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)

Five 7-week-old pups and four 4-week-old pups, all seronegative to canine parvovirus, were inoculated intravenously with 1000 haemagglutinating units of canine parvovirus originally isolated from the myocardium of a dog with naturally occurring myocarditis. After three days, pups in both litters became pyrexic, anorectic and depressed, with vomiting and diarrhoea. The 4-week-old pups were killed on day 4, and the 7-week-old pups died or were killed on day 5 post-inoculation. Histological examination showed degeneration and necrosis of intestinal crypt epithelial cells and villous atrophy. All pups had thymic atrophy caused by lymphoid depletion. Peyer's patches, mesenteric lymph node and spleen also had lymphoid depletion. Lymphoid necrosis was present occasionally in these tissues. In the bone marrow, granulocytes and granulocyte and erythroid precursors were depleted. Amphophilic intranuclear inclusion bodies were abundant in crypt epithelial nuclei, less so in myocardial nuclei. Canine parvovirus was isolated from intestinal contents, thymus, spleen, mesenteric lymph node and liver in most pups, but not from kidney or myocardium.
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PMID:Canine parvoviral disease: experimental reproduction of the enteric form with a parvovirus isolated from a case of myocarditis. 740 70

Single-treatment schedules in mice and dogs and multiple-treatment schedules in dogs and monkeys were used to evaluate the toxicity of 2,3-dihydro-1H-imidazo[1,2-b]pyrazole. The LD50 of the iv single dose in male and female mice collectively was 993 mg/kg (2980 mg/m2). The major target organs in mice, dogs, and monkeys were the bone marrow, lymphoid tissue, and gastrointestinal tract. Clinical signs at lethal and high toxic doses were weight loss, diarrhea, hematochezia, emesis, anorexia, mydriasis, dyspnea, lethargy, and stupor. The immediate toxic effect on blood cells was a depression of rbcs with suppression of lymphoid elements occurring later. In dogs, the most toxic schedule was single bolus injections. Attenuation of toxic responses occurred if rest periods were introduced between single or repeated daily dose schedules. The monkeys were more sensitive than the dogs to the high toxic dose on a milligram per meter squared basis, with similar sensitivity to the low toxic dose in the repeated daily injections.
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PMID:Preclinical toxicologic study of 2,3-dihydro-1H-imidazo[1,2-b] pyrazole (IMPY) in mice, dogs, and monkeys. 745 89

The incidence of SIADH (the syndrome of inappropriate antidiuretic hormone secretion) was analyzed retrospectively in 43 children who received marrow-ablative chemotherapy before autografts with peripheral blood stem cells for lymphoid malignancies. SIADH was documented in three children (ages 3, 13, and 13 years) who received chemotherapy, which included high-dose methyl 6-[3-(chloroethyl)-3-nitrosoureido]-6-deoxy-alpha-D-glucopyranoside (MCNU) and cyclophosphamide, under a concomitant overhydration protocol. SIADH was manifested as frequent vomiting in two patients and as generalized seizure in one. Hyponatremia (< 125 mEq/L), hypo-osmolality (< 260 mOsm/kgH2O), and continued urinary excretion of sodium (> 30 mEq/L) were used to diagnose SIADH in these three patients. All signs and symptoms subsided within 24 hours either by fluid restriction alone (n = 1) or by supportive care including anticonvulsant and D-mannitol, or hyperhydration with saline plus 5% glucose and diuretic. None of the patients died. Careful monitoring of the serum sodium level, as well as the osmolality of plasma and urine, should be incorporated into the patient management protocol for this type of high-dose chemotherapy.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion (SIADH) in children undergoing high-dose chemotherapy and autologous peripheral blood stem cell transplantation. 757 88

