Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malabsorption was present in 29 of 40 symptomatic patients with giardiasis. Twenty-three had impaired D-xylose absorption; in 20 vitamin B12 absorption was low, and 15 patients had steatorrhoea. More severe malabsorption was associated with more marked histological abnormalities. Metronidazole, 2-0 g as a single daily dose on three successive days, produced a parasitological cure rate of 91%. In contrast, the standard course of mepacrine, 100 mg thrice daily for 10 days, eradicated the parasite in only 63% of patients. Improvements in absorption and jejunal morphology followed anti-giardial treatment. Tetracycline in eight patients failed to eradicate the parasite, intestinal absorption was unaltered, and histological appearances of the jejunal mucosa often deteriorated.
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PMID:Giardiasis: clinical and therapeutic aspects. 87 19

The influence of metronidazole on the breath hydrogen response and symptoms of sucrose malabsorption was investigated in a double-blind, randomized and controlled study. Carbohydrate malabsorption was induced by the competitive alpha-glucosidase inhibitor, acarbose. Metronidazole reduced flatulence and the breath hydrogen response during sucrose malabsorption without a change in intestinal carbohydrate absorption, as indicated by serum levels of gastric inhibitory polypeptide, serum insulin and blood glucose. The effect of metronidazole suggests that anaerobic bacteria mediate both signs and symptoms of the colonic response to sucrose malabsorption. In contrast to previous reports on lactose malabsorption, it was not possible to quantify sucrose malabsorption by comparing the breath hydrogen response to sucrose malabsorption with the H2 response to a lactulose load.
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PMID:Influence of metronidazole on the breath hydrogen response and symptoms in acarbose-induced malabsorption of sucrose. 716 May 49

In the rapidly increasing elderly population, diarrhoea as a result of drug therapy is an important consideration. The elderly consume a disproportionately large number of drugs for multiple acute and chronic diseases. Drugs can compromise both immune and nonimmune responses. Aging decreases the quality and proportion of T cells which in turn reduces the production of secretory IgA, the primary immune response of the gut. Acid production in the stomach decreases with increasing age and this compromise its vital 'self-sterilising' function, thus increasing the risk of diarrhoea due to viral, bacterial and protozoal pathogens. Other nonimmune defence mechanisms include the motility of the small intestine and the host-protective commensal bacteria of the colon. Drug induced hypomotility may result in bacterial overgrowth, deconjugation of bile salts and diarrhoea. Less commonly, diarrhoea may occur due to hypermotility because of a cholinergic-like syndrome. In the colon the host-protective commensal bacteria provide a powerful defence against pathogens. Disruption of this commensal population by antibiotic therapy may result in Clostridium difficile supra-infection which causes diarrhoea through toxin production. This is especially important in the elderly patient on chemotherapy for malignancy and those with multiple diseases. The organism responds to vancomycin, metronidazole and bacitracin. Metronidazole is the suggested drug of choice, with vancomycin reserved for relapses. Drugs also cause diarrhoea by interfering with normal physiological processes. Drugs impair fluid absorption by activating adenylate cyclase within the small intestinal enterocyte which increases the level of cyclic AMP. This causes active secretion of Cl- and HCO3-, passive efflux of Na+, K+ and water and inhibition of Na+ and Cl- into the enterocyte. Examples of these drugs (secretagogues) are bisacodyl, misoprostol and chenodeoxycholic acid (used to dissolve cholesterol gallstones). Drugs may also affect a second mechanism that regulates water and electrolyte transport, the Na+, K+ exchange pump. The energy for this pump is provided by the ATPase mediated breakdown of ATP. ATPase may be inhibited by digoxin, auranofin, colchicine and olsalazine. A number of drugs cause osmotic diarrhoea including antacids containing magnesium trisilicate or hydroxide. Lactulose is being used increasingly in compensated liver disease to increase protein tolerance and prevent hepatic encephalopathy. Sorbitol, an osmotic laxative agent also used in some liquid pharmaceutical preparations, induces diarrhoea by virtue of its osmotic potential. Another mechanism by which drugs cause diarrhoea is by mucosal damage of the small and large bowel. In the small intestine mucosal damage causes diarrhoea and fat malabsorption, as may occur with neomycin and colchicine. In the colon, for example, gold salts and penicillamine cause colitis of varying severity. Though the causes of diarrhoea are diverse, a drug-associated aetiology should always be considered and actively sought and addressed to prevent the complications of dehydration, electrolyte imbalance and undernutrition.
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PMID:Mechanisms of drug-induced diarrhoea in the elderly. 978 28

Giardia lamblia, a flagellate protozoan is a protozoa, frequently associated with diarrhea in AIDS patients (adults and children). Transmission occurs via the fecal-oral route by ingestion of infectious cysts in contaminated food or drinking water. Giardia lamblia can cause diarrhea and intestinal malabsorption in both AIDS and non-AIDS patients. The prevalence rate of diarrhea caused by Giardia lamblia in AIDS patients is higher than in those without AIDS, due to humoral immune defect in AIDS patients. The most common symptoms are abdominal distress, watery diarrhea and weight loss. The clinical symptoms in AIDS patients are similar to those in non-AIDS patients. Diagnosis may be made by identifying either cysts or trophozoites in a stool sample, duodenal biopsy and aspirate. Metronidazole is the common drug of choice. Relapse may be found in AIDS patients. At present there is no vaccine. Prevention requires proper handling, good hygiene and treatment of water used for AIDS patients.
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PMID:Giardia lamblia in AIDS patients with diarrhea. 1051 66

