Cases reported "diarrhea"

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1/1207. microsporidia infection in transplant patients.

    BACKGROUND: microsporidia are the most common cause of chronic diarrhea in patients infected with human immunodeficiency virus. patients who have undergone organ transplantation may also be infected. The precise immune defect and the clinical picture in transplant patients have not been studied. methods: We report a case of microsporidia infection in a heart transplant patient and review three other cases reported in the literature. RESULTS: infection in three solid organ transplant patients occurred when the patients were receiving immunosuppressive therapy for rejection 1.5-3 years after transplantation. patients had chronic diarrhea, vomiting, dyspepsia, and weight loss for 1 month to 3 years. CONCLUSIONS: microsporidia may be the cause of chronic unexplained diarrhea and gastrointestinal disturbances in transplant patients. Defects in cell-mediated immunity probably play a role in maintaining the chronicity of this infection. Specific screening requests should be made to the microbiology laboratory when microsporidia infection is suspected. ( info)

2/1207. 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. ( info)

3/1207. Idiopathic bile acid catharsis.

    In the course of extensive routine screening for bile acid malabsorption a few patients were detected in whom chronic diarrhoea was apparently induced by excess bile acid loss which was neither associated with demonstrable conventional ileopathy nor with any other disorder allied to diarrhoea. In three patients subjected to scrutiny the results obtained were in harmony with a concept of idiopathic bile acid catharsis. Ingestion of cholestyramine was followed by immediate relief, but the diarrhoea recurred whenever this treatment was withdrawn. It it suggested that idiopathic bile acid catharsis should be suspected in patients with unexplained chronic diarrhoea and especially in those with a diagnosis of irritable colon with diarrhoea. ( info)

4/1207. 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. ( info)

5/1207. 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. ( info)

6/1207. Therapy of prednisone-refractory collagenous colitis with budesonide.

    Collagenous colitis is a rare cause of chronic watery diarrhea. No effective standard treatment has yet been established. Based upon anecdotal reports some anti-inflammatory and symptomatic drugs seem to have some therapeutic efficacy. prednisone is widely believed to be the most effective treatment. Here we describe three female patients with histologically confirmed collagenous colitis refractory to therapy with prednisone. Each had received prednisone with a high starting bolus and lower dose maintenance therapy for their disease. However, definite clinical remission could not be achieved. After the administration of 3 x 3 mg/day controlled ileal release (CIR) capsules of budesonide the symptoms resolved immediately. The mean follow-up after beginning budesonide was 11 months (range 7-18). Two patients are still on budesonide. One had had a quick relapse of diarrhea after stopping her treatment. budesonide therapy was therefore resumed. She has remained symptom-free on a lower daily dose of 2 x 3 mg/day budesonide. One patient has been in remission for more than 1 year after a 3-month course of budesonide. budesonide is a topically acting steroid with rapid absorption, high receptor affinity, and low systemic bioavailability, thus causing almost no side effects. As yet only few case reports have been published on the use of budesonide for collagenous colitis. We present here the first three cases of prednisone refractory collagenous colitis successfully treated with budesonide. ( info)

7/1207. Secretory villous adenomas that cause depletion syndrome.

    Secretory villous adenomas of the colon have been known to cause a depleting syndrome characterized by dehydration, prerenal azotemia, hyponatremia, hypokalemia, metabolic acidosis, obtundation, and, in severe cases, death. We describe 1 case of classic depleting syndrome and review the literature on possible mechanisms. Both cyclic adenosine monophosphate and prostaglandin E2 have been implicated as possible secretagogue compounds in the pathogenesis of this syndrome unique to the secretory variant form of villous adenomas. indomethacin as a prostaglandin inhibitor has been used with apparent benefit in controlling the volume of rectal effluent in patients with secretory villous adenomas. ( info)

8/1207. Successful salvage treatment with irinotecan (CPT-11) of recurrent malignant lymphoma in an aged patient; and CPT-11 pharmacokinetics.

    A 72-year-old patient with relapsed non-Hodgkin's lymphoma (diffuse large B-cell type) in the tongue was treated with irinotecan (CPT-11) as the 4th salvage therapy. A two-thirds reduced dose of 40 mg/m2 of CPT-11 was administered, as were granulocyte-colony stimulating factor and antidiarrheal agents. Complete remission was achieved. Although grade 3 leukopenia and grade 1 diarrhea were observed, these adverse reactions did not interrupt the treatment schedule and CPT-11 was administered without interruption for a total of 12 weeks. Despite the dose reduction, the area under the concentration-time curve of SN-38, the active metabolite of CPT-11, was nearly equal to the values reported in phase I and II studies of CPT-11. The patient's ratio of SN-38 to the SN-38 glucuronide (SN-38G) was low, suggesting a low risk of diarrhea. The optimal dose modification provided a sufficient amount of the active metabolite. Supportive therapy managed therapy-related toxicities and resulted in a stable treatment schedule. This is a rare case of a patient successfully treated with CPT-11 after a 4th relapse, in which the agent was administered at the total dose of 960 mg/m2, despite the patient's advanced age. ( info)

9/1207. Primary gastric T-cell lymphomas: report of two cases and a review of the literature.

    To understand more fully the clinicopathological features of primary gastric T-cell lymphomas (PGTL), we report two cases of PGTL and review the literature. The present cases were not associated with human T-cell leukemia virus type 1 (HTLV-1) and were at clinical stage IIE. In both cases, T-cell origin of the lymphoma cells was diagnosed immunohistochemically. The clinical courses of these two cases were different: one followed a very aggressive clinical course and the patient died 6 months after the diagnosis, whereas the other patient survived more than 2 years without adjuvant chemotherapy. Clinicopathological features of 23 patients with PGTL are summarized with regard to their differences from primary small intestinal T-cell lymphomas (PSITL) and by association with HTLV-1. The median age at onset of PGTL was 58 years. The gender ratio was male-dominant (M:F = 2.3:1). About two-thirds (10 of 17) of PGTL cases had evidence of HTLV-1 infection. The most common presenting symptom for PGTL was upper abdominal discomfort and/or pain (76%), whereas that in PSITL was weight loss (61%) and diarrhea (42%). Typical lesions for PGTL were large ulcerations at the corpus to antrum. Neoplastic cells had no typical morphological characteristics for PGTL including HTLV-1-associated cases. CD3 4 8- was the most frequently observed surface phenotype of PGTL cells. Laboratory findings at diagnosis were not informative. Most patients were treated by gastrectomy with or without chemotherapy. PGTL, excluding that with HTLV-1, showed better prognosis than PSITL, although PGTL with HTLV-1 had a poorer prognosis. ( info)

10/1207. 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. ( info)
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