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)

There have been reports of chemical attacks in which sulfur mustard might have been used (a) on Iranian soldiers and civilians during the Gulf War in 1984 and 1985 and (b) in an Iraqi chemical attack on the Iranian-occupied village of Halbja in 1988, resulting in many civilian casualties. Heavy use of chemical warfare in Afghanistan by the Soviet military is a recent innovation in military tactics that has been highly successful and may ensure further use of chemical agents in future military conflicts and terrorist attacks as a profitable adjunct to conventional military arms. Mustard is a poisonous chemical agent that exerts a local action on the eyes, skin, and respiratory tissue, with subsequent systemic action on the nervous, cardiac, and digestive systems in humans and laboratory animals, causing lacrimation, malaise, anorexia, salivation, respiratory distress, vomiting, hyperexcitability, and cardiac distress. Under extreme circumstances, dependent upon the dose and length of exposure to the agent, necrosis of the skin and mucous membranes of the respiratory system, bronchitis, bronchopneumonia, intestinal lesions, hemoconcentration, leucopenia, convulsions with systemic distress, and death occur. Severe mustard poisoning in humans is associated with systemic injury, which is manifested as headache, epigastric distresses, anorexia, diarrhea, and cachexia and is usually observed at mustard doses of 1000 mg/min/m3 with damage to hematopoietic tissues and progressive leucopenia. Sulfur mustard is a cell poison that causes disruption and impairment of a variety of cellular activities that are dependent upon a very specific integral relationship. These cytotoxic effects are manifested in widespread metabolic disturbances whose variable characteristics are observed in enzymatic deficiencies, vesicant action, abnormal mitotic activity and cell division, bone marrow disruption, disturbances in hematopoietic activity, and systemic poisoning. Indeed, mustard gas readily combines with various components of the cell such as amino acids, amines, and proteins. Although evidence of an association between lung cancer and mustard gas encountered on the battlefields of World War I is at best suggestive if not problematical (Case and Lea, 1955; Beebe, 1960; Norman, 1975), the epidemiological data accumulated from the poison gas factories in Japan (Yamada et al., 1953; Wada et al., 1968; Inada et al., 1978; Shigenobu, 1980; Nishimoto et al., 1983; Hirono et al., 1984; Takuoka et al., 1986), in Germany (Weiss, 1958; Hellmann, 1970a; Weiss and Weiss, 1975; Klehr, 1984) and in England (Manning et al., 1981; Easton et al., 1988) are substantial (International Agency for Research on Cancer, 1975). Unfortunately, attempts to seek confirmatory and substantial evidence in laboratory animals such as mice (Boyland and Horning, 1949; Heston, 1950; Heston, 1953a; McNamara et al., 1975) and rats (Griffin et al., 1951; McNamara et al., 1975; Sasser et al., 1996) have not been consistent. Sulfur mustard has been shown to be mutagenic in a variety of different species using many different laboratory techniques from fruit flies, microorganisms and mammalian cell cultures (Fox and Scott, 1980). Evidence is slowly accumulating from human data (Hellmann, 1970a; Lohs, 1975; Wulf et al., 1985). Evidence for the teratogenicity of mustard has been negative in assessment of fetotoxicity and adverse effects of mustard on the reproductive potential of both human and animal studies. Indeed, investigations of women adversely affected by mustard are minimal because most of the studies have been performed on former men employees of poison gas factories and have been negative or questionable. We have recently emphasized the need to assess the affect of a suspected teratogen on maternal toxicity in laboratory animals before any conclusions can be made.(ABSTRACT TRUNCATED)
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PMID:Toxicology and pharmacology of the chemical warfare agent sulfur mustard. 880 7

