of vitamin B12 and so can develop severe neurological disease (subacute combined degeneration of the spinal cord).

Patients with atrophic gastritis often have bacterial colonisation of the upper alimentary tract, with increased concentration of nitrite and carcinogenic N-nitroso compounds. These, coupled with excess growth of mucosal cells, may be linked to cancer. In chronic corpus gastritis, the risk of gastric cancer is about 3–4 times that of the general population.

Postgastrectomy mucosa The mucosa of the gastric remnant after surgical removal of the distal part of the stomach is usually in?amed and atrophic, and is also premalignant, with the risk of gastric cancer being very much greater than for patients with duodenal ulcer who have not had surgery.

Stress gastritis Acute stress gastritis develops, sometimes within hours, in individuals who have undergone severe physical trauma, BURNS (Curling ulcers), severe SEPSIS or major diseases such as heart attacks, strokes, intracranial trauma or operations (Cushing’s ulcers). The disorder presents with multiple super?cial erosions or ulcers of the gastric mucosa, with HAEMATEMESIS and MELAENA and sometimes with perforation when the acute ulcers erode through the stomach wall. Treatment involves inhibition of gastric secretion with intravenous infusion of an H2-receptorantagonist drug such as RANITIDINE or FAMOTIDINE, so that the gastric contents remain at a near neutral pH. Despite treatment, a few patients continue to bleed and may then require radical gastric surgery.

Gastric ulcer Gastric ulcers were common in young women during the 19th century, markedly fell in frequency in many western countries during the ?rst half of the 20th century, but remained common in coastal northern Norway, Japan, in young Australian women, and in some Andean populations. During the latter half of this century, gastric ulcers have again become more frequent in the West, with a peak incidence between 55 and 65 years.

The cause is not known. The two factors most strongly associated with the development of duodenal ulcers – gastric-acid production and gastric infection with H. pylori bacteria – are not nearly as strongly associated with gastric ulcers. The latter occur with increased frequency in individuals who take aspirin or NSAIDs. In healthy individuals who take NSAIDs, as many as 6 per cent develop a gastric ulcer during the ?rst week of treatment, while in patients with rheumatoid arthritis who are being treated long term with drugs, gastric ulcers occur in 20–40 per cent. The cause is inhibition of the enzyme cyclo-oxygenase, which in turn inhibits the production of repair-promoting PROSTAGLANDINS.

Gastric ulcers occur especially on the lesser curve of the stomach. The ulcers may erode through the whole thickness of the gastric wall, perforating into the peritoneal cavity or penetrating into liver, pancreas or colon.

Gastric ulcers usually present with a history of epigastric pain of less than one year. The pain tends to be associated with anorexia and may be aggravated by food, although patients with ‘prepyloric’ ulcers may obtain relief from eating or taking antacid preparations. Patients with gastric ulcers also complain of nausea and vomiting, and lose weight.

The principal complications of gastric ulcer are haemorrhage from arterial erosion, or perforation into the peritoneal cavity resulting in PERITONITIS, abscess or ?stula.

Aproximately one in two gastric ulcers heal ‘spontaneously’ in 2–3 months; however, up to 80 per cent of the patients relapse within 12 months. Repeated recurrence and rehealing results in scar tissue around the ulcer; this may cause a circumferential narrowing – a condition called ‘hour-glass stomach’.

The diagnosis of gastric ulcer is con?rmed by ENDOSCOPY. All patients with gastric ulcers should have multiple biopsies (see BIOPSY) to exclude the presence of malignant cells. Even after healing, gastric ulcers should be endoscopically monitored for a year.

Treatment of gastric ulcers is relatively simple: a course of one of the H2 RECEPTOR ANTAGONISTS heals gastric ulcers in 3 months. In patients who relapse, long-term inde?nite treatment with an H2 receptor antagonist such as ranitidine may be necessary since the ulcers tend to recur. Recently it has been claimed that gastric ulcers can be healed with a combination of a bismuth salt or a gastric secretory inhibitor

for example, one of the PROTON PUMP INHIBITORS such as omeprazole or lansoprazole

together with two antibiotics such as AMOXYCILLIN and METRONIDAZOLE. The long-term outcome of such treatment is not known. Partial gastrectomy, which used to be a regular treatment for gastric ulcers, is now much more rarely done unless the ulcer(s) contain precancerous cells.

