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)

Twenty-four hour urine and spot urine samples from 29 patients with metabolic acidosis were collected for evaluation of urine ammonium in relation to urine anion gap, urine osmolal gap (OG) and modified urine osmolal gap (MOG). Their underlying diseases included SLE in 8, RTA in 7, CRF in 6, RPGN in 2 (one with SLE), Lowe syndrome in 2, on acetazolamide in 2, gastroenteritis in 2, and CAH in one. Twenty-three patients had normal serum anion gap (< 14 mmol/L). Their mean CO2 was 13.77 (9.4-17.9) mmol/L, net acid excretion (NAE) was 33.18 +/- 35.36 mmol/24 hour, NH+4 excretion was 29.16 +/- 31.97 mmol/24 hour. Neither the 24-hour urine nor spot urine anion gap correlated with corresponding urine NH+4 with or without adding urine HCO-3 in the calculation. Spot urine NH+4 correlated well with urine OG (r2 = 0.82, p < 0.001) and less with MOG (r2 = 0.339, p < 0.006). The urine osmolality was well correlated with the sum of 2 (Na+ + K+ + NH+4) + urea for both spot (r2 = 0.990, p < 0.001) and 24 hour urine (r2 = 0.907, p < 0.001) collection. Twenty-four hour urine NH+4 did not correlate with the OG or the MOG. There was no correlation between spot urine NH4/Cr ratio and 24 hour urine NH4/Cr ratio (r2 = 0.243, p = 0.53) nor between spot NAE/Cr ratio and 24 hour urine NAE/Cr ratio (r2 = 0.380, p = 0.014). Therefore in the presence of low urine NH+4 (< 100 mmol/L), urine osmolal gap may be used to determine urine NH+4 indirectly with good correlation. Twenty-four hour urine collection is still necessary to assess renal acidification.
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PMID:Comparison of urine anion gap, urine osmolal gap and modified urine osmolal gap in assessing the urine ammonium in metabolic acidosis. 1073 May 27

A previously healthy 7-year-old white boy presented to St. Louis Children's Hospital with a 1-day history of headache, malaise, temperature of 38.7 degrees C, and a progressively erythematous, tender calf with central dusky purpura. On the morning of admission, his mother noticed a 2-mm crust on the patient's right calf with a 3-cm x 3-cm area of surrounding erythema. No history of recent trauma or bite was obtained. He had suffered two episodes of nonbloody, nonbilious emesis during the last day. In addition, over the previous 12 h, he presented brown urine without dysuria. His mother and brother had suffered from gastroenteritis over the previous week without bloody diarrhea. On initial physical examination, there was a 6-cm x 11-cm macular tender purpuric plaque with a central punctum on the right inner calf, which was warm and tender to the touch, with erythematous streaking towards the popliteal fossa (Fig. 1). The inguinal area was also erythematous with tender lymphadenopathy and induration, but without fluctuance. Laboratory studies included an elevated white blood cell count of 20, 800/microL with 6% bands, 86% segs, and 7% lymphocytes, hemoglobin of 12.5 g/dL, hematocrit of 35.1%, and platelets of 282,000/microL. The prothrombin time/activated partial tissue thromboplastin was 10. 4/28.0 s (normal PT, 9.3-12.3 s; normal PTT, 21.3-33.7 s) and fibrinogen was 558 mg/dL (normal, 192-379 mg/dL). Urinalysis showed 1+ protein, 8-10 white blood cells, too numerous to count red blood cells, and no hemoglobinuria. His electrolytes, blood urea nitrogen (BUN), and creatine were normal. The urine culture was negative. Blood culture after 24 h showed one out of two bottles of coagulase negative Staphylococcus epidermidis. The patient's physical examination was highly suggestive of a brown recluse spider bite with surrounding purpura. Over the next 2 days, the surrounding rim of erythema expanded. The skin within the plaque cleared and peeled at the periphery. The coagulase negative staphylococci in the blood culture were considered to be a contaminant. Cefotaxime and oxacillin were given intravenously. His leg was elevated and cooled with ice packs. The patient's fever resolved within 24 h. The lesion became less erythematous and nontender with decreased warmth and lymphadenopathy. The child was discharged on Duricef for 10 days. Because the patient experienced hematuria rather than hemoglobinuria, nephritis was suggested. In this case, poststreptococcal glomerulonephritis was the most likely cause. His anti-streptolysin-O titer was elevated at 400 U (normal, <200 U) and C3 was 21.4 mg/dL (normal, 83-177 mg/dL). His urine lightened to yellow-brown in color. His blood pressure was normal. Renal ultrasound showed severe left hydronephrosis with cortical atrophy, probably secondary to chronic/congenital ureteropelvic junction obstruction. His right kidney was normal.
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PMID:A child with spider bite and glomerulonephritis: a diagnostic challenge. 1080 79

