Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The main purpose of this work was to study changes in the balance of fluids, electrolytes and blood metabolites in neonatal piglets with severe transmissible gastroenteritis. Six two day old conventional piglets were infected with transmissible gastroenteritis virus while six others were used as normal controls. Blood samples were collected in heparin when the infected piglets were moribund. The following variables were measured: packed red cell volume, total plasma protein and bicarbonate, blood pH, blood urea nitrogen and plasma glucose, creatinine, chloride, inorganic phosphorus, sodium, potassium, magnesium and calcium. Vomiting and diarrhea appeared 12 to 24 hours postinoculation in the infected piglets and they were moribund one or two days later. Before becoming moribund, most of the piglets fell rapidly into a lethargic and comatose state. The most evident changes in their blood variables were an increase in packed cell volume, total protein, blood urea nitrogen, phosphorus and magnesium levels and a decrease in pH and bicarbonate concentration as well as a severe hypoglycemia. The results suggest that severe hypoglycemia coupled with metabolic acidosis and dehydration might be an important factor contributing to the high mortality rates caused by transmissible gastroenteritis in neonatal piglets. The hypoglycemia results from a combination of the inadequate glucose metabolism inherent to neonatal piglets and the acute maldigestion and malabsorption resulting from the diffuse and severe villous atrophy induced by the virus.
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PMID:Hypoglycemia: a factor associated with low survival rate of neonatal piglets infected with transmissible gastroenteritis virus. 647 97

A disease syndrome similar to the hemolytic uremic syndrome of people is described in three dogs with acute renal failure. In each dog, hemorrhagic gastroenteritis preceded the onset of anuric acute renal failure. Evidence of microangiopathic hemolytic anemia (schizocytes, thrombocytopenia, and increased concentrations of fibrin split products) was present in the three dogs. Serum chemistry results showed increased concentrations of blood urea nitrogen, creatinine, and phosphorus. Ultrasound examination performed in one dog revealed increased echogenicity of the renal cortices. Treatment for anuric acute renal failure using a continuous dopamine and furosemide infusion established urine production in one of three dogs. Microscopic examination of tissue from the two dogs that underwent necropsy showed occlusion of the renal vasculature by fibrin thrombi consistent with microangiopathic arteriolar thrombosis. The pathophysiology and current knowledge of human hemolytic uremic syndrome is compared with hemolytic uremic syndrome in these dogs.
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PMID:Hemolytic uremic syndrome in dogs. 824 11

One hundred and twenty patients with a mean age of 38 years (range 12-85 years; M 91, F 37) were studied over a period of 5 years in a teaching hospital in Dhaka. Sixty-two patients presented with probable anuria with 1-4 days' duration, 63 patients presented with oliguria, and 3 were nonoliguric. The causes of acute renal failure were medical (94), surgical (22), obstetrical (13). Of the medical cases, the causes were gastroenteritis in 42 cases, gastroenteritis with CNS involvement in 11 cases, rapidly progressive glomerulonephritis in 10 cases, acute viral hepatitis in 8 cases, and septicemia in 8 cases. Of 22 surgical cases, postoperative acute renal failure was the cause in 9, road traffic accident in 6, and renal calculus disease in 7. There were 13 cases in the obstetrics group, of whom 9 were due to abortion, 2 were due to preeclampsia, and the other 2 were postoperative. The mean blood urea of all cases was 35 mmol/L and serum creatinine was 988 mumol/L. Dialysis was required in 105 cases; of these, 72 were medical cases, 21 were surgical cases, and 12 were obstetric cases. The overall survival rate was 75%. The improved survival is probably due to timely referral and prompt medical management.
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PMID:Outcome of acute renal failure in adults in a teaching hospital in Bangladesh. 829 Jul 6

The hemolytic-uremic syndrome (HUS) is an acute disorder, characterized by the triad of microangiopathic hemolytic anemia, nephropathy and thrombocytopenia. The great majority of patients are children, usually under 4 years of age, although adults can be affected. The onset is abrupt and usually follows gastroenteritis or upper respiratory infection. Later, clinical manifestations based on the triad, such as pallor, jaundice, edema, hypertension and purpura soon develop. The urinary output is reduced and the urine may appear dark yellow or tea-colored. Laboratory tests of peripheral blood show severe hemolytic anemia associated with fragmented red blood cells and thrombocytopenia, usually below 50,000/microliters. The blood urea nitrogen, serum creatinine and lactate dehydrogenase concentrations are elevated. Proteinuria and microscopic hematuria, which are indicative of active glomerular damage are also seen. Profound understanding of these manifestations is sufficient to permit an early diagnosis of HUS.
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PMID:[Diagnosis and clinical features of hemolytic uremic syndrome]. 843 21