Cancer of the stomach Cancer of the stomach is common and dangerous and, worldwide, accounts for approximately one in six of all deaths from cancer. There are marked geographical di?erences in frequency, with a very high incidence in Japan and low incidence in the USA. In the United Kingdom around 33 cases per 100,000 population are diagnosed annually. Studies have shown that environmental factors, rather than hereditary ones, are mainly responsible for the development of gastric cancer. Diet, including highly salted, pickled and smoked foods, and high concentrations of nitrate in food and drinking water, may well be responsible for the environmental effects.

Most gastric ulcers arise in abnormal gastric mucosa. The three mucosal disorders which especially predispose to gastric cancer include pernicious anaemia, postgastrectomy mucosa, and atrophic gastritis (see above). Around 90 per cent of gastric cancers have the microscopic appearance of abnormal mucosal cells (and are called ‘adenocarcinomas’). Most of the remainder look like endocrine cells of lymphoid tissue, although tumours with mixed microscopic appearance are common.

Early gastric cancer may be symptomless and, in countries like Japan with a high frequency of the disease, is often diagnosed during routine screening of the population. In more advanced cancers, upper abdominal pain, loss of appetite and loss of weight occur. Many present with obstructive symptoms, such as vomiting (when the pylorus is obstructed) or di?culty with swallowing. METASTASIS is obvious in up to two-thirds of patients and its presence contraindicates surgical cure. The diagnosis is made by endoscopic examination of the stomach and biopsy of abnormal-looking areas of mucosa. Treatment is surgical, often with additional chemotherapy and radiotherapy.... stomach, diseases of

A protozoon normally present in the VAGINA of about 30–40 per cent of women. It sometimes becomes pathogenic and causes in?ammation of the genital passages, with vaginal discharge. A man may become infected as a result of sexual intercourse with an infected woman and suffer from a urethral discharge; it may also cause prostatitis (see under PROSTATE GLAND, DISEASES OF). METRONIDAZOLE is usually an e?ective treatment, and to obtain a satisfactory result it may be necessary to treat both partners. Should metronidazole not work, then tinidazole may be tried.... trichomonas vaginalis

The term used to describe several clinical entities caused by one or other of the nematode ?lariae; these include Wuchereria bancrofti/Brugia malayi, Onchocerca volvulus, Loa loa, Dracunculus medinensis (DRACONTIASIS or guinea-worm disease), Mansonella perstans, etc. These organisms have widely di?ering geographical distributions. Whereas lymphatic ?lariasis is present throughout much of the tropics and subtropics, ONCHOCERCIASIS (river-blindness) is largely con?ned to west and central Africa and southern America. Loaiasis is an infection of west and central Africa, and dracontiasis involves west and central Africa and western India only.

Clinically, the lymphatic ?lariases characteristically cause ELEPHANTIASIS (lymphoedema); onchocerciasis gives rise to ophthalmic complications (river-blindness), rashes and subcutaneous nodules; loaiasis causes subcutaneous ‘Calabar swellings’ and subconjunctival involvement; and dracontiasis predisposes to secondary bacterial infections (usually involving the lower limbs). Diagnosis is by ?nding the relevant ?larial nematode, either in blood (day and night ?lms should be examined), or in one or other of the body ?uids. An EOSINOPHILIA is often present in peripheral blood. Serological diagnosis is also of value. In onchocerciasis, skin-snips and the Mazotti reaction are valuable adjuncts to diagnosis.