The efficacy and safety of the angiotensin converting enzyme inhibitor enalapril in dogs with naturally acquired class III or class IV heart failure was evaluated in this study. Eighteen small-breed dogs with insufficiency of their mitral valves, but without other diseases were included in this study over a period of six months. When necessary due to massive pulmonary edema or high serum potassium concentrations, furosemide was added to the therapy with enalapril. No other drugs, including digitalis, were used in this study. The treatment was followed by anamnesis, clinical examinations, electrocardiography, radiography, echocardiography and laboratory diagnosis. Examinations were performed before treatment and after one week, after six weeks and after six months of treatment. 72% of the dogs improved in NYHA classification until the end of the study (p < 0.05). The incidence of seizures due to syncopes or severe respiratory distress decreased during this study (p < 0.01). For 28% of the dogs this treatment was not successful. In the electrocardiographic, radiographic and laboratory examinations statistically significant changes could not be recorded. The decrease in heart rate did not reach statistical significance. The echocardiographic investigation evaluated a significant decrease in fractional shortening and in the diastolic diameter of the left ventricular wall (p < 0.05 respectively p < 0.01), but no significant change in the diastolic or systolic diameter of the interventricular septum. The average oral dose of enalapril was 0.38 mg/kg body weight b.i.d., the average dose of furosemide was 0.37 mg/kg body weight b.i.d. in the first week of the study and was raised to 0.74 mg/kg body weight b.i.d. until the end of the study. Side effects like diarrhea, vomiting or reduced appetite did not increase during the course of the study. However one dog was excluded from the study because of repeated vomiting after six weeks of treatment. This study shows the beneficial clinical and hemodynamic effects and the security of the therapy with enalapril for dogs with heart failure due to mitral insufficiency.
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PMID:[Treatment of mitral valve insufficiency in dogs with the ACE inhibitor enalapril. A clinical progress study]. 953 70

Forty-three cases of diabetic ketosis were analysed to determine the mode of presentation, treatment modalities and outcome. Among these cases 62.8% were non-insulin dependent diabetes mellitus (NIDDM) patients and 37.2% belonged to the insulin dependent diabetes mellitus (IDDM) group. Six patients had blood glucose levels of more than 250 mg/dl but less than 300 mg/dl who were grouped separately for analysis under the term "euglycaemic diabetic ketoacidosis (EGDK)". Infection was the commonest precipitating factor in diabetic ketosis in all groups. Abdominal pain and vomiting occurred with NIDDM and EGDK cases. Drowsiness was common and coma was rare. Acute myocardial infarction (MI) and pulmonary oedema occurred with NIDDM cases. Shock, acidosis, acquired respiratory distress syndrome (ARDS) and mucor mycosis were seen with IDDM cases. Mortality was 7 out of 43(16.3%). Saline requirement was lower in NIDDM and EGDK cases. Intensive insulin therapy with hourly intravenous doses were needed for IDDM cases while majority of NIDDM cases could be managed with 6 hourly doses of insulin given subcutaneously or intramuscularly.
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PMID:Changing profile of diabetic ketosis. 956 97

Eleven neonates ranging in gestational age from 34 to 40 weeks presented with gastric necrosis. The 4 full-term neonates showed sudden-onset hemorrage and "coffee-ground" vomiting; in the 7 premature babies the initial clinical finding was abdominal distention. The criteria for diagnosis were: perinatal distress in prematures and transient neonatal respiratory distress in full-term babies. Radiographic evidence of gastric distention was typical and preceded clinical signs of hematemesis and gastric perforation. Surgery was performed in 8 patients; 3 received medical treatment. At surgery 1 total and 3 subtotal gastrectomies and 4 segmental gastric resections were performed. Three of these patients died post-operatively as a consequence of multiorgan failure; a second look was necessary in one patient 1 week after surgery because of prepyloric perforation due to ulcers. Biopsy specimens taken from the site of perforation demonstrated extensive necrosis; ulceration was disseminated in the surrounding gastric mucosa; no signs of phlogosis were detected. The diagnosis, treatment, and physiopathologic considerations are reviewed.
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PMID:Gastric necrosis in newborns: a report of 11 cases. 963 13

