Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Records and pedigrees of Soft Coated Wheaten Terriers (SCWT) with protein-losing enteropathy (PLE) or protein-losing nephropathy (PLN) were studied retrospectively. Criteria for inclusion were defined based on analysis of blood (panhypoproteinemia for PLE, hypoalbuminemia for PLN) and urine (proteinuria for PLN) and histopathologic examination of tissue. Two hundred twenty-two affected dogs (female:male ratio = 1.6, P < .001) were clinically identified. Dogs were diagnosed with PLE earlier (P < .005; mean +/- SD age: 4.7+/-2.6 years, n = 76) than with PLN (6.3+/-2.0 years, n = 84) or with both diseases (5.9+/-2.2 years, n = 62). Clinical signs included vomiting, diarrhea, weight loss, pleural and peritoneal effusions, and less commonly thromboembolic disease. Dogs with PLE generally had panhypoproteinemia and hypocholesterolemia; intestinal lesions included inflammatory bowel disease, dilated lymphatics, and lipogranulomatous lymphangitis. Dogs with PLN generally had hypoalbuminemia, proteinuria, hypercholesterolemia, and azotemia; renal lesions typically showed chronic glomerulonephritis/glomerulosclerosis, and less commonly endstage renal disease. Dogs with combined PLE/PLN had intermediate mean values (P < .001) for serum total protein, albumin, globulin, and cholesterol but had a higher mean urine protein:creatinine ratio than did PLN dogs (P < .05); intestinal and renal lesions in these dogs were similar to those in the other groups. Two dogs had incidental mild renal dysplasia. Pedigree analysis from 188 dogs demonstrated a common male ancestor, although the mode of inheritance is unknown. Both PLE and PLN are common diseases in this small breed population. The prognosis is poor. Compared with previously reported intestinal and renal diseases in dogs, a new, distinctive familial predisposition for both PLE and PLN has been recognized in the SCWT breed.
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PMID:Familial protein-losing enteropathy and protein-losing nephropathy in Soft Coated Wheaten Terriers: 222 cases (1983-1997). 1066 20

Unexplained hypercalcemia has been increasingly recognized in cats since 1990. In some instances, hypercalcemia has been associated with calcium oxalate urolithiasis, and some affected cats have been fed acidifying diets. We studied the laboratory findings, clinical course, and treatment of 20 cats with idiopathic hypercalcemia. Eight (40%) of the cats were longhaired and all 14 cats for which adequate dietary history was available had been fed acidifying diets. Clinical signs included vomiting (6 cats), weight loss (4 cats), dysuria (4 cats), anorexia (3 cats), and inappropriate urinations (3 cats). Hypercalcemia was mild to moderate in severity. and serum parathyroid hormone concentrations were normal or low. Serum concentrations of phosphorus, parathyroid hormone-related peptide, 25-hydroxycholecalciferol, and calcitriol were within the reference range in most cats. Diseases commonly associated with hypercalcemia (eg, neoplasia, primary hyperparathyroidism) were not identified despite thorough medical evaluations and long-term clinical follow-up. Azotemia either did not develop (10 cats) or developed after the onset of hypercalcemia (3 cats), suggesting that renal failure was not the cause of hypercalcemia in affected cats. Seven of 20 cats (35%) had urolithiasis, and in 2 cats uroliths were composed of calcium oxalate. Subtotal parathyroidectomy in 2 cats and dietary modification in 11 cats did not result in resolution of hypercalcemia. Treatment with prednisone resulted in complete resolution of hypercalcemia in 4 cats.
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PMID:Idiopathic hypercalcemia in cats. 1111 Mar 84

A 9-year-old spayed female Labrador Retriever was evaluated for anorexia, lethargy, and vomiting of 5 days' duration. Laboratory abnormalities included azotemia, high liver enzyme activities, hyperchloremic metabolic acidosis, glucosuria, ketonuria, proteinuria, and aminoaciduria. These laboratory abnormalities were diagnostic of proximal renal tubular acidosis and Fanconi syndrome. Results of initial and convalescent serologic tests for leptospirosis were negative. The dog was treated with amoxicillin, sodium bicarbonate, and potassium citrate at discharge. Repeated evaluations revealed resolution of the acidosis, azotemia, proteinuria, glucosuria, ketonuria, and high liver enzyme activities. Alkali administration was gradually discontinued, and the dog was clinically normal 8 months after discharge. The dog's clinical condition appeared to have been transient in nature, a phenomenon that is rarely seen in human or veterinary medicine.
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PMID:Transient proximal renal tubular acidosis and Fanconi syndrome in a dog. 1515 30

