Cases reported "Malabsorption Syndromes"

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1/130. Approaching the patient with chronic malabsorption syndrome.

    The causes of chronic malabsorption may be categorized as decreased intestinal absorption, most commonly caused by celiac sprue; or maldigestion caused by pancreatic insufficiency. The initial step in the evaluation of these patients should include stool studies to confirm fat malabsorption. If fat malabsorption is confirmed, endoscopy with small-bowel biopsies and aspirates for bacterial culture usually follows. A normal endoscopic examination should lead to assessment of pancreatic function. In the setting of normal pancreatic function and the absence of bile acid deficiency, a barium radiograph of the small bowel should be made, looking for anatomical abnormalities. Celiac sprue is an intolerance to gluten caused by a combination of genetic, environmental, and immunologic factors. It classically causes malabsorption. However, it is likely that many patients who exhibit only minor manifestations of the disease go unrecognized and untreated. A presumed diagnosis of celiac sprue is confirmed after a clinical and endoscopic response to a gluten-free diet. Serological markers are available with high degrees of sensitivity and specificity, but duodenal biopsy remains the gold standard for diagnosis. A minority of patients are unresponsive to a gluten-free diet, and intestinal lymphoma should be suspected in these cases.
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2/130. ceroid enteropathy and vitamin e deficiency.

    ceroid (polymerised peroxidised polyunsaturated fatty acids) deposition in the intestine is a result of chronic malabsorption and vitamin e deficiency. This gives the bowel a striking brown colour. Three patients are described with this condition. The macroscopic and microscopic appearances were similar, but the cause of the malabsorption differed. In one patient with polyarteritis there was regression of the pigments with improvement of the malabsorption after treatment with prednisone.
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3/130. fanconi syndrome following bowel surgery and hepatitis reversed by 25-hydroxycholecalciferol.

    A permature male infant required intravenous alimentation for six weeks following extensive surgery for ileal and cecal necrosis. At 3 months he developed evidence of hepatitis. Subsequently osteoporosis and the fanconi syndrome appeared. urine phosphate clearance was 83 percent of creatinine clearance at a serum phosphate concentration of 1.6 mg/dl. Concentration of plasma immunoreactive parathyroid hormone was elevated at 550 pg/ml. 25-Hydroxycholecalciferol was given at 240 mug/day. Aminoaciduria disappeared and bone healing occurred. serum phosphate rose to 6.5 mg/dl and phosphate clearance fell to 2 percent of creatinine clearance. Upon cessation of 25-OHCC therapy, the fanconi syndrome recurred despite administration of vitamin D2. 25-OHCC was then administered at 40 mug/day, and the urine abnormalities were reversed. The patient probably developed hyperparathyroidism, secondary malabsorption, and hepatitis. The fanconi syndrome was the consequence of the hyperparathyroidism. 25-OHCC therapy was more effective than vitamin d in reversing the disordered state, possibly because of impaired hepatic metabolism of vitamin D2.
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4/130. tetany, malabsorption, and mastocytosis.

    mastocytosis is characterized by increased proliferation of mast cells. Two patients had systemic mastocytosis involving the skin and gastrointestinal tract, complicated by malabsorption and tetany. Absorption studies in these patients suggested that the entire small bowel was involved and that the defect was mild in the absence of diarrhea. Small bowel biopsies disclosed infiltration of the lamina propria and submucosa by mast cells, and gastrointestinal tract x-ray films showed nodular densities, edema, and thickening of the bowel wall. tetany was due in part to combined hypocalcemia, hypomagnesemia, and hypokalemia. diarrhea and malabsorption were due to mast cell infiltration of the bowel rather than to histamine. patients with signs of systemic mastocytosis should have careful evaluations and be followed up to prevent development of malabsorption and tetany.
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5/130. strongyloides stercoralis infestation associated with septicemia due to intestinal transmural migration of bacteria.

    strongyloides stercoralis infestation is common in the tropics and is usually asymptomatic. patients with immunocompromised states may develop hyperinfection and fulminant disease. It has been suggested that bacteria accompany S. stercoralis during its passage across the bowel wall, resulting in systemic sepsis. Herein is a report on a 30-year-old man with S. stercoralis infestation and small bowel bacterial overgrowth presenting as malabsorption syndrome. He developed extensive duodenojejunal ulceration, septicemia and fatal hypokalemia. Blood and jejunal fluid grew escherichia coli with the same antibiotic sensitivity patterns. This supports the hypothesis of migration of bacteria from the intestinal lumen as a cause of septicemia in patients with fulminant S. stercoralis infestation.
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6/130. Enteric bacterial flora and bacterial overgrowth syndrome.