Clinical Confusion between human babesiosis and malaria is often reported in the literature. Headache, fever, chills, nausea, vomiting, myalgia, altered mental status, disseminated intravascular coagulation, anaemia with dyserythropoiesis, hypotension, respiratory distress, and renal insufficiency are common to both diseases. This remarkable similarity is not restricted to the human host. In the mouse, for example, the histological changes wrought by fatal malaria (Plasmodium vinckei) and babesiosis (Babesia rhodaini) are identical, and parasites of both genera cross-protect. Malarial disease pathogenesis is now generally associated with excessive production of pro-inflammatory cytokines , such as tumour necrosis factor. While this concept has not yet been examined in babesiosis, indirect evidence arises from noting the parasite density at which illness occurs in primary infections caused by either organism. Naive mice tolerate high loads of malarial or babesial parasites before they become ill, and are also tolerant to endotoxicity, which is mediated by these same cytokines. In contrast, humans require very much smaller loads of Plasmodium or Babesia spp. before becoming ill, and likewise are very sensitive to endotoxin, the harmful effects of which are mediated by the pro-inflammatory cytokines. For these reasons, as discussed in this review, the diseases caused by these two genera of intra-erythrocytic protozoan parasites will probably prove to be conceptually identical.
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PMID:Do babesiosis and malaria share a common disease process? 968 99

Although angiotensin-converting enzyme inhibitors (ACEIs) are well-known causes of orofacial angioedema, angioedema from these agents involving the bowel is not often considered. We report a case of simultaneous onset of small bowel and orofacial angioedema due to captopril. A 61-year-old black man with hypertension, coronary artery disease, and congestive heart failure had been treated with captopril for 5 years. He had sudden swelling of the lips, face, and tongue, followed by nausea, emesis, abdominal pain, and diarrhea. Other medications included aspirin, indomethacin, allopurinol, colchicine, and nifedipine. Examination showed swelling of the tongue, buccal mucosa, and neck; he also had midabdominal tenderness but no respiratory distress. Laboratory data were normal. A C1-esterase inhibitor level was normal. An ileus pattern was present on abdominal x-ray film. Angioedema was diagnosed, and all signs and symptoms resolved in 24 hours after captopril was discontinued. Clinicians need to be vigilant for bowel involvement from ACEI angioedema.
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PMID:Simultaneous mucosal and small bowel angioedema due to captopril. 982 92

Recently leukocytapheresis (LCAP) has attracted attention as a new therapy for ulcerative colitis. We reviewed the complications associated with LCAP carried out in our department during the period from December 1992 to September 1997. There were side effects during 195 (9.9%) of the 1,978 sessions performed, involving 47 (51.1%) of the 92 patients treated. Moderate reactions, which caused considerable discomfort to the patients and required the transient interruption of the administration or some medical treatment depending on the state, occurred during 31 (1.6%) of all therapy sessions, involving 15 (16%) patients. All patients recovered soon and never fell into a life-threateningly severe state. They also did not have any symptoms afterwards. The common side effects were nausea, vomiting, fever, chills, and nasal obstruction. Reactions such as palpitations, respiratory distress, or chest oppressions were common, especially when heparin sodium (HS) was used as the anticoagulant. The type and frequency of side effects depended somewhat on the length of the therapy series or the duration of one session. Other complications such as clotting in the leukocyte removal filter and/or blood line during administration were encountered frequently. These latter problems occurred during 46% of all sessions, but most of them had little significance. Sessions in which HS was used as the anticoagulant showed more severe clotting than those in which nafamostat mesilate (NM) was used. In our series, we experienced a relatively low rate of serious complications. We require, of course, careful observation during and after each session.
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PMID:Complications of leukocytapheresis. 1022 12

