Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Total 45 patients (male 27 and female 18) of acute renal failure (ARF) admitted in Nepal Medical College Teaching Hospital over a period of 12 months (1st of Baisakh 2064 BS to 31st of Chaitra 2064 BS) were enrolled in the study. Sixty four percent of study population were of age group 21-60 years. Acute Gastroenteritis 33, sepsis 5, hemorrhage 2, others 5 were the different causes of ARF. Serum creatinine of the study population before and after treatment was 4.35 +/- 2.72 and 1.38 +/- 0.72 mg/dl respectively. Similarly serum urea before and after treatment was 101.78 +/- 57.56 and 42.60 +/- 30.46 mg/dl respectively. Thirty three patients were managed by non dialytic modality of therapy and 12 patients needed hemodialysis. Blood urea of those patients who underwent nondialytic therapy was significantly less than of those who underwent hemodialysis (80.65 +/- 38.21 vs. 151.08 +/- 66.22; p = 0.004). Serum creatinine was also significantly lower in nondialytic therapy group (3.15 +/- 1.15 vs. 7.64 +/- 3.10; p = 0.000) ARF patients with very high urea, creatinine and disturbed electrolytes required dialysis. Average session of hemodialysis was 3.4. Thirty five patients were cured, 6 left against medical advice, 3 were discharged on request, and one patient of sepsis expired during the course of treatment. Acute gastroenteritis was the leading cause of ARF and outcome was excellent even without dialysis in most of the cases provided the treatment was started early and appropriately.
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PMID:Acute renal failure in Nepal Medical College Teaching Hospital. 1882 39

Convulsions sometimes occur in infants and toddlers with mild gastroenteritis. We retrospectively investigated the hospital records of 106 patients admitted to our hospital who had rotavirus gastroenteritis from February 2002 to April 2008. There were 23 patients with convulsions, including 13 with benign convulsions, 9 with febrile seizures, and 1 with epilepsy. Gastroenteritis in patients with benign convulsions was mild from the viewpoint of body weights and serum creatinine concentrations on admission and the duration of admission. Serum Na(+) and Cl(-) concentrations of patients with benign convulsions were relatively lower than those without convulsions on admission (P = .006, and P = .008, respectively). Twelve of thirteen patients had no other seizures after oral administration of 5 mg/kg of carbamazepine, while 1 patient had 1 convulsion 15 minutes after the therapy. In conclusion, carbamazepine therapy was effective for benign convulsions with rotavirus gastroenteritis.
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PMID:Clinical characteristics of benign convulsions with rotavirus gastroenteritis. 1916 32

Afebrile seizures in children usually necessitate investigations in order to determine the etiology and estimate the prognosis. Recently, convulsions that are described as benign but afebrile have been documented in children, in association with diarrhea, and are now recognized as a distinct entity. Benign afebrile seizures with mild gastroenteritis are defined as convulsions accompanying symptoms of mild diarrhea without dehydration or electrolyte derangement and without fever before and after the seizures in healthy children without meningitis, encephalitis or encephalopathy. The convulsions are short, symmetrical, generalized tonic-clonic seizures, occurring in clusters. Laboratory studies (full blood count, blood glucose, creatinine, serum electrolytes, cerebrospinal fluid, bacterial and viral cultures) are usually normal, and other investigations (neuroimaging and electroencephalogram) are not necessary. Prognosis is always favorable (normal psychomotor development, no recurrences of seizures), and anticonvulsant therapy is not warranted. Recognition of this benign infantile convulsion avoids extensive evaluation and long-term anticonvulsant therapy; physicians may reassure the parents regarding the lack of long-term sequelae. In conclusion, this type of seizure seems to be a new entity, but it awaits a correct place in the large group of infantile convulsion disorders.
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PMID:Afebrile benign convulsions with mild gastroenteritis: a new entity? 1943 78

