Cases reported "Diarrhea"

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1/18. Surreptitious abuse of magnesium laxatives as a cause of chronic diarrhoea.

    Surreptitious laxative abuse is increasingly considered as a possible cause of unexplained chronic diarrhoea. Laboratory services for detection of colonic stimulant laxatives are widely available; however, laboratory facilities for identifying patients with magnesium-induced diarrhoea are not commonly provided, making diagnosis difficult. We describe three patients who surreptitiously abused magnesium laxatives, and whose diagnoses were delayed, leading in each case to extensive investigations and lengthy in-patient stays. In all three cases, the diagnosis was eventually made by the simple measurement of magnesium in a random faecal sample. We would like to increase the awareness of surreptitious magnesium laxative abuse as a cause of chronic diarrhoea so that costly and unnecessary investigations may be minimized.
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2/18. Congenital sodium diarrhea with a partial defect in jejunal brush border membrane sodium transport, normal rectal transport, and resolving diarrhea.

    Defective jejunal sodium/proton exchange causes severe, congenital secretory diarrhea. We report a boy who presented typically in utero, but in whom diarrhea resolved during the first year of life. pregnancy was complicated by polyhydramnios, and an ultrasound at 31 weeks showed a distended fetal small intestine. The abdomen was grossly distended at birth, and profuse secretory diarrhea began immediately. He subsequently thrived on breast milk and electrolyte supplements. Studies of jejunal brush border sodium/proton exchange at 6 months showed a partial defect. Nonequilibrium rectal dialysis showed rectal sodium and potassium transport to be intact. diarrhea lessened after 9 months, and the patient subsequently required occasional laxatives. These observations suggest that there is a spectrum of congenital abnormality in this exchanger, and that in children with incomplete defects normal colonic sodium salvage can subsequently mask net small intestinal secretion.
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3/18. nephrolithiasis in a child with glucose-galactose malabsorption.

    glucose-galactose malabsorption (GGM) is a rare autosomal recessive disorder of intestinal transport of glucose and galactose, leading to watery diarrhea, dehydration, failure to thrive, or early death. We report a female newborn with GGM, whose clinical diagnosis was confirmed by mutational analysis of the SGTL1 gene. Bilateral nephrolithiasis was discovered after an episode of hematuria. Metabolic causes of nephrolithiasis were not found. The most likely explanation for the development of nephrolithiasis is chronic diarrhea leading to dehydration and highly concentrated urine. High fluid intake and rigorous prevention of dehydration is therefore advised for these patients. Furthermore, life-long monitoring of their renal status, including regular ultrasound examinations, is warranted.
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4/18. Butyrate as an effective treatment of congenital chloride diarrhea.

    BACKGROUND & AIMS: Many therapeutic attempts have demonstrated to be ineffective in reducing the severity of congenital chloride diarrhea and its long-term complications. The short-chain fatty acid butyrate stimulates intestinal water and ion absorption through a variety of mechanisms, including the activation of a parallel Cl-/butyrate and Na /H exchanger. In this case report, we report the therapeutic efficacy of butyrate on an 11-year-old patient affected by congenital chloride diarrhea. methods: The efficacy of increasing doses of oral butyrate (from 50 to 100 mg/kg/day) was investigated through the daily evaluation of stool volume, bowel movements, fecal incontinence, serum, and stool electrolytes concentrations. The modifications in transepithelial intestinal ion transport elicited by butyrate were examined by rectal dialysis study. RESULTS: A butyrate dose of 100 mg/kg/day induced a normalization of stool pattern and of serum and fecal electrolytes concentration. The rectal dialysis study demonstrated a proabsorptive effect induced by butyrate on Na , Cl-, and K intestinal transport. Butyrate therapy was well tolerated during the entire 12-month observation period, and the stool pattern and fecal and serum ion concentrations remained stable within the normal ranges. No clinical adverse events or episodes of dehydration requiring hospital care were observed. CONCLUSIONS: Butyrate could be effective in treating congenital chloride diarrhea. It is easily administered, useful in preventing severe dehydration episodes, and may be a promising therapeutic approach for a long-term treatment in this rare and severe condition.
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5/18. Pharmacokinetic changes of irinotecan by intestinal alkalinization in an advanced colorectal cancer patient.