The mainstay of chemotherapy consists of diethylcarbamazine (aimed predominantly at the larval stage of the parasite). However, ivermectin (not available in the UK) is e?ective in onchocerciasis, and metronidazole or one of the benzimidazole compounds have limited value in dracontiasis. Suramin has been used to kill adult ?larial worms. Prevention consists of eradication of the relevant insect vector.... filariasis

A group of drugs used to treat amoebiasis. Examples are diloxanide, and metronidazole.... amoebicides

a condition caused by overgrowth of certain species of the bacteria that are normally present in the vagina (e.g. Bacteroides, *Gardnerella vaginalis). One of the most common vaginal infections, it is marked by a greyish watery vaginal discharge with a characteristic fishy odour. Treatment is with clindamycin or metronidazole.... bacterial vaginosis

acute painful gingivitis with ulceration, in which the tissues of the gums are rapidly destroyed. Occurring mainly in debilitated patients, it is associated with anaerobic microorganisms (see Fusobacterium; Bacteroides) and is accompanied by an unpleasant odour. Treatment is with *metronidazole and a careful and thorough regime of oral hygiene supplemented with oxidizing mouthwashes. In the past ulcerative gingivitis has been called acute necrotizing ulcerative gingivitis (ANUG), Vincent stomatitis, or Vincent’s angina. A rare complication of severe ulcerative gingivitis is a *noma.... ulcerative gingivitis

The LIVER may be extensively diseased without any obviously serious symptoms, unless the circulation through it is impeded, the out?ow of BILE checked, or neighbouring organs implicated. JAUNDICE is a symptom of several liver disorders, and is discussed under its separate heading. ASCITES, which may be caused by interference with the circulation through the portal vein of the liver, as well as by other reasons, is also considered separately. The presence of gallstones is a complication of some diseases connected with the liver, and is treated under GALLBLADDER, DISEASES OF. For hydatid cyst of the liver, see TAENIASIS. Liver diseases in a tropical environment are dealt with later in this section.

In?ammation of the liver, or HEPATITIS, may occur as part of a generalised infection or may be a localised condition. Infectious hepatitis, which is the result of infection with a virus, is one of the most common forms. Many di?erent viruses can cause hepatitis, including that responsible for glandular fever (see MONONUCLEOSIS). Certain spirochaetes may also be the cause, particularly that responsible for LEPTOSPIROSIS, as can many drugs. Hepatitis may also occur if there is obstruction of the BILE DUCT, as by a gall-stone.

Cirrhosis of the liver A disorder caused by chronic damage to liver cells. The liver develops areas of ?brosis or scarring; in response, the remaining normal liver cells increase and form regeneration nodules. Those islands of normality, however, suffer from inadequate blood supply, thus adversely affecting liver function. Alcohol is the most common cause of cirrhosis in the United Kingdom and the USA, and the incidence of the disorder among women in the UK has recently risen sharply as a consequence of greater consumption of alcohol by young women in the latter decades of the 20th century. In Africa and many parts of Asia, infection with hepatitis B virus is a common cause. Certain drugs – for example, PARACETAMOL – may damage the liver if taken in excess. Unusual causes of cirrhosis include defects of the bile ducts, HAEMOCHROMATOSIS (raised iron absorption from the gut), CYSTIC FIBROSIS, cardiac cirrhosis (the result of heart failure causing circulatory congestion in the liver), and WILSON’S DISEASE (raised copper absorption).

Symptoms Some people with cirrhosis have no signs or symptoms and the disease may be diagnosed at a routine medical examination. Others may develop jaundice, OEDEMA (including ascites – ?uid in the abdomen), fever, confusion, HAEMATEMESIS (vomiting blood), loss of appetite and lethargy. On examination, cirrhotic patients often have an enlarged liver and/ or SPLEEN, and HYPERTENSION. Liver function tests, cholangiography (X-ray examination of the bile ducts) and biopsy of liver tissue will help to reach a diagnosis.

Treatment Nothing can be done to repair a cirrhosed organ, but the cause, if known, must be removed and further advance of the process thus prevented. In the case of the liver, a high-protein, high-carbohydrate, low-fat diet is given, supplemented by liver extract and vitamins B and K. The consumption of alcohol should be banned. In patients with liver failure and a poor prognosis, liver TRANSPLANTATION is worthwhile but only after careful consideration.

Abscess of the liver When an ABSCESS develops in the liver, it is usually a result of amoebic DYSENTERY, appearing sometimes late in the disease – even after the diarrhoea is cured (see below). It may also follow upon in?ammation of the liver due to other causes. In the case of an amoebic abscess, treatment consists of oral metronidazole.

Acute hepatic necrosis is a destructive and often fatal disease of the liver which is very rare. It may be due to chemical poisons, such as carbontetrachloride, chloroform, phosphorus and industrial solvents derived from benzene. It may also be the cause of death in cases of poisoning with fungi. Very occasionally, it may be a complication of acute infectious hepatitis.

