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)

Clinical and immunologic responses of sheep to vaccination and subsequent bluetongue virus (BTV) challenge exposure were studied and compared with those of non-vaccinated sheep. Sheep were vaccinated with inactivated BTV administered with aluminum hydroxide and cimetidine or levamisole. After sheep were vaccinated, precipitating group-specific antibodies to BTV were detected, but serotype-specific neutralizing antibodies were not detected. Cellular immune responses (lymphocyte blastogenesis) to BTV were not detected. After virulent BTV challenge exposure, vaccinated and nonvaccinated sheep developed acute clinical disease of similar severity. Clinical signs included hyperemia and petechiae of oral mucosa and coronary bands of the feet, excess salivation, nasal discharge with crusting, ulceration of the muzzle, and edema of lips and intermandibular space. Marked increases in serum creatine kinase activity were associated with stiff gait, reluctance to move, and vomiting. Fever and leukopenia were detected in most of the challenge-exposed sheep. Viremia and neutralizing antibodies were detected in vaccinated and nonvaccinated sheep after challenge exposure. Bluetongue virus-specific reaginic antibodies were not detected in sera from any of the sheep when the passive cutaneous anaphylaxis test was used.
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PMID:Experimental bluetongue virus infection of sheep; effect of previous vaccination: clinical and immunologic studies. 301 26

Ten sheep were inoculated with bluetongue virus (BTV) serotype 17. Six of the sheep had been vaccinated before challenge exposure, 4 sheep served as nonvaccinated challenge-exposed controls, and 2 additional sheep served as nonvaccinated, nonchallenge-exposed, contact controls. Biopsy specimens (oral labial mucosa and skin) were obtained periodically after challenge exposure. Sheep were killed 8 to 13 days after challenge exposure, and necropsy was done. Vaccination did not seem to affect the nature or severity of the lesions observed. The changes in the mucosa of the cranial portion of the digestive tract included hyperemia, edema, inflammation, petechiae, erosions, ulcers, and surface encrustations. Lesions of skeletal, cardiac, and smooth muscles included hemorrhage, edema, myofiber degeneration, and necrosis. Lesions in cardiac muscles were sometimes widespread, indicating that cardiac failure may have been the major contributor to pulmonary congestion, edema, and eventual death during acute BTV infection. Damage to esophageal musculature resulted in vomiting. Hemorrhage was observed within the base of the pulmonary artery of all challenge-exposed sheep. Using immunofluorescence, bluetongue viral antigens were detected in small blood vessels of the skin, oral labial mucosa, tongue, esophagus, rumen, reticulum, urinary bladder, and pulmonary artery and in skeletal and cardiac muscles. Viral antigens were present in tissues obtained 3 to 11 days after inoculation. Ultrastructurally, changes in small-caliber blood vessels included congestion, hemorrhage, swollen degenerated endothelial cells, and occasional fibrin-platelet thrombi. Tubular structures and virus-like particles were observed within some of these endothelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experimental bluetongue virus infection of sheep; effect of vaccination: pathologic, immunofluorescent, and ultrastructural studies. 301 27

High risk splenectomy is often encountered in cases of hypersplenism with massive splenomegaly (10 times usual weight of 150-200 g) resulting from myelophthisic processes. Intra-operative ligation of the splenic artery through the lesser sac is a technically useful method of gaining vascular control prior to mobilizing the challenging spleen. However, a massive or inaccessible spleen imposes mechanical limitations during surgery and may be complicated by torrential intra-operative hemorrhage in the setting of severe thrombocytopenia refractile to platelet transfusions. The authors describe pre-operative intravascular proximal splenic artery control in four adult patients (3 men, 1 woman) with extreme splenomegaly (2,250-10,000 g). The massive splenomegaly in this group resulted from chronic myelogenous leukemia (n = 2), isolated splenic lymphoma (n = 1), and agnogenic myeloid metaplasia (n = 1). Chief symptom manifestations included left upper quadrant abdominal pain, early satiety, post-prandial emesis, dyspnea, petechiae, and associated easy bruising. Prior to surgery, all the patients were taken to the radiology suite where either detachable silastic balloons or stainless steel coils were placed selectively into the splenic artery under fluoroscopic guidance requiring approximately 35 minutes. Splenic artery occlusion aided normalization of thrombocytopenia (average increases 19,000/microliter to 215,000/microliter) with prolongation in survival of platelets. Successful splenectomy was subsequently performed with no additional transfusion requirements and was made technically easier by reducing splenic bulk. There were no adverse consequences of intravascular occlusion and no peri-operative morbidity or mortality. Preoperative intravascular selective splenic artery occlusion, used as an important potential adjunct to anticipated high risk splenectomy, is recommended.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Preoperative splenic artery occlusion as an adjunct for high risk splenectomy. 317 46