Rhabdomyolysis is a life-threatening condition that involves muscle cell destruction. Among its etiologies, severe hypernatremia is a less common cause. We report a teenage girl with congenital central hypoventilation syndrome and hypothalamus dysfunction syndrome who presented with extreme hypernatremia (sodium, 211 mmol/L) with rhabdomyolysis (creatine kinase, 32,850 U/L) and acute renal failure (creatinine, 6.1 mg/dL) following gastroenteritis with 7-kg weight loss. Rhabdomyolysis subsequently led to acute renal failure and hyperkalemia. Acute hemodialysis was initiated on hospital day 3 for hyperkalemia. This resulted in a 13 mmol/L fall in serum sodium in 3 hours despite using a 156 mmol/L sodium bath, but without the development of cerebral edema or neurological defect. This report highlights an unusual cause of rhabdomyolysis in children and the experience of managing such a difficult clinical situation.
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PMID:Extreme hypernatremia combined with rhabdomyolysis and acute renal failure. 1983 53

We report on 2 infants with acute renal failure caused by bilateral obstructive ureteral stones associated with rotavirus gastroenteritis. A 28-month boy and a 13-month boy with several days history of watery diarrhea and vomiting were referred to our hospital because of anuria. They were diagnosed acute post-renal failure due to obstructive bilateral ureteral stones based on the findings of ultrasound scan and computed tomography. Immediately, percutaneous nephrostomy tubes were inserted for urinary drainage, serum levels of creatinine and uric acid returned to normal within several days. Sandy stones were excreted through the nephrostomy tubes with urine after urinary alkalization, which were proved to be mainly ammonium acid urate. Ammonium acid urate is rare in developed countries, but some cases of bilateral urolithiasis causing acute renal failure in infants with rotavirus gastroenteritis were reported in recent years. It has been known that the cause of acute renal failure is renal azotemia resulting from sustained hypovolemia, but post-renal causes due to ammonium acid urate stones should be taken into consideration.
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PMID:[Two cases of infants with acute renal failure due to bilateral obstructive ureteral stones associated with rotavirus gastroenteritis]. 2015 76

Two men (61 and 81 years old) with mild impaired kidney function developed acute renal failure due to dehydration combined with the use of inhibitors of the renin-angiotensin-aldosterone system (RAAS). After rehydration, correction of hyperkalaemia and stopping RAAS-inhibition and diuretics, they recovered completely. Many patients using RAAS-inhibitors have impaired renal function. In the case of dehydration due to gastroenteritis or prolonged fever they risk developing acute renal failure. The high risk groups are elderly patients, patients with atherosclerosis or heart failure and those with co-medication of diuretics or NSAIDs. The underlying mechanism is that the normal pathways to protect kidney perfusion in case of hypovolaemia are blocked by the use of RAAS-inhibitors or NSAIDs. In the case of dehydration in patients with chronic kidney disease using RAAS-inhibitors, serum creatinine and potassium levels should be monitored. Temporary discontinuation of RAAS-inhibitors or diuretics is often necessary.
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PMID:[Acute renal failure due to RAAS-inhibitors combined with dehydration]. 2069 27

An ameliorating effect of Ocimum sanctum on the toxic effect of meloxicam, a new non-steroidal anti-inflammatory drug was studied by evaluating haemato-biochemical parameters, oxidative stress, gross and histopathological changes in various organs of Wistar rats. A total of thirty-six male rats were divided in six experimental groups each comprising of six rats and numbered from G(1) to G(6). Meloxicam toxicity was induced by oral feeding of meloxicam at 1.2 mg/kg and 2.4 mg/kg body weight in G(2) and G(3) respectively for 28 days. Group G(4) and G(5) were fed with 1.2-mg/kg body weight and 2.4-mg/kg body weight of meloxicam along with 200 mg/kg body weight of aqueous extract of Ocimum sanctum. Group G(1) serve as control while group G(6) was kept as treatment control and fed only aqueous extract of Ocimum sanctum at 200 mg/kg body weight. Clinical finding showed mild diarrhea from 23(rd) day onwards in-group treated with 2.4-mg/kg body of meloxicam. Significant reduction of hemoglobin and packed cell volume (PCV) was observed in both the group treated with 1.2 mg/kg and 2.4-mg/kg body wt. of meloxicam. Ocimum sanctum could restore the hemoglobin and PCV value in-group treated with meloxicam at low dose level. Serum alkaline phosphatase, serum glutamic pyruvic transaminase, Serum glutamic oxaloacetic transaminase and total bilirubin were found elevated in meloxicam treated groups and indicated hepatotoxic activity of meloxicam. Ocimum sanctum could reduce hepatotoxic activity of meloxicam in group G4 receiving meloxicam at lower dose rate along with Ocimum sanctum failed to regulate creatinine level in meloxicam treated groups. In meloxicam toxicity elevated Lipid peroxidation values was noticed in liver and kidneys, while superoxide dismutase and glutathione did not revealed any change. Stomach and intestine revealed hemorrhagic gastroenteritis and ulcers. Perivascular necrosis with infiltration with inflammatory cells was evident in liver. Interstitial nephritis, myocardial necrosis and spongiform encephalopathy were important lesions. The Ocimum sanctum could only counteract the toxic effect of meloxicam in liver and gastrointestinal tract.
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PMID:Ameliorative effect of ocimum sanctum on meloxicam induced toxicity in wistar rats. 2197 18

