Cases reported "Diarrhea"

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1/87. 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.
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2/87. Toxic epidermal necrolysis and graft vs. host disease: a clinical spectrum but a diagnostic dilemma.

    We describe a 53-year-old man who developed partial and full thickness skin loss associated with pyrexia, diarrhoea, liver, renal and bone marrow failure, during treatment for an aggressive B cell lymphoblastic lymphoma. The clinical features and histology were compatible with both toxic epidermal necrolysis and graft vs. host disease, causing a diagnostic and therapeutic dilemma. We discuss the possibility that methotrexate was the causative drug, with review of its cutaneous side-effects. Histologically our patient demonstrated the sparse dermal infiltrate with full thickness epidermal necrosis typical of toxic epidermal necrolysis and graft vs. host disease. We discuss this finding with respect to the pathogenesis of toxic epidermal necrolysis.
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3/87. life-threatening toxicity in a dihydropyrimidine dehydrogenase-deficient patient after treatment with topical 5-fluorouracil.

    In humans, 80-90% of an administered dose of 5-fluorouracil (5-FU) is degraded by dihydropyrimidine dehydrogenase (DPD; EC 1.3.1.2), the initial rate-limiting enzyme in pyrimidine catabolism. Cancer patients with decreased DPD activity are at increased risk for severe toxicity including diarrhea, stomatitis, mucositis, myelosuppression, neurotoxicity, and, in some cases, death. We now report the first known cancer patient who developed life-threatening complications after treatment with topical 5-FU and was shown subsequently to have profound DPD deficiency. RT-PCR and genomic PCR methodologies were used to identify a G to A mutation in the GT 5' splicing recognition sequence of intron 14, resulting in a 165-bp deletion (corresponding to exon 14) in this patient's DPD mRNA. immunoprecipitation and Western blot analysis were then used to demonstrate that the aberrant DPD mRNA is translated into a nonfunctional DPD protein that is ubiquitinated. We conclude that the presence of this metabolic defect combined with topical 5-FU (a drug demonstrating a narrow therapeutic index) results in the unusual presentation of life-threatening toxicity after treatment with a topical drug. These data further suggest that degradation by the ubiquitin-proteosome-mediated system plays a role in the elimination of the DPD protein.
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4/87. 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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5/87. 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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6/87. Increased tacrolimus levels in a pediatric renal transplant patient attributed to chronic diarrhea.

    tacrolimus is an immunosuppressant used to prevent rejection of transplanted organs. It is metabolized in both the gut and the liver by the cytochrome P450 (CYP) 3A4 enzyme system and is a substrate for the p-glycoprotein (P-gp) drug efflux pump. As CYP3A4 enzymes and P-gp are present at differing concentrations throughout the gastrointestinal tract, the bioavailability of tacrolimus may be influenced by changes in gastrointestinal transit time in addition to changes in hepatic metabolism. We report the case of a pediatric renal transplant patient who experienced a three-fold increase in serum tacrolimus concentrations during an episode of gastroenteritis with chronic diarrhea.
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7/87. ceftriaxone-resistant salmonella infection acquired by a child from cattle.

    BACKGROUND: The emergence of resistance to antimicrobial agents within the salmonellae is a worldwide problem that has been associated with the use of antibiotics in livestock. Resistance to ceftriaxone and the fluoroquinolones, which are used to treat invasive salmonella infections, is rare in the united states. We analyzed the molecular characteristics of a ceftriaxone-resistant strain of salmonella enterica serotype typhimurium isolated from a 12-year-old boy with fever, abdominal pain, and diarrhea. methods: We used pulsed-field gel electrophoresis and analysis of plasmids and beta-lactamases to compare the ceftriaxone-resistant S. enterica serotype typhimurium from the child with four isolates of this strain obtained from cattle during a local outbreak of salmonellosis. RESULTS: The ceftriaxone-resistant isolate from the child was indistinguishable from one of the isolates from cattle, which was also resistant to ceftriaxone. Both ceftriaxone-resistant isolates were resistant to 13 antimicrobial agents; all but one of the resistance determinants were on a conjugative plasmid of 160 kb that encoded the functional group 1 beta-lactamase CMY-2. Both ceftriaxone-resistant isolates were closely related to the three other salmonella isolates obtained from cattle, all of which were susceptible to ceftriaxone. CONCLUSIONS: This study provides additional evidence that antibiotic-resistant strains of salmonella in the united states evolve primarily in livestock. Resistance to ceftriaxone, the drug of choice for invasive salmonella disease, is a public health concern, especially with respect to children, since fluoroquinolones, which can also be used to treat this disease, are not approved for use in children.
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8/87. loperamide therapy in a patient with diarrhea and resistant hypertension.

    A 65-year-old man was admitted to our hospital for resistant essential hypertension. He had a past history of bowel resections due to Crohn's disease. We assumed that in this patient insufficient drug absorption might be a cause of resistant hypertension and that even increased antihypertensive regimens would fail to decrease blood pressure. We administered loperamide, which may increase drug absorption from the residual intestine. blood pressure was successfully decreased, with a concomitant increase in blood concentration of antihypertensive drugs. In patients with impaired drug absorption, we should make an effort to restore drug obstruction before considering increased drug regimens.
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9/87. Colorectal cancer: dilemmas regarding patient selection and toxicity prediction.

    Irinotecan (Campto, Rhone-Poulenc Rorer) is probably the most studied drug used as second-line treatment for colorectal cancer. Its main disadvantages are toxicity and cost. Delayed diarrhea and neutropenia are the most common toxic side effects, both of which can usually be predicted, by knowing the criteria for patients who are at increased risk for those side effects. These criteria include poor performance status (>2), bulky disease, previous abdominal-pelvic irradiation, hyperleukocytosis and increased bilirubin >1.5 x normal upper range. There are some other less common toxic effects of irinotecan, such as pneumonitis, cardiac arrhythmia, paralytic ileus, liver dysfunction, tumor lysis syndrome. While these side effects are very rare, physicians should be able to recognize them, because the number of patients being treated with irinotecan is increasing. The authors report four cases of probable irinotecan-related toxicity with fatal outcome in all 4 patients. Two of these 4 patients were not in the known risk categories for irinotecan toxicity. One patient died with signs of hepato-renal syndrome, the other with signs of rapid tumor lysis-like syndrome. Two other patients with bulky disease and performance status 2, had increased urea, creatinine and bilirubin serum levels after irinotecan administration, that could not be explained as manifestation of disease progression only. Data on all uncommon irinotecan toxic effects should be gathered and analyzed so that toxic effects, other than diarrhea and neutropenia, are better defined and predicted.
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10/87. diarrhea as a side effect of mesalamine treatment for inflammatory bowel disease.

    tablets of coated 5-aminosalicylate (5-ASA) called mesalazines are among the most widely prescribed preparations for the treatment of colitis, including ulcerative, Crohn's disease (CD), collagenous and lymphocytic colitis, and-to a lesser extent-CD of the small bowel. Mesalamines have, to a large extent, replaced the parent drug sulfasalazine because they produce fewer side effects. Although mesalamines have been known from earlier studies to produce occasional diarrhea, the true incidence of this effect is not known and is not always recognized. We are presenting the cases of five patients in whom oral mesalamines produced severe and persistent diarrhea-made worse by increasing doses of the drug-and intensified the colitis in two. Recognition of the problem is by symptom analysis after careful history taking. Changing the therapeutic regimen or discontinuing the medication is usually required to reverse this potentially debilitating and occasionally life-threatening side effect.
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