Fifty-five patients with psoriatic arthritis were treated with a low dose of cyclosporin A (CyA) (mean dose 2.7 mg/kg per day) for a period of 6 months to investigate the efficacy of CyA on disease parameters. Significant improvement in the joint complaints and inflammation parameters was observed including a decrease in the number of painful (-46%) and swollen (-45%) joints, tenderness (Ritchie Index: -50%) and degree of swelling (-46%), patient's assessment of pain (-35%), the duration of morning joint stiffness (-37%), as well as a decrease in C-reactive protein (-52%). A 50% reduction of joint complaints required a total of 24 weeks, whereas a 50% reduction of skin involvement was achieved after 5-6 weeks of treatment. Four patients left the study due to adverse events: creatinine level increase in two patients, hypertension in one patient and gastroenteritis in the fourth patient. Joint scintigraphy in 18 patients indicated an improvement or stable condition in 61% of cases after a mean follow-up of approximately 8 months. The results of this prospective study show that low-dose CyA effectively improves not only skin lesions, but also joint complaints in psoriatic arthritis.
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PMID:Anti-inflammatory efficacy of low-dose cyclosporin A in psoriatic arthritis. A prospective multicentre study. 897 76

We created a predictive model for the area under the concentration versus time curve (AUC) of cyclosporin A (CsA) using routine monitoring results, and examined its clinical utility. Based on 48 clinical time courses accumulated from renal transplant patients, the AUC predictive model was created. An estimate of the AUC0-8 (integrated from time zero to 8 h) was then given as follows: AUC0-8 = 5673.1 x log(TL) + 9342.8 x log(OB) + 64.1 x Dprd x 869.4 x DTK - 168.9 x HCT - 161.2 x SCr - 11.3 x GPT + 3.0 x PL - 588.6 x SEX - 24794.5. In this model, the AUC0-8(ng.h/ml) is given as a function of the CsA through levels (TL, ng/ml), obesity (OB, %), daily dose of prednisolone (Dprd, mg/d), donor type of kidney (DTK), hematocrit (HCT, %), serum creatinine (SCr, mg/dl), glutamate-pyruvate transaminase activity (GPT, IU/l), plasma lipids (PL, mg/dl) and sex distinction (SEX). The Statistical significance of the multiple regression was p < 0.00001 (R2 = 0.862, n = 48), and the day after transplantation, neither the administered oral dose of CsA, or the patient's age had any contribution to the regression. The predictive performance of this model was almost equal to that of the existing method which used 3-point data on the concentration versus time curve. In clinical adaptation for renal transplant patients, the steady-state concentration of CsA (Css) based on the AUC0-8 predictive model was significantly decreased during acute gastroenteritis or before acute rejection, whereas nephrotoxicity was increased, even though CsA trough levels were within a normal therapeutic range (100-200 ng/ml). These findings suggest that the created AUC0-8 predictive model using routine monitoring results, i.e., the trough level of CsA, biochemical tests, a daily dose of predorinsolone (PRD), and basic patient information, is convenient as a monitoring device for CsA therapy, and is satisfactory in clinical practice.
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PMID:A predictive model for area under the concentration versus time curve of cyclosporin A using several routine monitoring results in renal transplant patients. 930 Jan 38

Glutaric aciduria type III is a rare metabolic abnormality leading to persistent isolated glutaric acid excretion. We report the clinical and biochemical phenotypes of three affected children. The first patient is a boy with dysmorphic features and a chromosomal deletion (monosomy 6q26-qter) in whom a persistent glutaric aciduria (500 mmol/mol creatinine, normal <10) was detected during a routine metabolic investigation. The second boy suffered from acute gastroenteritis and hyperthyroidism, when an excessively high urinary glutaric acid excretion was identified (1460 mmol/mol creatinine). The third patient is a girl with constantly elevated glutaric acid in her urine (290 mmol/mol creatinine) but no symptoms of significant disease. In all our patients, glutaric aciduria type I (glutaryl-CoA dehydrogenase deficiency), glutaric aciduria type II (multiple acyl-CoA dehydrogenation defect), and secondary forms of glutaric aciduria (for example due to intestinal infections or mitochondrial dysfunction) could be excluded. Loading with the precursor amino acid lysine in all patients as well as with pipecolic acid in the third case led to an increase in urinary glutaric acid excretion, proving the endogenous origin of glutarate. Glutaric aciduria type III (a defect reported to be caused by peroxisomal glutaryl-CoA oxidase deficiency) is our presumptive diagnosis. However, peroxisomal glutaryl-CoA oxidase is not well characterized and no reliable approach for the direct determination of this enzyme is available to us. To our knowledge, in the English language literature only a single patient with glutaric aciduria type III has been described. Our cases reported here confirm the earlier assumption that glutaric aciduria type III is not related to a distinctive phenotype. Glutaric aciduria type III appears to be a rare metabolic abnormality, presumably of peroxisomal metabolism. However, its pathophysiological impact still needs further investigation.
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PMID:Glutaric aciduria type III: a distinctive non-disease? 1255 41