Amyloidosis is the most common and devastating complication of familial Mediterranean fever (FMF). Renal transplantation is the choice of treatment of in most end-stage renal disease (ESRD). We report our experience on the outcomes in eight patients who underwent renal transplantation for ESRD due to FMF secondary to amyloidosis, and we provide a discussion on the current evidence on this topic of study. The clinical charts of eight renal transplant patients (seven male, one female) who underwent ESRD due to FMF-related amyloidosis were investigated. Five patients underwent living-donor renal transplantation and three patients underwent deceased-donor renal transplant. The mean follow-up period was 35 months (range 3-72). All patients were on triple immunosuppressive treatment and received colchicine. All allografts are currently functioning well with a mean serum creatinine level of 1.4 (range 0.7-2.6) mg/dL. Posttransplantation complications included acute rejection (n = 4), chronic rejection (n = 1), severe gastroenteritis (n = 2), and erythrocytosis (n = 5). None of the patients had proteinuria. During follow-up, we did not observe clinically severe FMF attack, septicemia, rhabdomylosis, symptoms related to vasculitis, and clinical neuropathy. The clinical outcome of the patients in this cohort was similar to that of other renal transplant patients with ESRD due to other causes. This study shows favorable prognosis of eight ESRD patients due to amyloidosis caused by FMF after renal transplantation. Renal transplantation is a safe procedure for ESRD patients having amyloidosis due to FMF. Regular use of colchicine after transplantation should be mentioned.
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PMID:Renal transplantation in patients with familial Mediterranean fever. 2256 68

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as information on the importance of medication compliance.
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PMID:Diabetic ketoacidosis: evaluation and treatment. 2354 50

Diarrhea is a frequent complication after kidney transplantation, with an incidence rate between 22% and 51%. In many cases, the cause remains unknown. We describe here the first case, to our knowledge, of persistent diarrhea associated with Coxsackievirus A19 (CVA19) in a kidney transplant recipient. The patient was a 46-year-old man who received a deceased-donor kidney. He experienced delayed graft function because of donor kidney donation after circulatory determination of death. Maintenance immunosuppression consisted of low-dose cyclosporine, high-dose mycophenolate mofetil (MMF) (3 g/day), and prednisone (10 mg/day). He had severe diarrhea for 2 weeks associated with acute renal failure. No pathogens were found in the stool cultures. Enterovirus detection was positive by real-time polymerase chain reaction, and sequence analysis found CVA19 (from Enterovirus C group). Area under the curve of MMF was 48 mg.h/L. Because of the persistence of diarrhea, MMF was stopped and replaced by azathioprine. The diarrhea disappeared, but serum creatinine did not return to baseline. CVA19 rarely causes gastroenteritis. This case illustrates that MMF is not always the direct cause of diarrhea, and that new clinical infectious diseases will be detected with the expansion of molecular-based DNA diagnostics.
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PMID:Acute enteritis associated with Coxsackievirus A19 in a kidney transplant patient. 2462 88


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