The toxicity of CI-949, an effective inhibitor of allergic mediator release in pharmacology models, was evaluated in rodents and dogs. Median lethal doses at 24-hr postdose ranged from 343 to 453 mg/kg in mice and 806 to 2058 mg/kg in rats. Delayed toxicity was observed at 300 mg/kg and greater in mice and at 500 mg/kg and greater in rats. Mortality and clinical intolerance occurred in rats at 200 and 400 mg/kg in the subacute studies, and at 100 and 150 mg/kg in the 13-week study. In rats, dose-dependent lymphoid tissue atrophy and depletion or necrosis of lymphocytes in lymphoid tissues were seen in deaths and moribund terminations. Although doses up to 60 mg/kg administrated for 2 weeks to dogs were well tolerated, 60 and 120 mg/kg in the 13-week dog study were poorly tolerated. Cutaneous sores, mucocutaneous purulent discharge, emesis, diarrhea, and weight loss were identified at these lethal doses. Histopathologic changes in dogs included myocardial, vascular and soft tissue inflammation, and gastric ulceration at 60 and 120 mg/kg, and thymic atrophy at 20 mg/kg and greater. Doses of 10 and 50 mg/kg were no-effect doses in 13-week repeated dose studies in dogs and rats, respectively. These results were used to support initial human clinical trials of CI-949.
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PMID:Toxicity of CI-949, a novel anti-allergy agent. 825 91

We describe the clinicopathologic characteristics of three patients with chronic intestinal pseudo-obstruction and malabsorption. The patients were young women (average age, 25 years) who presented with abdominal pain, nausea, vomiting, diarrhea, and weight loss that led to extreme inanition and death in two patients despite multiple treatment schemes. The evolution of the process averaged 8 years. No case manifested evidence of malignant lymphoproliferative progression. Histologically, a diffuse lymphoplasmacytic infiltrate that affected all the layers of the intestinal wall was observed in full-thickness biopsy specimens. The proliferating lymphocytes were small and mixed with mature plasma cells that proved to be polyclonal on immunohistochemical analysis. An outstanding finding in all three cases was extensive damage to submucosal and myenteric nerve plexus associated with a lymphoid infiltrate. Quantification of the myenteric plexus by using immunohistochemical and morphometric techniques also revealed a marked reduction in their number. We concluded that diffuse lymphoplasmacytic infiltration of the small intestine associated with damage to the intestinal nerve plexus constitutes a specific disorder that is different from other diseases that produce intestinal pseudo-obstruction.
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PMID:Diffuse lymphoplasmacytic infiltration of the small intestine with damage to nerve plexus. A cause of intestinal pseudo-obstruction. 834 45

A lymphosarcoma originating from kidneys, which metastasized to the ovaries, oviducts, heart and pancreas, was pathologically diagnosed in a 3-year-old female Japanese dog (Shiba dog). Clinically, the dog exhibited vomiting, diarrhea, oliguria and abdominal enlargement, associated with hypoglycemia. Grossly, the kidneys were enlarged and neoplastic masses were also seen in the ovaries and heart. Histologically, a majority of glomeruli and renal tubules were obliterated due to diffuse invasion by tumor cells. There were no metastatic lesions in the mesenteric and tracheobronchial lymph nodes, spleen and bone marrow. Most of the tumor cells were small- to medium-sized lymphoid cells with a large nucleus and scanty cytoplasm.
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PMID:Bilateral renal lymphosarcoma in a dog. 839 50

Yersinia pseudotuberculosis is an enteric pathogen that induces a variety of clinical symptoms, fever, scarlatiniform rash, diarrhea, vomiting, and arthritis. Characteristic histopathologic findings in Y. pseudotuberculosis infection such as lymphoid hyperplasia, typically seen in mesenteric lymph nodes, suggest that the stimulation of a large proportion of T lymphocytes may be involved in the pathogenesis of this infection. In this study, we assessed the mitogenic activity of culture supernatants of the clinical isolates of Y. pseudotuberculosis and investigated the mechanism by which these culture sups activate T cells. The culture sups, as well as partially purified fractions obtained by gel filtration, were found to selectively stimulate T cells bearing V beta 3, V beta 9, V beta 13.1, and V beta 13.2 compared with stimulation by anti-CD3. Furthermore, fibroblasts transfected with different HLA class II molecules, either HLA-DPw9, -DQw6, -DR1, or -DR4 Dw15, were capable of presenting Y. pseudotuberculosis culture supernatants to purified T cells. The T cell response to this sup was not restricted by donor HLA-DR types and was not neutralized by antibodies against the known staphylococcal superantigens, Staphylococcal enterotoxin (SE)A, SEB, SEC2, SED, SEE, and TSST1. These results suggest that Y. pseudotuberculosis produces superantigenic toxins that may mediate some of the systemic illnesses associated with infection by this organism.
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PMID:Evidence for superantigen production by Yersinia pseudotuberculosis. 840 95