The architecture of transmissible gastroenteritis coronavirus includes three different structural levels, the envelope, an internal core, and the nucleocapsid that is released when the core is disrupted. Starting from purified virions, core structures have been reproducibly isolated as independent entities. The cores were stabilized at basic pH and by the presence of divalent cations, with Mg(2+) ions more effectively contributing to core stability. Core structures showed high resistance to different concentrations of detergents, reducing agents, and urea and low concentrations of monovalent ions (<200 mM). Cores were composed of the nucleoprotein, RNA, and the C domain of the membrane (M) protein. At high salt concentrations (200 to 300 mM), the M protein was no longer associated with the nucleocapsid, which resulted in destruction of the core structure. A specific ionic interaction between the M protein carboxy terminus and the nucleocapsid was demonstrated using three complementary approaches: (i) a binding assay performed between a collection of M protein amino acid substitution or deletion mutants and purified nucleocapsids that led to the identification of a 16-amino-acid (aa) domain (aa 237 to 252) as being responsible for binding the M protein to the nucleocapsid; (ii) the specific inhibition of this binding by monoclonal antibodies (MAbs) binding to a carboxy-terminal M protein domain close to the indicated peptide but not by MAbs specific for the M protein amino terminus; and (iii) a 26-residue peptide, including the predicted sequence (aa 237 to 252), which specifically inhibited the binding. Direct binding of the M protein to the nucleoprotein was predicted, since degradation of the exposed RNA by RNase treatment did not affect the binding. It is proposed that the M protein is embedded within the virus membrane and that the C region, exposed to the interior face of the virion in a population of these molecules, interacts with the nucleocapsid to which it is anchored, forming the core. Only the C region of the M protein is part of the core.
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PMID:The membrane M protein carboxy terminus binds to transmissible gastroenteritis coronavirus core and contributes to core stability. 1115 4

Norovirus (NV), a member of the family Caliciviridae, is one of the important causative agents of acute gastroenteritis. In the present study, we found that virus-like particles (VLPs) derived from genogroup II (GII) NV were bound to cell surface heparan sulfate proteoglycan. Interestingly, the VLPs derived from GII were more than ten times likelier to bind to cells than were those derived from genogroup I (GI). Heparin, a sulfated glycosaminoglycan, and suramin, a highly sulfated derivative of urea, efficiently blocked VLP binding to mammalian cell surfaces. The reagents known to bind to cell surface heparan sulfate, as well as the enzymes that specifically digest heparan sulfate, markedly reduced VLP binding to the cells. Treatment of the cells with chlorate revealed that sulfation of heparan sulfate plays an important role in the NV-heparan sulfate interaction. The binding efficiency of NV to undifferentiated Caco-2 (U-Caco-2) cells differed largely between GI NV and GII NV, whereas the efficiency of binding to differentiated Caco-2 (D-Caco-2) cells did not differ significantly between the two genogroups, although slight differences between strains were observed. Digestion with heparinase I resulted in a reduction of up to 90% in U-Caco-2 cells and a reduction of up to only 50% in D-Caco-2 cells, indicating that heparan sulfate is the major binding molecule for U-Caco-2 cells, while it contributed to only half of the binding in the case of D-Caco-2 cells. The other half of those VLPs was likely to be associated with H-type blood antigen, suggesting that GII NV has two separate binding sites. The present study is the first to address the possible role of cell surface glycosaminoglycans in the binding of recombinant VLPs of NV.
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PMID:Genogroup II noroviruses efficiently bind to heparan sulfate proteoglycan associated with the cellular membrane. 1504 97

