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)

Untreated hyperthyroidism during pregnancy is associated with increased maternal and perinatal morbidity. Some features of this disease simulate preeclampsia, which may encourage delivery of the fetus. We report a case of poorly controlled hyperthyroidism associated with generalized seizures, where patient management was directed at a diagnosis of preeclampsia-eclampsia. Although the presence of eclampsia and marked hyperthyroidism is very rare, this case illustrates the importance of aggressive medical management of hyperthyroidism. A 17-year-old gravida was diagnosed with hyperthyroidism at 15 weeks' gestation. At 26 weeks' gestation, she was admitted to the hospital after noting edema of the upper and lower extremities, nausea, vomiting, shortness of breath, and a cough. At admission, she was hypertensive, tachycardic, and dyspneic. The patient was believed to have preeclampsia with pulmonary edema complicated by hyperthyroidism. We initiated magnesium sulfate therapy and administered several bolus doses of hydralazine, with little effect on blood pressure. Oliguria was noted, and a pulmonary artery catheter was inserted. Hours later, generalized seizure activity occurred, and a decision was made for abdominal delivery. Postoperatively, cardiovascular function stabilized. On postoperative day 3, we received the results of the thyroid function tests obtained at admission, which suggested a markedly hyperthyroid condition. Untreated or poorly treated hyperthyroidism may present a clinical picture similar to preeclampsia. In our case, both disease processes coexisted in their severest forms. It is possible, although completely unproven, that a relationship exists between poorly controlled hyperthyroidism and preeclampsia-eclampsia. More importantly, accurate diagnosis of hyperthyroidism should lead to prompt medical or surgical management, thereby decreasing maternal and perinatal morbidity.
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PMID:Hyperthyroidism and seizures during pregnancy. 761 94

Rocky Mountain spotted fever occurs during seasonal tick activity. A history of exposure to tick-containing habitats within the 3- to 12-day incubation period is a key epidemiological factor. The signs of fever, headache, myalgia, nausea, vomiting, and anorexia at onset of infection are difficult to distinguish from those of self-limited viral infections. Rash usually appears later and, if present, progresses through a sequence of stages and distribution that are never pathognomonic. The effects of disseminated Rickettsia rickettsii infection of endothelial cells include increased vascular permeability, edema, hypovolemia, hypotension, prerenal azotemia, and, in life-threatening cases, pulmonary edema, shock, acute tubular necrosis, and meningoencephalitis. In severe cases, fluid management is a challenge. The clinical diagnosis, which is difficult, is rarely assisted by laboratory findings because antibodies are usually detected only in convalescence, and immunohistologic methods for detection of rickettsiae are unavailable in most clinics. Doxycycline is the treatment of choice except for pregnant or allergic patients, who are treated with chloramphenicol.
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PMID:Rocky Mountain spotted fever: a seasonal alert. 761 84

The pathology of aerosolized staphylococcal enterotoxin B (SEB) was studied in the nonhuman primate. Six juvenile rhesus monkeys that received multiple lethal inhaled doses of SEB developed diarrhea and vomiting within 24 hr followed by depression, dyspnea, and shock. Three of 6 animals died by 52 hr. The most striking gross lesion in all 6 monkeys was diffuse severe pulmonary edema. Histologically, edema fluid was present within the peribronchiolar, peribronchial, and perivascular interstitium, alveolar septa, and alveoli. The adventitia of pulmonary vessels was infiltrated by lymphocytes, macrophages, and fewer neutrophils. Numerous large lymphocytes with occasional mitotic figures were within pulmonary vessels, often occluding alveolar capillaries. These cells were strongly immunoreactive with monoclonal antibodies against CD3, establishing them as T cells. Ultrastructurally, endothelial cell junctions were intact, and endothelial cells and type I pneumocytes contained numerous pinocytotic vesicles. Alveolar septal interstitial spaces were expanded by edema. The mechanism of these SEB-induced pulmonary lesions was not determined. We hypothesize that cytokine production by activated T cells may have caused vascular permeability changes leading to widespread pulmonary edema and shock.
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PMID:Aerosolized staphylococcal enterotoxin B-induced pulmonary lesions in rhesus monkeys (Macaca mulatta). 765 51

