Cases reported "Malabsorption Syndromes"

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1/23. An uncommon association: celiac disease and dermatomyositis in adults.

    We describe the case of a patient with a two-year history of adult dermatomyositis (DM) who developed malabsorption revealing celiac disease. Our observation raises the question of an association between DM and celiac disease as part of a continuum, suggesting that celiac disease may be included within the spectrum of the gastrointestinal manifestations of DM and polymyositis (PM). From a practical point of view, our data indicate that the diagnosis of celiac disease should be suspected in PM/DM patients exhibiting malabsorption syndrome. Based on our findings, we further emphasize that an evaluation for celiac disease, including anti-gliadin antibodies, anti-endomysium antibody and tissue trans-glutaminase antibodies should be considered in PM/DM patients presenting with unusual and unexplained gastrointestinal features. This could lead to the early management of such patients, resulting in decreased morbidity (i.e., malnutrition and malignancy) related to misdiagnosed celiac disease.
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2/23. Torulopsis glabrata pneumonia in a malnourished woman.

    A middle-aged woman developed malabsorption and severe protein-calorie malnutrition after a near-total gastrectomy for a perforated gastric ulcer. A transbronchial lung biopsy showed pulmonary infection with Torulopsis glabrata. Improvement in the patient's nutritional status was followed by clearing of the pneumonia without the need for antifungal chemotherapy.
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3/23. Interrelationships between the B-vitamins in B12-deficiency neuromyelopathy. A possible malabsorption-malnutrition syndrome.

    Five patients presenting clinically with a form B12-deficiency neuromyelopathy, with cord involvement in all and proximal muscle weakness in two of them, were investigated for their neurologic, hematologic and vitamin status. Megaloblastosis and achlorhydria were present in all, and impaired absorption of 57Co vitamin B12 and of D-xylose was detected in four. Total cyanide extracted vitamin B12 (A) was lowered in all cases and noncyanide extractable (B) in four of the five, being zero in three. All five responded to injections of hydroxocobalamin. In two patients sequential estimations showed that both A and B, especially the latter, rose steeply initially, normalizing at 50% of A after some weeks. Moiety B is suggested to be physiologically the more active and dissociable form of vitamin B12. Markedly elevated initial serum folate levels, and their subsequent fall under treatment with B12, indicated the operation of the "methyltetrahydrofolate trap". Blood levels of thiamin, nicotinic acid and pantothenic acid were within normal limits. However, serum riboflavin (B2) total vitamin B6 and pyridoxal were reduced in all where tested. Vitamin B6 deficiency could have resulted from its own malabsorption and have contributed to be B12 deficiency. Vitamin B2 and B6 levels also corrected themselves on B12 therapy. The B-vitamin deficiencies in our patients probably resulted from intestinal malabsorption, with a possible factor of malnutrition consequent to their strictly vegetarian diet.
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4/23. Chronic pancreatitis and maldigestion.

    patients with chronic pancreatitis may suffer from maldigestion and malnutrition. Longstanding inflammation and fibrosis in the gland can destroy exocrine tissue, leading to inadequate delivery of digestive enzymes to the duodenum in the prandial and postprandial period and subsequent maldigestion. Maldigestion is augmented by inadequate bicarbonate delivery to the duodenum, with secondary inactivation of enzymes and bile acids by gastric acid. abdominal pain, sitophobia, nausea, vomiting, postprandial satiety, and on-going alcohol abuse may contribute to poor oral intake. Gastric dysmotility and mechanical gastric outlet obstruction from fibrosis in the pancreatic head may contribute to malnutrition and clinical decline. patients with chronic pancreatitis may at times experience profound steatorrhea and weight loss. In this article, we examine the natural history of exocrine insufficiency in chronic pancreatitis, outline the important nutritional issues in these patients, review the methods of diagnosis of maldigestion, and discuss the approach to therapy.
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5/23. 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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6/23. Bleeding, salicylates, and prolonged prothrombin time: three case reports and a review of the literature.

    Fourteen cases of ASA induced hypoprothrombinemic bleeding, including three patients reported by the authors, are reviewed. Predisposing factors toward bleeding include malnutrition and malabsorption syndrome. Although the bleeding is usually benign, it may be serious on occasion. The importance of this rarely considered cause of ASA associated bleeding lies in the fact that it is readily corrected with vitamin k.
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7/23. 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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8/23. A study of digestive absorption in four cases of Down's syndrome. Down's syndrome, malnutrition, malabsorption, and Alzheimer's disease.

    Many data suggest that patients with Down's syndrome (DS) suffer from digestive malabsorption. A fecal test of absorption (search for undigested meat fibers following the ingestion of a measured diet) was conducted in 4 patients with DS. The results point to malabsorption in these patients and support the hypothesis of malabsorption in DS. The etiology of probable malabsorption in DS is discussed. Data are presented suggesting that chronic malnutrition caused by malabsorption could be the cause of the neuropathologic signs of Alzheimer's disease occurring at or slightly before the fourth decade in all patients with DS.
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keywords = malnutrition
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9/23. Elevated levels of serum pancreatic secretory trypsin inhibitor (PSTI) in patients with malabsorption syndrome.

    serum pancreatic secretory trypsin inhibitor (PSTI) was measured by radioimmunoassay in 5 patients with malabsorption syndrome. The serum level of PSTI was elevated to 123.8 /- 25.8 ng/ml (Mean /- SE) in patients with malabsorption syndrome, which was significantly higher than the 16.6 /- 0.7 ng/ml level seen in 116 healthy control subjects. serum PSTI levels in 5 patients with malabsorption syndrome showed inverse correlations with serum levels of cholesterol, cholinesterase and amylase, and not with serum levels of vitamin e, carotene, apoprotein A-IV, albumin, nor with immunoreactive elastase 1, respectively. These results suggest that elevated levels of serum PSTI represent a state of malnutrition due to impaired intestinal absorption.
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10/23. Malabsorption: common causes and their practical diagnosis.

    Malabsorption may present as non-specific ill health and malnutrition in the elderly. Outside major medical centers, however, investigation is often thought to be difficult and unrewarding, and screening tests unreliable. Therefore, a direct approach is suggested to identify treatable small bowel disease in those elderly patients with a clinical possibility of malabsorption. It is based on the use of plain abdominal x-ray, endoscopy with duodenal biopsy, and small bowel meal.
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