A 46-year old man suffered from fever, sweating, vomiting, abdominal pains, and watery diarrhea during two weeks. The abdomen was tender on pressure. Laboratory findings revealed increased leucocytes to 18,500/microliters, increased thrombocytes to 513,000/microliters, an increased sedimentation rate of 105/129 mm, CRP of 18.2 mg/dl and slightly elevated activities of the amino-transferases. Ultrasonography showed a tumor of the liver with a diameter of 10 cm and a echocomplex wheel-spoke structure. The tumor was confirmed by computed tomography, nuclear resonance tomography, angiography, and scintigraphy without signs of malignity. Fine needle biopsy was negative. Bisegment resection of the liver revealed a tumor of the liver with focal necrosis, with the histological aspect of fibrous tissue with lymphoid infiltration and multiple abscesses. The diagnosis was "inflammatory pseudotumor of the liver" (IPT). Postoperatively the follow-up half a year later was normal. The IPT ist an important differential diagnosis of the hepatocellular carcinoma. The review of 80 cases shows that operative resection of the tumor is the treatment of choice, because the benign diagnosis cannot maintained without doubts. But the pathognomonic trias of symptoms 1. Inflammatory signs, 2. solid tumor of the liver, 3. normal liver tissue allows to make this exceptional diagnosis. The question is whether the operation of the tumor can be avoided by conservative medical therapy.
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PMID:[Inflammatory pseudotumor of the liver. Case report of a rare differential diagnosis of hepatocellular carcinoma]. 865 89

A nine months old boy was admitted to the hospital with the diagnosis of meningoencephalitis 15 days after having a clinically diagnosed chickenpox. Lumbar puncture showed clear CSF with 0.23 g/l of proteins, 57 mg/dl of glucose, 30 red cells/mm3 and 5 leukocytes/mm3. Blood count showed a packed red cell volume of 22%, a hemoglobin of 7 g/dl, 14800 leukocytes with 1% eosinophils, 5% band and 39% segmented neutrophils, 50% lymphocytes and 5% monocytes and a decreased platelet count. On the fourth hospitalization day, the patient had vomiting, irritability and stiff neck. A new lumbar puncture showed a clear CSF that differed from the former only in the glucose level that increased to 102 mg/dl. The patient died and the necropsy showed a congestive and enlarged brain and congestive meninges infiltrated with lymphocytes. There was lymphoid follicle hyperplasia in the small bowel and enlarged mesenteric lymph nodes. Samples of brain, brain stem, spinal cord and stools were sent for virological study. A Coxsackie B-5 virus was isolated from the spinal cord sample.
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PMID:[Isolation of Coxsackieviruses B5 in a fatal case of meningoencephalitis]. 873 69

The pathophysiology and clinical features of TA-GVHD are reviewed. Engrafted donor derived lymphocytes in TA-GVHD mainly target the immune system, i.e. myeloid and lymphoid as a result of recognition of "foreign" recipient transplantation antigens. The pathophysiology of acute GVHD has been described as a "cytokine storm" at the barrier of the immunobiological defence in the skin, liver, and intestine. TA-GVHD is mostly an acute syndrome, and predominantly associated with a pan-cytopenia, severe immunosuppression, a skin eruption, hepatitis, and gastrointestinal dysfunction, clinically manifested nausea, vomiting and diarrhea. The overall risk of TA-GVHD is unknown and is probably higher than the approximately 300-350 cases reported in the literature. TA-GVHD is often unrecognized in the setting of complex medical situations, where target organs are already dysfunctional. Furthermore, incomplete manifestations of the triad of GVHD may be present, or the syndrome may be mild or atypical. Finally, the potential diagnosis may be missed. We present an atypical case of fatal TA-GVHD in an immunocompetent diabetic patient after CABG operation, showing leukocytosis throughout the clinical course.
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PMID:[Clinicopathological features of transfusion-associated graft-versus-host disease]. 930 Dec 85


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