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

Five children with AML were treated with high-doses of Ara-C (2 g/m2) during consolidation. After 17 cycles the toxicity was evaluated. Granulocytopenia (< 0.5 x 10(9)/l) and thrombocytopenia (< 25 x 10(9)/l) were stated after 15/17 and 13/17 cycles respectively. The nadir of bone marrow suppression appeared between day 10 and 14. In one case treatment related death during severe myelosuppression was noted. In individual cases jaundice with elevated activity of aminotransferases, paralytic ileus and pulmonary oedema were observed. All these adverse reactions were reversible. Other toxicities such as nausea/vomiting, stomatitis, diarrhea, infections and drug related fever were transient. No neurologic toxicity was seen. There is a need for developing a new way of the administration of high-dose Ara-C which could substantially reduce toxicity of the drug.
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PMID:[Preliminary evaluation of adverse effects after administration of arabinoside cytosine (Ara-C) in high doses to children with acute myelogenous leukemia]. 820 12

Eighty-seven cats with histologically confirmed malignant tumors were used in a prospective study to determine the toxicity of mitoxantrone, a dihydroxyquinone derivative of anthracene, which was administered at 21-day intervals at dosages ranging from 2.5 to 6.5 mg/m2 of body surface, IV. Eleven of these cats were treated concurrently with radiation but were evaluated separately. Each cat was evaluated for signs of toxicosis for 3 weeks after each dose was administered or until the cat developed progressive disease, or until the cat's quality of life diminished to an unacceptable level as determined by the owner or attending veterinarian. Although the primary purpose of this study was to determine a clinically useful dosage and to characterize the toxicoses associated with mitoxantrone administration, each cat was monitored for response to treatment. Forty-nine cats had been refractory to 1 or more treatment modalities prior to inclusion in this study. The most common signs of toxicosis after treatment with mitoxantrone were vomiting, anorexia, diarrhea, lethargy, sepsis secondary to myelosuppression, and seizures. Two cats died of complications that may have been attributed to mitoxantrone: 1 of cardiomyopathy and the other of pulmonary edema of an undetermined cause. Older cats were more likely to develop signs of toxicosis after the third or fourth mitoxantrone treatment than younger cats (P < or = 0.05). Cats with signs of toxicosis during the 21-day interval after administration of the first dose of mitoxantrone were significantly (P < or = 0.05) more likely to develop signs of toxicosis during the 21-day interval between the second and third doses of mitoxantrone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Toxicoses and efficacy associated with administration of mitoxantrone to cats with malignant tumors. 832 Jan 52

The purpose of this study was to review our experience with the use of OKT3 (a murine monoclonal CD3 antibody) used as immune prophylaxis for pediatric heart transplant recipients. Orthotopic heart transplantation was performed in 18 pediatric patients, 8 girls and 10 boys, ranging in age from 17 days to 17 years. OKT3 therapy was initiated intraoperatively at a dose of approximately 0.2 mg/kg and was administered at a dose of approximately 0.1 to 0.2 mg/kg/day for a period of 11.5 +/- 2.5 days. Daily average OKT3 levels were 1132 +/- 469 ng/ml. Side effects that occurred during OKT3 therapy were fever (59%), diarrhea (24%), headaches (24%), vomiting (18%), encephalopathy (12%), pulmonary edema (6%), and rash (6%). Infections occurred in 24% of patients, all within 6 months of transplantation. In the first year after transplantation, patients experienced 3.4 +/- 2.4 episodes of mild rejection and 1.0 +/- 0.8 episodes of moderate rejection. No patient experienced severe rejection. Five of the surviving 14 patients (36%) have been weaned from chronic steroid therapy, and 42% are being maintained on alternate-day prednisone at a dose of 0.06 +/- 0.02 mg/kg/day. Coronary artery disease developed in three patients; two of whom died. Actuarial survival was 83% at 1 year and 73% at 2 years. This report shows that OKT3 prophylaxis in pediatric heart transplantation can be used with acceptable short-term adverse side effects and overall survival.
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PMID:Murine monoclonal CD3 antibody (OKT3)-based early rejection prophylaxis in pediatric heart transplantation. 832 14