There are three clinical presentations of anthrax in humans: cutaneous (>95% of cases), orogastric and inhalational. The infectious form, the spore, enters the body and is thought to germinate within macrophages either at the site of inoculation (cutaneous or orogastric) or in the regional lymph node (inhalational). The bacillus then synthesizes its antiphagocytic capsule and the lethal and oedema toxins which interfere with the non-specific host defences leading to the characteristic locally destructive lesion and spread by lymphatics to the systemic circulation and other organs. The cutaneous form begins as a papule which progresses over several days to a vesicle and then ulcerates. There is often oedema, sometimes massive, probably due to the oedema toxin that surrounds the lesions which then develop a characteristic black eschar. The patient may be febrile with mild to severe systemic symptoms of malaise, headache and toxicity. Oropharyngeal anthrax presents with severe sore throat or an ulcer in the oropharyngeal cavity associated with neck swelling, fever, toxicity and dysphagia. Gastrointestinal anthrax begins with anorexia, nausea, vomiting and abdominal pain which may be similar to an acute abdomen. There may be diarrhoea and ascites, both of which may be haemorrhagic. Inhalational anthrax begins with non-specific symptoms of malaise, fever, myalgia and non-productive cough. After a period of 2-3 days, this is followed by a sudden onset of severe respiratory distress associated with diaphoresis, cyanosis and increased chest pain. There may be a widened mediastinum and pleural effusions on chest X-ray. Death follows in 24-36 h from respiratory failure, sepsis and shock. The diagnosis of anthrax is easy if it is considered. The organism is readily observed by Gram or Wright stain in local lesions or blood smear and can be easily cultured from the blood and other body fluids. However, because of its rarity, it is not often included in the differential diagnosis and in inhalational disease the diagnosis is rarely made until the patient is moribund. More rapid diagnostic tests are under development. Penicillin, combined with supportive care, remains the mainstay of treatment, although the organism is susceptible in vitro to many antibiotics. In recent years, there have been significant advances in our knowledge of the organism and its toxins and it is anticipated that similar progress will be made in the future in developing more rapid diagnostic tests and new modalities of treatment.
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PMID:Clinical aspects, diagnosis and treatment of anthrax 1047 74

Acute pancreatitis is one of the complications associated with severe primary and secondary hypertriglyceridemia. The frequency of hypertriglyceridemia in patients with pancreatitis ranges from 4 to 53%. The elevation in serum triglycerides probably induces the release of free fatty acids, responsible for the pancreatic damage. During a three year study, nine patients with acute pancreatitis due to hypertriglyceridemia were followed up at the University Hospital of Federal University and at the "Hospital Monte Sinai" (Juiz de Fora, MG, Brazil). Suggestive clinical manifestations, especially superior abdominal pain, nausea, vomiting and ileus, were found in all the patients; however, only three showed elevated serum amylase levels. All had triglyceride levels above 1000 mg/dl (11.3 mmol/L). The evolution after clinical treatment was good in eight patients (two needed parenteral nutrition). The only death observed was due to shock and acute respiratory distress, refractory to clinical management. The maintenance treatment aimed at withdrawing the predisposing conditions and reduction of the triglyceride levels prevented recurrence of acute pancreatitis episodes during the 23 months of follow-up.
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PMID:[Hyperlipemic pancreatitis: clinical course]. 1051 73

An eight-year-old intact male Bernese mountain dog was referred with a history of chronic vomiting, coughing and signs of respiratory distress. Other historical findings included lethargy, weight loss and choking. On presentation, clinical findings were Horner's syndrome, ipsilateral laryngeal hemiplegia, coughing, gagging, respiratory distress and vomiting. Lateral cervical radiographs showed ill-defined mineralisation in the soft tissue ventral to the third cervical vertebra, while ultrasonography of the neck revealed a well marginated heterogeneous mass with focal hyperechogenic lesions and acoustic shadowing. Results of an ultrasound-guided fine needle aspirate suggested neoplasia. At necropsy, a large tumour was detected in the ventral cervical region, originating from the right vagosympathetic trunk. In view of the infiltrating pattern, the cellular pleomorphism and the numerous mitoses on histopathological examination, the tumour was classified as a malignant peripheral nerve sheath tumour.
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PMID:Cervical neoplasia originating from the vagus nerve in a dog. 1075 81


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