    The prevention of irinotecan (CPT-11)-induced diarrhea, a well-known adverse reaction to the drug, by treatment with intestinal alkalinization has been carried out in patients with colorectal cancer in japan. Under acidic conditions, CPT-11 and its active metabolite, SN-38, exists preferably as the lactone form, whereas both exist as the carboxylate form under basic conditions. It has been suggested that the lactone forms of both CPT-11 and SN-38 are diffused passively across the intestinal mucosal membranes, whereas the carboxylate forms are actively transported. The intestinal uptake rate of both forms appears to be pH sensitive under physiological conditions, but it remains unclear whether intestinal alkalinization treatment affects the pharmacokinetics of CPT-11 and SN-38. This study was designed to evaluate the pharmacokinetics of CPT-11 and SN-38 in a colorectal cancer patient with or without alkalinization treatment. We found that intestinal alkalinization significantly decreased the plasma levels of CPT-11 and SN-38. In particular, the AUC of SN-38 was markedly decreased to 56 from 107 ng.h/mL. Intestinal alkalinization was effective in preventing CPT-11-induced diarrhea, but this treatment changed the pharmacokinetics of CPT-11 and SN-38 in the body.
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6/18. Stimulated active potassium secretion in a patient with colonic pseudo-obstruction: a new mechanism of secretory diarrhea.

    BACKGROUND & AIMS: Secretory diarrhea is caused by inhibition of intestinal active sodium absorption and stimulation of active chloride secretion. The resulting increase in fecal sodium salts causes an isotonic increase in fecal water output. Abnormalities in potassium transport are not known to be a cause of secretory diarrhea. The aim of our report is to describe a patient with secretory diarrhea that was mediated by excess intestinal secretion of potassium. methods: A 78-year-old woman developed colonic pseudo-obstruction, complicated by severe diarrhea and hypokalemia. Her stools were collected quantitatively on 11 occasions and analyzed for electrolyte concentrations. Rectosigmoid potential difference was measured. RESULTS: The diarrheal fluid had a very high potassium concentration (130-170 mEq/L) and a very low sodium concentration (4-15 mEq/L). Stool potassium losses were as high as 256 mEq/day (normal, 9 mEq/day), and fecal sodium losses were never higher than 13 mEq/day. Potential difference between colonic lumen and a peripheral reference electrode was -14 mV (lumen side negative). CONCLUSIONS: Fecal potassium salts were the exclusive driving force for severe secretory diarrhea in a patient with colonic pseudo-obstruction. The high fecal output of potassium was due to stimulation of active colonic potassium secretion, possibly because of changes in autonomic nervous system activity and distention of the colon in association with colonic pseudo-obstruction. The extremely low fecal excretion of sodium indicates that active sodium absorption was not inhibited. This case study reveals an ion transport mechanism of secretory diarrhea that has not been previously appreciated.
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7/18. Acute renal failure associated with an accidental overdose of colchicine.

    CASE SUMMARY: A 47-year-old man with a history of polyarticular gout was admitted to the nephrology service because of severe renal insufficiency (creatinine 6.25 mg/dl). Three days before admission he had a pain crisis in his knees and ankles and self-administered 20 x 1 mg granules of colchicine p.o. over a period of 4 - 5 hours together with six suppositories each containing 100 mg of indomethacin. The patient began vomiting within 24 hours, experienced diarrhea which persisted for three days and then came to the hospital. The patient reported oliguria during the preceding 24 hours. In hospital, attempts to correct water and electrolyte balance were initiated. The patient became stabilized hemo-dynamically, the diarrhea disappeared within 24 hours, diuresis resumed and the renal function progressively improved. leukopenia and thrombopenia were diagnosed, the transaminases increased: AST = 79 U/l, ALT = 132 U/l on the eighth day after taking the colchicine. The serology for hepatitis a, B, C and hiv viruses was negative; the serology for CMV and VEB revealed a previous infection. After being discharged from hospital 11 days after admission, the patient presented with the following parameters: hematocrit 39%, leukocytes 5,920/microl (3 470 neutrophils), prothrombin time 13 seconds, urea 44 mg/dl, creatinine 1.29 mg/dl, AST 16 U/l and ALT 35 U/l. DISCUSSION: The patient mistakenly ingested 20 mg ofcolchicine p.o. (0.22 mg/kg). The intoxication was associated with gastroenterocolitis, dehydration and renal failure during the first three days after ingestion. The patient also developed leukopenia, thrombopenia and mild hepatocellular injury. Renal failure due to colchicine intoxication is due to various factors such as depletion of volume/hypotension, rhabdomyolysis and multiorgan failure. In this case, the hypovolemia was probably the fundamental cause of the acute renal insufficiency as demonstrated by the quick recovery after administering fluids. It is possible that indomethacin may have enhanced the toxic effect of colchicine on the kidneys and bone marrow. Some colchicine intoxications, as in this case, are caused by an error in interpreting the dose for treating an acute attack of gout. A way to prevent these errors would be to use a low-dose treatment protocol.
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8/18. Intestinal lymphangiectasia: a forgotten cause of chronic diarrhea.