Patients with symptomatic collagenous-lymphocytic colitis should eliminate dietary secretagogues such as caffeine- or lactose-containing food from their diet. When possible, use of nonsteroidal anti-inflammatory drugs should be discontinued. If steatorrhea is documented, a low-fat diet may be helpful. In the presence of bile salt malabsorption, binding resins such as cholestyramine might be useful. Nonspecific diarrheal agents such as loperamide hydrochloride, diphenoxylate hydrochloride and atropine, deodorized tincture of opium, or codeine might prove effective in some patients. Antibacterial agents such as bismuth subsalicylate (8 chewable 262-mg tablets daily) have been effective in symptom control. Metronidazole and erythromycin achieve response rates of 60%. Sulfasalazine, at the usual dose of 2 to 4 g daily, used in collagenous-lymphocytic colitis, demonstrated cessation of diarrhea in 1 to 2 weeks for 50% of patients. Other 5-aminosalicylic (5-ASA) compounds are preferred for patients with a history of sulfa allergy, and those who experience adverse reactions to sulfasalazine. Adrenocorticoid medication is reserved for patients whose conventional treatment with sulfasalazine or 5-ASA has failed. Resolution of diarrhea has been documented in 80% to 90% of patients within 1 week of treatment, however, in most patients, long-term therapy is required. Surgical management is reserved for those patients with disease refractory to medical therapy. Colectomy with ileostomy resulted in clinical and histologic resolution in small case series. If there is no abatement of symptoms, rule out other etiologies of diarrhea such as thyroid dysfunction, celiac disease, or bacterial overgrowth.
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PMID:Lymphocytic and Collagenous Colitis. 1109 41

Intestinal parasites cause significant morbidity and mortality. Diseases caused by Enterobius vermicularis, Giardia lamblia, Ancylostoma duodenale, Necator americanus, and Entamoeba histolytica occur in the United States. E. vermicularis, or pinworm, causes irritation and sleep disturbances. Diagnosis can be made using the "cellophane tape test." Treatment includes mebendazole and household sanitation. Giardia causes nausea, vomiting, malabsorption, diarrhea, and weight loss. Stool ova and parasite studies are diagnostic. Treatment includes metronidazole. Sewage treatment, proper handwashing, and consumption of bottled water can be preventive. A. duodenale and N. americanus are hookworms that cause blood loss, anemia, pica, and wasting. Finding eggs in the feces is diagnostic. Treatments include albendazole, mebendazole, pyrantel pamoate, iron supplementation, and blood transfusion. Preventive measures include wearing shoes and treating sewage. E. histolytica can cause intestinal ulcerations, bloody diarrhea, weight loss, fever, gastrointestinal obstruction, and peritonitis. Amebas can cause abscesses in the liver that may rupture into the pleural space, peritoneum, or pericardium. Stool and serologic assays, biopsy, barium studies, and liver imaging have diagnostic merit. Therapy includes luminal and tissue amebicides to attack both life-cycle stages. Metronidazole, chloroquine, and aspiration are treatments for liver abscess. Careful sanitation and use of peeled foods and bottled water are preventive.
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PMID:Common intestinal parasites. 1502 17

Giardia lamblia is the causative agent of giardiasis, one of the most common parasitic infections of the human intestinal tract. This disease most frequently affects children causing abdominal pain, nausea, vomiting, acute or chronic diarrhea, and malabsorption syndrome. In undernourished children, giardiasis is a determining factor in retarded physical and mental development. Antigiardial chemotherapy focuses on the trophozoite stage. Metronidazole and other nitroimidazoles have been used for decades as the therapy of choice against giardiasis. In recent years many other drugs have been proposed for the treatment of giardiasis. Therefore, several synthetic and natural substances have been tested in search of new giardicidal compounds. This study is a review of drugs used in in vitro and in vivo tests, and also drugs tested in clinical trials (nonrandomized and randomized).
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PMID:The old and new therapeutic approaches to the treatment of giardiasis: where are we? 1970 15

Eosinophilic colitis is a rare inflammatory disorder of the digestive tract with chronic evolution and unknown pathophysiological mechanisms. The article describes the case of a 64-year old woman with a history of asthma and hypereosinophilia, who presented to a surgical department for persistent abdominal pain in the past 4 months, weight loss and malabsorption. She was diagnosed with eosinophilic colitis based on the colonoscopic result indicating extensive eosinophilic infiltration of the colonic mucosa correlated with the laboratory data and abdominal CT scan results. Following the colonoscopy, the patient developed fever, hypotension and diarrhea and was transferred to an Infectious Diseases Department with a presumptive diagnosis of abdominal sepsis. Treatment with ertapenem was immediately started. Metronidazole was also added due to a PCR positive stool test for Clostridioides difficile toxins encoding-genes. The patient displayed a rapid remission of the fever and of the intestinal complaints following antibiotic therapy and was discharged after 14 days. During a 3 months follow-up, the patient remained asymptomatic with normal values of laboratory parameters except for a persistent hypereosinophilia. The case outlines two distinguishing features: a histopathologic diagnosis of eosinophilic colitis, a rare diagnosis of a patient with chronic abdominal pain and an unexpected and rapid remission of the eosinophilic colitis following the antibiotic treatment and the restoration of the intestinal eubiosis.
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PMID:Eosinophilic Colitis and Clostridioides difficile Sepsis With Rapid Remission After Antimicrobial Treatment; A Rare Coincidence and Its Pathogenic Implications. 3290 97