Headache, nausea, vomiting, insomnia and peripheral edema are the most important symptoms of acute mountain sickness (AMS), which occur within 6 to 12 h. after exposure to altitudes of more than 2500 m a. s. l. Usually, these symptoms resolve spontaneously; however, they may progress to life-threatening cerebral edema in some cases. High-altitude pulmonary edema (HAPE) is a noncardiogenic edema, which is often preceded by acute mountain sickness. Frequency and severity of these illnesses depend on the altitude, the rate of ascent and the degree of individual susceptibility. A low hypoxic ventilatory drive, sodium and water retention as well as increased capillary permeability are the most important pathophysiological factors which contribute to hypoxemia and edema formation in AMS. They are also important in the pathophysiology of HAPE. In addition, excessive hypoxic pulmonary artery hypertension is most likely crucial in the pathogenesis of HAPE. Constitutional factors which regulate ventilation and pulmonary artery pressure under hypoxia are considered the most important determinants of susceptibility to AMS and HAPE.
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PMID:[Clinical aspects and pathophysiology of altitude sickness]. 837 71

Ten cases of acute renal failure (ARF) were seen in the period from July 1990 to August 1991 in the Nephrology Department of the SIMS Hospital, Srinagar. All were males in the age group of 18-28 years and in apparent good health when apprehended by the police. There was alleged history of physical torture of different types. All had been beaten on the buttocks, back and limbs; in addition, 2 cases had been given repeated electric shocks and 1 case put to 'sit-and-stand' exercise for about 3 h. The interval between the first day of torture till they came to our observation varied from 4 to 11 days. The main clinical features at the time of presentation were generalized aches and weakness (10), oligoanuria (9), vomiting (8), hypertension (6), acidosis (10), facial puffiness and pedal edema (6), fever and shivering (3), pulmonary edema (2), stupor (4), and hyperkalemia (5). All the cases had an established ARF (serum creatinine 668-1,997 mumol/l and serum urea 21.8-71.8 mmol/l) when first seen. Muscle enzymes, creatine phosphokinase, lactic dehydrogenase and serum glutamic oxaloacetic transaminase were all significantly raised indicating rhabdomyolysis. All showed evidence of myoglobin casts in urine. Nine had oliguric and 1 had nonoliguric ARF. All except the 1 case with nonoliguric ARF were managed with peritoneal dialysis and/or hemodialysis. All recovered. Early recognition of ARF is important since the main attention in such cases is directed towards the surgical aspect.
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PMID:Acute renal failure following physical torture. 845 79

Acute mountain sickness (AMS) affects, to varying degrees, all travelers to high altitudes (elevations greater than 5280 feet). In a small percentage of patients, AMS can lead to high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE). Symptoms of AMS range from a combination of headache, insomnia, anorexia, nausea, and dizziness, to more serious manifestations, such as vomiting, dyspnea, muscle weakness, oliguria, peripheral edema, and retinal hemorrhage. Although the primary cause of these symptoms is related to the reduced oxygen content and humidity of the ambient air at high altitudes, the physiologic pathway relating hypoxemia to AMS and its sequelae remains unclear. Tips on self-diagnosis and symptom recognition are critical elements to be included in educating patients who are contemplating a trip to high altitudes. Preventive strategies include allowing 2 days of acclimatization before engaging in strenuous exercise at high altitudes, avoiding alcohol, and increasing fluid intake. Conditioning exercise for patients older than 35 years is also recommended before departure. A high-carbohydrate, low-fat, low-salt diet can also aid in preventing the onset of AMS. Acetazolamide (125 mg two or three times daily, or once at bedtime) has also been shown to reduce susceptibility to AMS and the incidence of HAPE and HACE. Although effective in treating cerebral symptoms of AMS, dexamethasone is not routinely recommended as a prophylactic agent for AMS.
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PMID:A trek to the top: a review of acute mountain sickness. 855 56


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