Bacterial infections are frequent events in premature and newborn infants. The reason is a defective specific and nonspecific defence of bacterial organisms. Some immunoglobulins like IgM and IgA including secretory IgA are absent. Premature infants also show a decreased level of IgG. Cellular immunity is anatomically intact but functionally defective. A number of complement factors are lacking, the activation of the alternative pathway is impaired. Newborn infants with perinatal problems like asphyxia or difficult delivery, show defects of leucocyte function like decreased deformability, defective chemotaxis and defective killing of ingested bacteria. Certain diseases, like hypoxia and malformations of immature organ functions in this age group (decreased acid production in the stomach), facilitate bacterial colonization of surface epithelia and the invasion of tissues. Consequences of these pathogenetic mechanisms are an unimpaired propagation of bacterial organisms into the blood and meninges without localization of the infecting organisms at the entry site. Bacterial meningitis is not considered a separate disease entity but a complication of bacteremia and sepsis. Clinical symptoms are nonspecific at the onset of the infection. Fever is frequently absent; decreased appetite, vomiting, a bloated abdomen, diarrhea, tachycardia, tachypnea are early signs of a bacterial infection, a grey mottled appearance, cyanosis, jaundice, petechiae, apneic spells, seizure activity and a metabolic acidosis are symptoms of advanced infection. Successful treatment at this stage is often not possible. Every sign of a decreased well being of a newborn of premature infant warrants laboratory and bacteriologic work up for septicemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chemotherapy of severe bacterial infections in pediatrics]. 631 69

The aim of this work was to describe the endoscopic features and clinical outcome of the duodenal complications in anaphylactoid purpura. Over a 3-year period, 20 patients were hospitalized in our unit because of purpura rheumatica. Duodenal complications occurred in 5 cases warranting endoscopic assessment. All patients had bilious vomiting and epigastric pain, constantly associated with low-grade purpuric rash. Plasma factor XIII concentrations were always decreased. The duodenal complication was suspected radiologically in 2 cases when "thumbprint" impressions were seen. Petechiae, oedema and intramural hematoma with superficial erosions were present endoscopically in 3 cases. The lesions were severe and extensive, involving the entire duodenum in 3 cases and the jejunum in one case. In one patient, there was a stricture of the upper part of the second duodenum. Treatment consisted of parenteral nutrition (using a central catheter: 3 cases, or a peripheral vein: 2 cases) and cimetidine (30 mg/kg.bw). The clinical outcome was favorable in 4 patients; the symptoms vanished and the endoscopic lesions were reversible (including the stricture) with restitutio ad integrum after 10 days. The last patient died the 8th day of treatment, 3 days after digestive improvement; the cause of death was probably iatrogenic and related to accidental migration of the central catheter. These results suggest that endoscopic examination should be performed in all patients with anaphylactoid purpura presenting with bilious vomiting. Endoscopy seems to be of great value in deciding if parenteral nutrition is indicated--or not--and perhaps in order to contraindicate the use of steroid therapy in the case of ulcerated hematomas.
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PMID:[Duodenal complications of rheumatoid purpura. Endoscopic aspects]. 643 33

Clinical and serological studies were carried out on 114 patients admitted to hospital in Havana, Cuba with Dengue Haemorrhagic Fever and Dengue Shock Syndrome (DHF/DSS). Serological confirmation of dengue was obtained in 90% of cases, with 5% of cases primary and 95% secondary. Fever, haemorrhagic manifestations, vomiting and headache were the most frequent signs and symptoms. Among haemorrhagic manifestations, petechiae and vaginal bleeding were reported in a larger number of patients. 21 patients presented shock and, of these, 20 were secondary infections. The disease appeared more frequently in white persons and in women. The aetiopathogenicity of the syndromes is discussed. 95% of the cases could be explained on the basis of the secondary infection hypothesis.
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PMID:Dengue haemorrhagic fever in Cuba. II. Clinical investigations. 646 14