Australian Aboriginal children hospitalized with diarrhoeal disease have severe manifestations with acidosis, hypokalaemia, osmotic diarrhoea and abnormal small bowel permeability. Nitric oxide (NO) production is increased in diarrhoeal disease, but its relationship to mucosal function and diarrhoeal complications is not known. We examined the relationship between NO production and complications of acute diarrhoea in Aboriginal and non-Aboriginal children between February 1998 and February 2000. We enrolled 318 children admitted to Royal Darwin Hospital into one of three groups: acute diarrhoea, non-diarrhoeal controls with no inflammatory illness, and non-diarrhoeal controls with inflammatory illness. Nitric oxide production was measured by urine nitrate-creatinine (NOx/Cr) excretion on a low nitrate diet. Small bowel intestinal permeability was measured by the lactulose-rhamnose (L/R) ratio on a timed blood specimen. The NOx/Cr ratios were markedly elevated in Aboriginal diarrhoeal cases (geometric mean [GM] = 1.23, 95% confidence interval [95% CI] 1.07-1.44), lowest in non-Aboriginal non-inflammatory controls (GM = 0.13, 95% CI 0.10-0.16) and intermediate in all other groups (GM = 0.35, 95% CI 0.28-0.43). Convalescent levels (day 5) in the Aboriginal diarrhoeal group (GM = 1.02, 95% CI 0.82-1.28) were slower to fall than L/R ratios. Multivariate analysis in the diarrhoeal group indicated that high NO production was associated with abnormal permeability, hypokalaemia and malnutrition, but not with the severity of diarrhoea, acidosis or osmotic diarrhoea. We concluded that increased NO production may contribute to impaired mucosal barrier function and hypokalaemia in acute gastroenteritis, which may be the cost of the known gut-protective and antimicrobial effects mediated by NO in acute intestinal inflammation.
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PMID:Increased nitric oxide production in acute diarrhoea is associated with abnormal gut permeability, hypokalaemia and malnutrition in tropical Australian aboriginal children. 1288 17

Hemolytic uremic syndrome (HUS) is an nonexceptional complication of infectious gastroenteritis. No one has already been reported in Senegalese publications. We made a retrospective study of the record of 7 patients with HUS among 256 cases of children with bloody diarrhea presenting to the pediatric unit of Aristide Le Dantec between august 1998 and july 1999. The mean age of the children was 33,14+/-25 months and the weight was -2,29 DS. The diagnosis is supported by the findings of an acute renal failure with urea at 1,28+/-0,51g/ l and creatinine at 41,46+/-25,48mg/l. An hemolytic anemia was constant, the blood film revealed schizocytes. We found a thrombocytemia only in two cases. A hight white blood cell count (more than 50000/mm3) was noted in for cases. Only one child made a good recovery. We insist on preventing gastroenteritis and aggressive and adapted management of the HUS.
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PMID:[Hemolytic uremic syndrome: a complication of acute gastroenteritis in children]. 1577 51

In this study, we aimed to compare bone calcium system changes from children with diabetic ketoacidosis or acute metabolic acidosis due to dehydration to find out the relative contribution of metabolic acidosis and diabetes-related factors on expected negative calcium balance. We studied a set of non-invasive parameters of bone remodeling in 16 children with diabetic ketoacidosis due to new onset type 1 diabetes and 25 children with acute metabolic acidosis due to dehydration complicating acute gastroenteritis before and after the correction of acidosis. The two groups of subjects were matched for age, sex, pubertal status, and degree of metabolic acidosis and dehydration. A group of 18 age and sex-matched healthy children served as the control group. Plasma ionized calcium levels were increased in both groups, significantly more so in diabetic ketoacidosis. While osteoblastic markers, osteocalcin and alkaline phosphatase, were depressed to a comparable degree in both groups, urinary calcium/creatinine ratio and hydroxyproline excretion were significantly greater in diabetic ketoacidosis. No significant changes in calcitrophic hormone (intact PTH, calcitonin, 25-hydroxy vitamin D3) levels were observed. All study parameters except for serum phosphate levels behaved in parallel in both clinical conditions, and abnormalities disappeared with the correction of acidosis except for IGF-1, which remained low in diabetic subjects. In conclusion, our results suggest that, in diabetic ketoacidosis, the observed severe negative calcium balance occurred through diminished bone formation mediated by metabolic acidosis per se and increased bone mineral dissolution and bone resorption because of severe insulin deficiency and secondarily via metabolic acidosis. Observed changes appear to be independent of calcitrophic hormones.
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PMID:Bone calcium changes during diabetic ketoacidosis: a comparison with lactic acidosis due to volume depletion. 1586 25


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