Cases reported "Diarrhea"

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1/179. Lymphocytic colitis: a clue to an infectious trigger.

    We present a 19-year-old patient who was admitted for evaluation of prolonged watery diarrhea. Previous study showed one stool culture positive for campylobacter jejuni, which was treated with appropriate antibiotics with no response. She underwent colonoscopy with multiple biopsies, which led to a diagnosis of lymphocytic colitis. We believe that the patient's disease was due to the infectious process, which triggered an autoimmune response and caused the lymphocytic colitis.
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2/179. INR elevation associated with diarrhea in a patient receiving warfarin.

    OBJECTIVE: To report a case of international normalized ratio (INR) prolongation in a patient receiving warfarin who experienced several episodes of diarrhea. CASE SUMMARY: A 56-year-old white woman, previously controlled on warfarin therapy (INR 2.5-3.5) after aortic valve replacement, experienced six episodes of INR elevation, each associated with an acute bout of diarrhea lasting from one to four days. The patient had not received additional warfarin or new medications (including nonprescription medications and herbal remedies) prior to the episodes. The patient had no obvious signs of bleeding (except bruising on 1 episode) or signs of infection determined through physician evaluation of the patient and her stools. In addition, she had no diagnosis of liver disease or acute or chronic malabsorption. The patient did report that her dietary intake decreased to 25-50% of normal during these episodes of diarrhea, which may result in decreased vitamin k ingestion. DISCUSSION: This is one of the first case reports documenting a trend of INR elevation specifically with episodes of diarrhea. Since most of the common reasons for acute INR elevation have been eliminated, diarrhea with decreased oral intake are the most probable causes for these observed changes in the INR. Several reports suggest that acute diarrhea results in malabsorption of vitamin k, which can predispose patients taking warfarin to INR elevations, but in many of these reports patients had other risk factors for INR elevation. Although the effect of diarrhea on vitamin k absorption and the INR is difficult to quantify, the INR elevation reported here seemed to be directly associated with the duration of each diarrheal episode. CONCLUSIONS: diarrhea episodes in patients receiving warfarin can result in prolongation of the INR and possible bleeding. patients who experience diarrhea or decreased oral intake resulting in elevated INRs should have their INRs evaluated more frequently and their warfarin doses adjusted appropriately.
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3/179. Autoimmune enteropathy with distinct mucosal features in T-cell activation deficiency: the contribution of T cells to the mucosal lesion.

    BACKGROUND: Autoimmune enteropathy is normally characterised by crypt hyperplastic villous atrophy with enterocyte autoantibodies, activation of mucosal lymphocytes and increased epithelial HLA-DR. This case involved a severely affected Portuguese infant who was found to have lymphocyte activation deficiency and demonstrated correspondingly distinct mucosal features. methods: A female infant of nonconsanguineous parents was treated for vomiting and diarrhoea, first with milk exclusion and then with parenteral nutrition. lymphocyte subsets and immunoglobulin concentrations were normal, but in vitro testing showed no activation in response to phytohaemagglutinin, candida, or purified protein derivative, although the response to interleukin (IL)-2 was intact. interleukin-2 deficiency was excluded. Analysis of jejunal biopsy specimens revealed only mild villous blunting with absent goblet cells, normal epithelial proliferation, and no crypt hyperplasia. The dense infiltrate of CD8 and CD4 T lymphocytes showed normal CD2 and CD3 expression but no activation or proliferation markers. HLA-DR was not increased on epithelium or lymphocytes. Thus, in addition to in vitro evidence for lymphocyte activation deficiency, the mucosal specimens showed no evidence of in situ T-cell activation. RESULTS: After development of overwhelming septicaemia, the patient died at 18 months, just before a planned bone marrow transplant. CONCLUSIONS: These findings confirm significant heterogeneity within autoimmune enteropathy. Formal immune function testing should be performed in all affected infants to identify T-cell activation deficiencies. The distinct mucosal findings suggest that activated T cells usually induce the crypt hyperplastic villous atrophy characteristic of classic autoimmune enteropathy.
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4/179. An unusual case of ileocaecal tuberculosis in an 80-year-old Caucasian male.

    An 80-year-old Caucasian male presented with a seven-week history of diarrhoea and weight loss. Distal duodenal biopsies showed partial villous atrophy but he failed to respond to a gluten-free diet. Subsequently he developed a right iliac fossa mass associated with radiological evidence of ileocaecal ulceration. Colonoscopic biopsies from the caecum showed non-caseating granulomata and Ziehl-Neelsen (ZN) staining and culture for acid-fast bacilli (AFB) were negative. Crohn's disease was diagnosed and he was started on steroids. Although he showed an initial response, his condition then deteriorated and he died after six weeks. ZN staining of tissue at postmortem showed AFBs. Although a rare diagnosis in the UK, a high index of suspicion should be maintained for ileocaecal TB in patients with appropriate clinical features, even if classical risk factors for TB are absent.
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5/179. association of lymphocytic colitis with linear IgA dermatosis.

    The case of a 66-year-old female patient is presented, who suffered from chronic watery diarrhea. In addition, she developed linear IgA dermatosis after oral treatment of a presumed yeast infection with nystatin. To evaluate the reason for her diarrhea, colonoscopy was performed. The macroscopic aspect of the colon mucosa was described as normal with no specific alterations for chronic inflammatory bowel disease or for bacterial infections. In contrast, the histologic examination revealed the typical characteristics of lymphocytic colitis. This disease is thought to be caused by immunological reactions against as yet unknown luminal antigens. After treatment with steroids and dapsone the diarrhea as well as the skin disease disappeared. To our knowledge, the present report describes for the first time the association of linear IgA dermatosis with lymphocytic colitis after oral treatment with nystatin. A possible causative link between these two disease entities is discussed.
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6/179. Diabetic microangiopathy in the small bowel.