The most common cause of ureteral obstruction in dogs and cats is ureteral calculi. Common clinical signs associated with ureteral obstruction include abnormalities in urination, persistent urinary tract infection, abdominal pain, vomiting, anorexia, weight loss,and depression or lethargy. Medical management of ureteral obstruction includes fluid diuresis, muscle relaxants, and treatment of azotemia using nephrostomy tubes or hemodialysis. Surgical techniques used to restore patency to the ureter include ureterotomy,partial ureterectomy and ureteroneocystostomy, and ureteral resection and anastomosis. Lithotripsy has been used in dogs to remove ureteral calculi. Renal function can be preserved if complete ureteral obstruction is relieved within several days of onset.
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PMID:Management of ureteral obstruction. 1522 12

Acute zinc poisoning has been observed in dogs following the ingestion of metallic zinc objects. A 1 1/2-y-old female miniature bull terrier exhibiting anorexia, vomiting, depression, fever (39.9 C), icterus and intravascular hemolysis was diagnosed with acute zinc poisoning. Anemia, Heinz body production, azotemia and bilirubinemia were also evident. Abnormal pancreatic, hepatic and renal functions were also apparent. A radio opaque object was observed in the stomach. Based upon an elevated plasma zinc level of 28.6 ppm, a tentative diagnosis of zinc poisoning was made. Following surgical removal of the metallic zinc object, a blood transfusion and fluid therapy were given to restore the normal blood volume. Heparin, Cephazolin and Raniditine were also given, although chelation therapy was not provided. Zinc levels in the plasma declined in a steady fashion (half-life = 7.6 d). Complications, such as disseminated intravascular coagulation, chronic pancreatitis, renal or hepatic failure, were not observed. By 20 d post surgery, only mild elevation of liver enzymes was evident. Measurements of the half-life of zinc may provide a useful indication of prognosis and the success of treatment.
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PMID:Diagnosis and treatment of zinc poisoning in a dog. 1548 53

This study was conducted with 3 objectives in mind: first, to identify the toxic fraction (aqueous or organic) in leaves and flowers; second, to identify diagnostic marker(s) of toxicosis in cats; and, third, to evaluate the morphologic effects of intoxication. The study was conducted in 2 phases. Phase 1 was to identify which extract, organic or aqueous, was nephrotoxic and also to determine the appropriate dose for use in the phase 2 studies. Results indicated that only the aqueous extracts of leaves and flowers were nephrotoxic and pancreotoxic. To identify the proximate toxic compound, cats in the phase 2 study were orally exposed to subfractions of the aqueous flower extract, 1 subfraction per cat. Results confirmed vomiting, depression, polyuria, polydipsia, azotemia, glucosuria, proteinuria, and isosthenuria as toxic effects of the Easter lily plant. Another significant finding in serum was elevated creatinine kinase. Significant histologic kidney changes included acute necrosis of proximal convoluted tubules and degeneration of pancreatic acinar cells. Renal ultrastructural changes included swollen mitochondria, megamitochondria, edema, and lipidosis. Subfraction IIa3 of the aqueous floral extract contained most of the toxic compound(s). These studies reproduced the clinical disease, identified the most toxic fraction of the Easter lily, and helped characterize the clinical pathology, histopathology, and ultrastructural pathology associated with the disease.
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PMID:A comprehensive study of Easter lily poisoning in cats. 1558 68

Gallstones are usually asymptomatic in the majority of patients. Gallstones can migrate through a cholecysto-duodenal fistula and may cause an intestinal obstruction anywhere along the gastrointestinal tract. The obstruction usually occurs at the level of the ileocecal valve. In most cases, the clinical presentation includes symptoms related to the intestinal obstruction including abdominal pain and vomiting. We report an unusual case of gallstones presented with acute prerenal azotemia as the major manifestation.
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PMID:Unusual presentation of gallstones. 1599 Sep 39