Cancer of the liver is not uncommon, although it is rare for the disease to begin in the liver – the involvement of this organ being usually secondary to disease situated somewhere in the stomach or bowels. Cancer originating in the liver is more common in Asia and Africa. It usually arises in a ?brotic (or cirrhotic) liver and in carriers of the hepatitis B virus. There is great emaciation, which increases as the disease progresses. The liver is much enlarged, and its margin and surface are rough, being studded with hard cancer masses of varying size, which can often be felt through the abdominal wall. Pain may be present. Jaundice and oedema often appear.... liver, diseases of

Linn.

Family: Compositae; Asteraceae.

Habitat: Tropical and subtropical countries of the world.

English: Congress Grass.

Folk: Pichhi, Machhipatri.

Action: Anti-amoebic, antidysen- teric, febrifuge, analgesic, emmena- gogue.

The grass was introduced into India during 1950 s (it first appeared in Pune).

The grass exhibits in vitro anti- amoebic activity against axenic and polygenic cultures of Entamoeba his- tolytica, comparable to the standard drug for amoebiasis, Metronidazole.

Parthenin and some of its derivatives exhibited significant antimalarial activity against a multi drug-resistant strain of Plasmodium falciparum.

The main toxic constituent of the grass responsible for causing dermatitis and other forms of allergy are parthenin and coronopilin. Parthenin in present up to 8% in the capitulum and 5% in the leaves.... parthenium hysterophorus

A variety of drugs with di?ering actions are available for the treatment of peptic ulcer, the composite title covering gastric ulcer (see STOMACH, DISEASES OF) and DUODENAL ULCER. Peptic ulceration may also involve the lower OESOPHAGUS, and after stomach surgery the junction of the stomach and small intestine.

The drugs used in combination are:

The receptor antagonists, which reduce the output of gastric acid by histamine H2receptor blockade; they include CIMETIDINE, FAMOTIDINE and RANITIDINE.

ANTIBIOTICS to eradicate Helicobacter pylori infection, a major cause of peptic ulceration. They are usually used in combination with one of the PROTON-PUMP INHIBITORS and include clarithomycin, amoxacillin and metronidazole.

BISMUTH chelates.

The prostaglandin analogue misoprostol has antisecretory and protective properties.

Proton-pump inhibitors omeprazole, lansoprazole, pantaprazole and rabeprazole, all of which inhibit gastric-acid secretion by blocking the proton pump enzyme system.... ulcer healing drugs

An infection caused by the amoeba ENTAMOEBA HISTOLYTICA, a tiny single-celled parasite that lives in the human large intestine. Amoebiasis is spread through drinking water or eating food contaminated by human excreta containing cysts of the amoeba.

Some people carry the amoeba in their intestines and excrete cysts but have no symptoms.

However, some strains invade and ulcerate the intestinal wall, causing diarrhoea and abdominal pain, which may develop into full-blown dysentery.

The amoebae may spread via the bloodstream to the liver, or, rarely, the brain or lung, where they cause abscesses.

Symptoms of an amoebic liver abscess are chills, fever, weight loss, and painful enlargement of the liver.

Treatment of all forms of amoebiasis is with drugs such as metronidazole or diloxanide, which kill the parasite within a few weeks, leading to full recovery.... amoebiasis

Painful infection and ulceration of the gums due to abnormal growth of bacteria that usually exist harmlessly in small numbers in gum crevices. Predisposing factors include poor oral hygiene, smoking, throat infections, and emotional stress. In many cases the disorder is preceded by gingivitis or periodontitis. The condition is uncommon, primarily affecting people aged 15–35.

The gums become sore and bleed at the slightest pressure. Crater-like ulcers develop on the gum tips between teeth, and there may be a foul taste in the mouth, bad breath, and swollen lymph nodes. Sometimes, the infection spreads to the lips and cheek lining (see noma).

A hydrogen peroxide mouthwash can relieve the inflammation.

Scaling is then performed to remove plaque.

In severe cases, the antibacterial drug metronidazole may be given to control infection.... gingivitis, acute ulcerative