    Under certain conditions, colonic bacterial flora can colonize the upper small bowel in concentrations sufficient to cause mucosal damage and malabsorption of nutrients, vitamin B12, and fat-soluble vitamins. This situation, known as small bowel bacterial overgrowth syndrome (SBBOS) may be an under-appreciated cause of malnutrition in elderly people. The diagnosis of SBBOS should be considered when patients with known or suspected predisposing conditions have symptoms or findings compatible with this syndrome. However, proof of small bowel bacterial overgrowth requires specialized testing that is not readily available. Moreover, disagreement persists as to how best to test definitively for this disease. Therefore, on a practical level and despite the potential drawbacks of such a decision, SBBOS is usually diagnosed when a compatible syndrome responds to an empirical trial of appropriate oral antibiotics. Improvements on this approach to SBBOS will be built on more widespread access to sensitive, specific, and less cumbersome testing than is currently available.
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7/130. Tropical malabsorption.

    Tropical malabsorption remains an important clinical problem for both the indigenous population of tropical countries and for short-term visitors and longer-term residents from the industrialized world. In young children, persistent diarrhea and malabsorption can result in severe retardation of growth and development. The most common cause is an intestinal infection notably the small intestinal protozoa including giardia intestinalis, cryptosporidium parvum, isospora belli, cyclospora cayetanensis, and the microsporidia. Tropical sprue still remains an important diagnostic option but is less common than it was 20 to 30 years ago. It is important to attempt to make a specific microbiological diagnosis as this will influence the choice of antibiotic. However, if laboratory facilities are not available, it is possible to offer empirical therapy although this may involve a trial of more than one antibiotic.
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8/130. Diffuse nodular lymphoid hyperplasia of the large bowel without hypogammaglobulinemia or malabsorption syndrome: a case report and literature review.

    Diffuse nodular lymphoid hyperplasia (DNLH) of the intestine is an extremely rare lymphoproliferative disorder occasionally associated with non-Hodgkin lymphomas. We report an unusual case of DNLH of the entire colon, which resembled malignant lymphoma (particularly low-grade B-cell lymphoma) both on clinical and pathologic grounds. The patient was a 62-year-old Japanese woman who was found to have multiple polypoid lesions along the entire large intestine by colonoscopy. Abdominal computed tomography revealed hepatosplenomegaly and multiple mesenteric lymphadenopathy. Histologically, the lesion was characterized by numerous lymphoid follicles with active germinal centers and a diffuse infiltrate of lymphoid cells in the mucosa and submucosa. The present case appears to be an essentially benign condition bearing a resemblance, both clinically and histologically, to malignant lymphoma, and from which it can be distinguished by use of immunohistochemical or molecular analysis.
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9/130. Glucose-galactose malabsorption with renal stones in a Saudi child.

    A case of glucose-galactose malabsorption in an 18-month-old Saudi girl is presented. She had associated bilateral renal stones with impaired renal function. Dietary therapy improved her malabsorption and the renal stones were cleared by extracorporeal shortwave lithotripsy.
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10/130. Severe villus atrophy and chronic malabsorption induced by azathioprine.

    azathioprine is commonly prescribed for autoimmune hepatitis and inflammatory bowel disease. An acute gastroenteritis-like syndrome has been ascribed to azathioprine use, but chronic diarrhea has not. We report a patient with autoimmune hepatitis who developed severe small-bowel villus atrophy and chronic diarrhea after azathioprine was initiated (50 mg/day). We present a case report of a patient followed up prospectively. Duodenal mucosal histology and expression of brush border enzyme dipeptidyl peptidase IV and peptide transporter PepT1 messenger rna levels were determined before and after azathioprine discontinuation. Chronic diarrhea developed several weeks after the initiation of azathioprine and resulted in micronutrient depletion and severe protein-calorie malnutrition, which was unresponsive to oral pancreatic enzyme therapy or a gluten-free diet. Severe malabsorption required parenteral nutrition support for longer than 1.5 years; this was complicated by unstable blood glucose control, acute calculous cholecystitis, catheter sepsis, and severe venous thrombosis. When the temporal association between azathioprine and diarrhea was identified, the drug was tapered while the patient consumed an unrestricted diet. Within 2 weeks after azathioprine was discontinued, diarrhea had completely resolved, and parenteral nutrition was discontinued. Mucosal biopsies obtained before and 4 months after azathioprine discontinuation showed complete reversal of severe duodenal villus atrophy and marked up-regulation of mucosal dipeptidyl peptidase IV and PepT1 messenger rna. The patient has subsequently maintained normal liver function tests on low-dose prednisone alone, with normal stools and stable nutritional status for longer than 4 years. azathioprine can induce severe small-bowel villus atrophy, diarrhea, and malabsorption that is reversible with drug discontinuation.
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