KW2083 7-N-(p-hydroxyphenyl) mitomycin C is a mitomycin C derivative, but not its masked compound. KW2083 differs from mitomycin C in various points. A phase I study of KW2083 by single intravenous injection was performed in 21 patients with advanced solid tumor. The dose limiting factor of this drug is marrow depression, and 70mg/m2 causing marked thrombocytopenia was determined as maximum tolerated dose. The thrombocyte count and the WBC count reached to nadir the minimum 2 to 3 weeks after and 1 to 2 weeks after the administration and recovered in 1 to 2 weeks and in 2 to 3 weeks respectively. As gastrointestinal symptoms, nausea or vomiting (38.1%), and anorexia (28.6%) occurred soon after the administration, and stomatitis and diarrhea were also observed in one case each. In addition, petechia, hemorrhagic tendency and fever were found in one case each. Patients receiving 70mg/m2 showed slight alopecia and transient slight in GOT and GPT elevation.
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PMID:[Phase I study of KW2083 7-N-(p-hydroxyphenyl) mitomycin C]. 718 79

We describe two siblings affected by chronic relapsing thrombotic thrombocytopenic purpura from infancy. The elder brother, a 12-year-old boy had 50 such episodes characterized by acute onset of fever, headache, drowsiness, vomiting, dark urine, thrombocytopenia and anemia. The younger sister, a 6-year-old girl, had 8 episodes with the same clinical manifestations. Petechiae and ecchymoses on the extremities were present throughout their lives. Furthermore, anemia with evidence of red blood cell fragmentation and thrombocytopenia were present chronically. Periodical transfusion of frozen fresh plasma prevented recurrent episodes. These cases suggest that there is a congenital variant of thrombotic thrombocytopenic purpura.
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PMID:A congenital variant of thrombotic thrombocytopenic purpura in two siblings. 771 55

The clinical characteristics of serologically verified nephropathia epidemica, the Scandinavian form of hemorrhagic fever with renal syndrome, were studied in Swedish children who were < 15 years of age. In 1990 to 1992, 14 cases were prospectively followed. A retrospective survey during 1984 to 1990 disclosed another 18 cases. Among the 32 cases (20 boys, 12 girls, 3 to 15 years of age; median age, 11 years), the most common symptoms were fever (100%), headache (100%), abdominal pain (93%), vomiting (91%) and back pain (76%). Laboratory findings included elevated serum creatinine concentration (19 of 28) and thrombocytopenia (7 of 22). Urinalysis showed proteinuria (31 of 31 patients) and hematuria (24 of 30). Six children had mild hemorrhagic manifestations (epistaxis, metrorrhagia, and petechiae). No severe complications occurred. The clinical symptoms of children with nephropathia epidemica seem to be similar to those found among adult nephropathia epidemica cases.
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PMID:Nephropathia epidemica (hemorrhagic fever with renal syndrome) in children: clinical characteristics. 790 97

In a prospective case controlled study, we evaluated the adverse effects of long-term fluoride ingestion on the gastrointestinal tract. Ten patients with otosclerosis who were receiving sodium fluoride 30 mg/day for a period of 3-12 months, and 10 age- and sex-matched healthy volunteers were included. They were all evaluated clinically and subjected to a real time ultrasound examination, upper gastrointestinal endoscopy, and biopsies from the gastric antrum and duodenum. The biopsies were subjected to a rapid urease test as well as light and electron microscopic examinations. Ionic fluoride was estimated in the serum, urine, and drinking water using an ION 85 Ion Analyzer. Seven subjects (70%) ingesting fluoride had abdominal pain, vomiting, and nausea. Petechiae, erosions, and erythema were seen on endoscopy in all the subjects, but not in the controls. Histological examination of the gastric antral biopsy showed chronic atrophic gastritis in all the subjects but in only one (10%) healthy volunteer. Scanning electron microscopic examination showed "cracked-clay" appearance, scanty microvilli, surface abrasions, and desquamated epithelium in the subjects ingesting fluoride, but not in the controls. We conclude that long-term fluoride ingestion is associated with a high incidence of dyspeptic symptoms as well as histological and electron microscopic abnormalities.
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PMID:Toxic effects of chronic fluoride ingestion on the upper gastrointestinal tract. 803 13


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