A 62-year-old male died of colchicine poisoning after accidental ingestion of Colchicum autumnale (meadow saffron). He ate a salad of plant with green leaves regarded as wild garlic (Allium ursinum). A few hours later he developed symptoms of gastroenteritis and was admitted to hospital. In spite of gastric lavage, activated charcoal and supportive measures, multi-organ system failure developed over the next two days. Laboratory analysis showed highly elevated blood concentrations of hepatic enzymes, creatine kinase, lactate dehydrogenase and blood urea nitrogen, as well as leukocytopenia and thrombocytopenia. Mechanical ventilation, dopamine, noradrenaline, crystalloid solutions and fresh frozen plasma were applied but despite treatment the patient died five days after the ingestion. Post-mortem examination revealed hepatic centrilobular necrosis, nephrotoxic acute tubular necrosis, petechial bleeding in fatty tissue, blunt and shortened intestinal villi and cerebral toxic edema. Botanical identification of incriminated plant gave Colchicum autumnale which confirmed colchicine poisoning. Although the accidental ingestion of Colchicum autumnale is rare and to our knowledge only five such cases have been described in detail, this is the second fatal case in Croatia described in the last 3 years.
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PMID:Fatal colchicine poisoning by accidental ingestion of meadow saffron-case report. 1574 68

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

The records of children with Salmonella gastroenteritis only (n = 97), and those with associated bacteraemia (n = 64), seen in one medical centre during a 12-year period, were analysed retrospectively. Mean patient age was 2.24 +/- 2.8 years (range, 0.05-16 years), and 49% were male. Children with bacteraemia presented after a longer duration of symptoms (7.0 +/- 6.9 vs. 3.9 +/- 4.6 days, p 0.0002), and had higher erythrocyte sedimentation rates (45 +/- 22 vs. 33 +/- 22 mm/h, p < 0.02) and lactate dehydrogenase values (924 +/- 113 vs. 685 +/- 165 IU/L, p 0.001). There was a trend in bacteraemic children towards immunosuppression (6.3% vs. 1.0%, p 0.08) and a lower number of siblings (2.9 +/- 1.9 vs. 3.8 +/- 2.7, p 0.063). Non-bacteraemic children had a more severe clinical appearance, and a higher percentage had a moderate to bad general appearance (51.5 vs. 29.7%, p < 0.01), with dehydration (37.1 vs. 18.8%, p 0.02) and vomiting (58.8 vs. 39.0%, p 0.02). Laboratory dehydration indicators were also markedly worse in non-bacteraemic children, with urine specific gravity of 1020 +/- 9.4 vs. 1013 +/- 9.0 (p 0.0002), base excess of - 4.2 +/- 3.0 vs. - 2.5 +/- 3.4 mEq/L (p 0.01), and blood urea nitrogen of 10.1 +/- 7.0 vs. 7.4 +/- 4.5 mg% (p 0.002). Thus, the clinical presentation of bacteraemic children was more gradual, and associated gastroenteritis and dehydration was less pronounced. These findings may contribute in part to the inadvertent discharge of bacteraemic children from the emergency department.
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PMID:Non-Typhi Salmonella gastroenteritis in children presenting to the emergency department: characteristics of patients with associated bacteraemia. 1600 18

The purpose of this study was to investigate clinical and metabolic effects of combined parenteral and oral nutrition compared with parenteral nutrition in young dogs with haemorrhagic gastroenteritis in a prospective clinical study. Dogs with acute gastroenteritis received either parenteral nutrition (group PN, n = 9) or combined parenteral and early enteral nutrition (group EN, n = 10). Infusions were compounded from amino acids, lipids, glucose and electrolyte/glucose solutions [149 g/l glucose, 20 g/l triglycerides, 40 g/l amino acids and 4009 kJ metabolizable energy/l (957 kcal ME/l)], and supplemented with potassium, phosphate and trace elements. Group EN received additionally a hydrolysed diet (74 kJ/kg BW(0.75) on day 2 and 148 kJ/kg BW(0.75) on days 3 and 4). Glucose, triglycerides, protein, albumin, fibrinogen, urea, creatinine, alkaline phosphatase, glutamate dehydrogenase and glutamate pyruvate transaminase were measured before and during the infusions, haematological traits only before the infusions. Statistics included two-factorial anova and subsequent t-test or Wilcoxon test (P < 0.05). All dogs of group EN survived compared with seven of nine patients in group PN. Most dogs in the EN group vomited within half an hour after introduction of oral feeding on day 2 but tolerance for food increased on days 3 and 4. The general health status and faecal and blood parameters of the surviving dogs were similar (P > 0.05) between the groups. In all dogs leucocytes increased during the treatment period, haematocrit and haemoglobin levels declined. Infusions increased blood glucose and triglycerides (P < 0.05); however, no adverse signs were observed. Early enteral nutrition was possible after a short period of adaptation, however, vomiting can be a severe problem. The evaluation of clinical benefits of early enteral nutrition in young dogs with haemorrhagic gastroenteritis requires further investigations.
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PMID:Early enteral nutrition in young dogs suffering from haemorrhagic gastroenteritis. 1610 6