    Intestinal lymphangiectasia is a rare autosomal dominant disorder or acquired condition that leads to lymph obstruction, poor chyle transport and concomitant problems. We describe the cases of two women with chronic diarrhea in whom the common signs of lymphagiectasia-hypoalbuminemia, lymphopenia and distal edema- were found. One of them also had pleural effusion and chylous ascites. The diagnosis was performed by intestinal biopsy. We herein review the histopathologic, radiographic and endoscopic features of this disorder and case reports in Mexican population.
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keywords = transport
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9/18. Microvillus inclusion disease. in vitro jejunal electrolyte transport.

    Microvillus inclusion disease is an inherited intestinal brush border membrane defect that causes severe fluid and electrolyte malabsorption. In an infant with microvillus inclusion disease (confirmed by electron microscopic evaluation of rectal, jejunal, and gallbladder mucosae), basal stool output was massive (greater than 125 mL . kg-1 . day-1) and was not altered by treatment with clonidine or octreotide. A proximal jejunostomy with mucous fistula was placed, allowing separation of proximal from distal tract outputs (60 mL . kg-1 . day-1 and 100 mL . kg-1 . day-1, respectively). A 10-cm jejunal segment was excised during surgery and mounted in Ussing chambers for determination of transepithelial Na and Cl fluxes. Compared with intestine of normal infants, this infant's epithelium showed transmural conductance and unidirectional ion fluxes that were only 30% of normal. With respect to both Na and Cl, the excised jejunum was in a net secretory state. theophylline (5 mmol/L) increased net Cl secretion slightly. In response to mucosal D-glucose (30 mmol/L), jejunal mucosal-to-serosal Na flux doubled. In the infant, glucose-electrolyte solution administered intrajejunally did not significantly change stool output, suggesting that all of the solution (40 mL/kg) was absorbed. Subtotal enterocolectomy, in theory, could have decreased purging by 66% in this infant with microvillus inclusion disease, but diarrhea would still have been significant.
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10/18. Effect of two new antisecretory drugs on fluid and electrolyte transport in a patient with secretory diarrhoea.

    The effect of oral lidamidine hydrochloride and subcutaneous long acting somatostatin analogue, SMS 201-995, on stool output and salt and water transport in the small intestine was investigated in a patient with gross secretory diarrhoea caused by a vasoactive intestinal polypeptide (VIP) secreting tumour in the liver. Transport in the jejunum and ileum were assessed by steady state perfusion techniques. Under basal conditions, the patient was absorbing fluid and electrolytes from the jejunum and ileum, but at rates that were abnormally low. Lidamidine had no effect on either intestinal transport or stool frequency and output. SMS 201-995 increased intestinal absorption in the jejunum and ileum, reduced plasma VIP concentrations, daily stool frequency and weight, and enabled the patient to resume a normal diet without oral or intravenous fluid and electrolyte supplements. After two months of treatment, medical control was becoming increasingly difficult and stool output had risen again to 2 litres per day. Surgical resection, fortunately, was possible and led to resolution of symptoms and normal plasma VIP concentrations.
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