Brown spider (Loxosceles genus) venom can induce dermonecrotic lesions at the bite site and systemic manifestations including fever, vomiting, convulsions, disseminated intravascular coagulation, hemolytic anemia and acute renal failure. The venom is composed of a mixture of proteins with several molecules biochemically and biologically well characterized. The mechanism by which the venom induces renal damage is unknown. By using mice exposed to Loxosceles intermedia recombinant dermonecrotic toxin (LiRecDT), we showed direct induction of renal injuries. Microscopic analysis of renal biopsies from dermonecrotic toxin-treated mice showed histological alterations including glomerular edema and tubular necrosis. Hyalinization of tubules with deposition of proteinaceous material in the tubule lumen, tubule epithelial cell vacuoles, tubular edema and epithelial cell lysis was also observed. Leukocytic infiltration was neither observed in the glomerulus nor the tubules. Renal vessels showed no sign of inflammatory response. Additionally, biochemical analyses showed such toxin-induced changes in renal function as urine alkalinization, hematuria and azotemia with elevation of blood urea nitrogen levels. Immunofluorescence with dermonecrotic toxin antibodies and confocal microscopy analysis showed deposition and direct binding of this toxin to renal intrinsic structures. By immunoblotting with a hyperimmune dermonecrotic toxin antiserum on renal lysates from toxin-treated mice, we detected a positive signal at the region of 33-35 kDa, which strengthens the idea that renal failure is directly induced by dermonecrotic toxin. Immunofluorescence reaction with dermonecrotic toxin antibodies revealed deposition and binding of this toxin directly in MDCK epithelial cells in culture. Similarly, dermonecrotic toxin treatment caused morphological alterations of MDCK cells including cytoplasmic vacuoles, blebs, evoked impaired spreading and detached cells from each other and from culture substratum. In addition, dermonecrotic toxin treatment of MDCK cells changed their viability evaluated by XTT and Neutral-Red Uptake methodologies. The present results point to brown spider dermonecrotic toxin cytotoxicity upon renal structures in vivo and renal cells in vitro and provide experimental evidence that this brown spider toxin is directly involved in nephrotoxicity evoked during Loxosceles spider venom accidents.
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PMID:Brown spider dermonecrotic toxin directly induces nephrotoxicity. 1600 84

The purpose of this study was to review recent cases of leptospirosis seen at referral centers in New York State and to identify differences in clinical or clinicopathologic aspects of the disease among different suspected infecting serogroups. Medical records at the Cornell University Hospital for Animals and the Animal Medical Center in New York City were reviewed to identify dogs diagnosed with leptospirosis from September 1996 to August 2002. Records of 55 dogs met the inclusion criteria for the study. The suspected infecting serogroups included 21 occurrences of Grippotyphosa, 12 of Pomona, 6 of Autumnalis, 5 of Bratislava, 2 of Hardjo, and 1 of Canicola. Five dogs had equal titers to serogroups Grippotyphosa and Pomona, and 3 had equal titers to 2 other serogroups. Common clinical signs included lethargy, anorexia, and vomiting. Common clinicopathologic findings included anemia, thrombocytopenia, azotemia, hyperphosphatemia, high liver enzyme activity, and hyperbilirubinemia. Forty-three of 55 dogs were discharged from the hospital. Serogroup-specific analysis indicated that dogs with suspected serogroup Pomona infection were more likely to suffer from vomiting (P = .01), thrombocytopenia (P = .009), severe azotemia (P = .04), and hyperphosphatemia (P = .006) than dogs with other serogroups and were less likely to be discharged alive from the hospital (P = .03). This study suggests that only minor clinically relevant differences exist among serogroups. Leptospira serogroup Pomona caused more severe renal disease and was associated with a worse outcome compared with disease caused by other serogroups.
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PMID:Influence of infecting serogroup on clinical features of leptospirosis in dogs. 1673 79

HELLP syndrome is a multi-organ disorder unique to pregnancy. It is characterized by hemolysis, elevated liver enzymes, and low platelets in patients with pre-eclampsia or eclampsia. In King Abdulaziz Oncology Center, Jeddah, seven patients with HELLP syndrome were admitted over a period of four years (1991-94). Retrospective analysis of data was done to study the clinical profile of HELLP syndrome. The incidence of HELLP syndrome in our institution was 1 per 2285 deliveries. One patient was Saudi and six were non-Saudis. The age range was 23 to 44 years, with a mean of 29 years. All patients were multipara. The disorder occurred between 24 to 33 weeks of gestational age, the average being 29 weeks. The most commonly encountered clinical feature was right upper quadrant/epigastric pain. Other features included nausea/vomiting, jaundice, hepatic encephalopathy, azotemia, hypotension and grand mal convulsions. All patients had severe pre-eclampsia pr eclampsia. Indirect hyperbilirubinemia was in the range of 2 to 8 mg/dL and elevated transaminases up to 229 U/L (n<40 U/L) were noted. Various degrees of peripheral thrombocytopenia (<150x10(9)/L) were present in seven patients. Four patients had elevated prothrombin and partial thromboplastin time with postive fibrinogen degradation products. Laboratory abnormalities returned to normal within 10 days following delivery. Four patients were delivered by cesarean section and three had vaginal deliveries. We had two maternal deaths (mortality 34%). One died of multi-organ failure and the other with adult respiratory distress syndrome. There was one stillbirth and the second baby died soon after birth due to prematurity (infant perinatal mortality 34%). We conclude that HELLP syndrome is rare among pregnant women in our institution. It should always be suspected in women with pre-eclampsia or eclampsia when they present with upper abdominal pain. Multipara seem to be more afflicted. Subclinical disseminated intravascular coagulation was detected in 55% of the patients. A majority of our patients presented late to the hospital.
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PMID:HELLP syndrome: Clinical profile of seven patients. 1737 23


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