    AIMS: Microangiopathic changes in the gastrointestinal tract of patients with diabetes mellitus are frequently mentioned in the clinical literature. To our knowledge, pathological studies documenting these changes in bowel biopsies have not been previously reported. In this report, we describe striking duodenal biopsy findings of diabetic microangiopathy in a patient with long-standing insulin-dependent diabetes mellitus and chronic diarrhoea. methods AND RESULTS: The diagnosis was based on the histopathological and immunohistochemical findings in the appropriate clinical setting. blood vessels within the duodenum displayed prominent mural thickening and luminal narrowing secondary to accumulation of hyaline material, which was periodic acid-Schiff positive and intensely stained with monoclonal antibodies against type IV collagen. CONCLUSIONS: This is the first report of diabetic microangiopathy in a bowel biopsy. The pathogenesis, specificity and significance of these angiopathic changes, controversies about diabetic microangiopathy in the gastrointestinal tract, and the association with hypertension are discussed.
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7/179. clostridium difficile diarrhea and colitis: a clinical overview.

    Infection with toxin-producing strains of clostridium difficile is common and potentially life-threatening. It occurs mostly in patients in the hospital or nursing home who are taking or have recently taken antibiotics. Two toxins, A and B, damage the colonic mucosa, resulting in symptoms ranging from mild diarrhea to bloody diarrhea with fever and abdominal pain, colitis, or even pseudomembranous colitis. Severe cases may involve dehydration, toxic megacolon, or colonic perforation. This article reviews the microbiology, epidemiology, clinical manifestations, diagnosis, treatment, and prevention of this disease.
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8/179. 5-fluorouracil-induced small bowel toxicity in patients with colorectal carcinoma.

    BACKGROUND: diarrhea and oral mucositis are the most frequently reported gastrointestinal side effects caused by 5-fluorouracil (5-FU). diarrhea may be severe in 10-30% of patients and is schedule-dependent. 5-FU-induced gastrointestinal toxicity predominantly affects the upper and the lower gastrointestinal tract. The current study describes 5-FU-induced small bowel toxicity as an entity that to the authors' knowledge has not been reported previously in patients with colon carcinoma receiving 5-FU-based therapy. methods: The authors report a series of six patients with colorectal carcinoma who developed acute small bowel toxicity after treatment with 5-FU and leucovorin. RESULTS: Six patients developed a clinical picture of acute abdominal pain and diarrhea. Small bowel damage was documented by laparotomy in two patients, by colonoscopy in one patient, and by abdominal computed tomography scan in three patients. The course was complicated by recurrence of symptoms in one patient who was rechallenged with 5-FU and leucovorin, but the remaining four patients were rechallenged safely with lower doses of 5-FU and leucovorin after the acute toxicity episode. A possible explanation for this toxicity is 5-FU-induced vasospasm and/or decrease in fibrinolytic activity that results in decreased mucosal blood flow. CONCLUSIONS: 5-FU-induced small bowel toxicity is a potentially severe toxicity that may occur in patients with colon carcinoma or other malignancies who are receiving 5-FU-based therapy. [See editorial on pages 1099-100, this issue.] copyright 1999 american cancer society.
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9/179. Microscopic colitis syndrome: lymphocytic colitis and collagenous colitis.

    Microscopic colitis is a syndrome consisting of chronic watery diarrhea, a normal or near-normal gross appearance of the colonic lining, and a specific histological picture described as either lymphocytic colitis or collagenous colitis. Since its initial descriptions a quarter of a century ago, microscopic colitis has become a frequent diagnosis in patients with chronic diarrhea. Understanding of the cause and pathogenesis of microscopic colitis remain incomplete, but potentially important clues have been discovered that shed light on predisposing factors. In particular, specific HLA-DQ genotypes may be permissive for the development of microscopic colitis, and suggest a linkage to the pathogenesis of celiac sprue. Although the differential diagnosis of chronic watery diarrhea is broad, the diagnosis of microscopic colitis is straightforward, involving endoscopic inspection of the colonic mucosa and proper pathologic interpretation of biopsy specimens. As the limitations of drugs ordinarily used for other forms of inflammatory bowel disease are being recognized, new approaches, such as the use of bismuth subsalicylate, are being evaluated. The prognosis of patients with microscopic colitis syndrome remains good, and symptomatic improvement can be expected in most patients.
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10/179. Lymphocytic colitis, induced by ticlopidine.

    Lymphocytic colitis is a chronic inflammatory colonic disease characterized by watery diarrhea and a dense infiltration of the colonic mucosa with lymphocytes. The etiology is unknown but an immune reaction to various immunostimulatory agents including pathogenic or commensal bacteria, products of bacterial metabolism of dietary degradation, or antigens derived directly from the diet, and autoimmune phenomena are discussed. We observed a patient with all features of lymphocytic colitis characterized by a prominent intraepithelial T-cell component. The colitis resolved completely when therapy with ticlopidine--an agent inhibiting platelet aggregation--was stopped. This observation suggests that medical history concerning drug ingestion may reveal the etiology of lymphocytic colitis and allows cure of this otherwise difficult to treat disorder.
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