From July 1998 to July 1999, 45 cases of acute renal failure were treated at Bir Hospital, Kathmandu. Out of which 24 were male and 21 were female. Age ranged from 11 months to 84 years with mean age being 35 years and 9 cases were below 10 years. Four cases with pre-renal azotaemia and twenty five cases of acute tubular necrosis (ATN) accounted for 64% of all cases. These were due to gastroenteritis 10, sepsis 6, post surgical 1, trauma 1 and obstretical complications 5. Multiple hornet stings were responsible for acute renal failure in 3 cases, acute urate nephropathy in 1 case and miscellaneous causes in 2 cases. Glomerulonephritis / vasculitis accounted for 17.7%, acute interstitial nephritis 4.4%, haemotytic uraemic syndrome (HUS) 6.6%, and post renal azotaemia in 6.6% of all cases. Mean serum creatinine was 8 mg/dl, mean blood urea 190 mg/dl. Eight cases were treated only conservatively, eighteen received haemodialysis, fourteen received peritoneal dialysis, three received both and two refused for dialysis. Average duration of hospital stay was 13.6 days. Out of the forty-five cases twenty-nine recovered normal renal function, ten expired, two recovered partially, two progressed to chronic renal failure and two left against medical advice. Overall mortality was 22.2%. Common causes of acute renal failure in our setting were gastroenteritis (22%) and sepsis (20%). HUS was exclusively seen in children following bacillary dysentery. Multiple hornet stings is an important cause of acute renal failure in our country.
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PMID:Acute renal failure in a tertiary care center in Nepal. 1655 67

Campylobacter is now recognized as the most common bacterial agent of gastroenteritis. The adhesion of bacteria to intestinal cells is a major step in human colonization. The binding of Campylobacter jejuni cells to fibronectin (Fn), a component of the extra cellular matrix, is mediated by a 37,000 outer membrane protein termed CadF for Campylobacter adhesion to Fn. CadF protein is very hard to purify from Campylobacter membranes. In order to study the conformation of this protein, we set out to clone, express, purify, and re-fold the CadF protein. The nucleotide sequence encoding the N-terminal domain of the CadF protein was cloned in a pET-based expression vector. The recombinant protein was further produced in Escherichia coli, purified from inclusion bodies, and refolded. More specifically, the purification experiments were set-up as follows: (i) protein aggregates were collected from cell-lysates, solubilized in urea and enriched by ion-exchange chromatography; (ii) refolding was achieved by drop-by-drop dilution method in detergent containing buffer and monitored by CD measurements; (iii) the protein was finally purified to homogeneity by gel filtration chromatography. In spite of our success in purifying the N-terminal domain of the CadF protein, repeated attempts to express and purify the entire cadF gene in E. coli failed. Using a novel approach, we found it possible to express the entire cadF gene fused to a hexa-histidine encoding nucleotide sequence in C. jejuni. This allowed the expression, synthesis, and purification of the recombinant CadF-His tagged protein from C. jejuni by nickel affinity chromatography followed by gel filtration chromatography. In summary, we developed a novel strategy to produce significant quantities of a recombinant N-terminal portion of the CadF protein (46.5 microg/mg of bacterial dry weight) and of the native CadF protein (3.5 microg/mg of bacterial dry weight) for further studies.
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PMID:Expression and purification of native and truncated forms of CadF, an outer membrane protein of Campylobacter. 1662 Sep 52


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