Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen patients with Hodgkin's (10) and non-Hodgkin's (6) lymphoma were treated by the "ABCD scheme", which is a combination of adriamycin (25-30 mg/m2 day 1), bleomycin (15 mg day 1-5), CCNU (60 mg/m2 day 1) and DIC (90-100 mg/m2 day 1-5). 15 results are evaluable and included 5 complete remissions, 5 partial remissions, 2 stabilizations, 2 progressions and 1 early death (remission rate: 66%). 45 ABCD courses were given. 8 patients received more than one course (maximum 7 courses). Toxicity was tolerable and consisted mainly of myelodepression, nausea, vomiting and muco-cutaneous alterations. Two patients died following toxicity, one from myelosuppression and the other from interstitial pulmonary fibrosis. The results suggest that this combination can be useful where the usual chemotherapy combination fails.
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PMID:[Simultaneous combination of adriamycin, bleomycin, cyclohexyl-chloroethyl nitrosourea with dimethyl-triazeno imidazole carboxamide in the treatment of Hodgkin's lymphoma]. 6 45

Seven children (aged 8--17 years) presented with a high fever, headache, confusion, conjunctival hyperaemia, a scarlatiniform rash, subcutaneous oedema, vomiting, watery diarrhoea, oliguria, and a propensity to acute renal failure, hepatic abnormalities, disseminated intravascular coagulation, and severe prolonged shock. One patient died, one had gangrene of the toes, and all have had fine desquamation of affected skin and peeling of palms and soles during convalescence. Five patients were studied prospectively. Staphylococcus aureus related to phage-group I was isolated from mucosal (nasopharyngeal, vaginal, tracheal), or sequestered (empyema, abscess) sites, but not from blood. This organism produces an exotoxin which causes a positive Nikolsky sign in the newborn mouse and which is biochemically, pathologically, and immunologically distinct from phage-group-II stapphylococcal exfoliatin.
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PMID:Toxic-shock syndrome associated with phage-group-I Staphylococci. 8 81

Seven patients, aged 12 to 19 years, had atypical measles. Prodromal symptoms of fever, malaise, myalgia, headache, nausea, and vomiting were commonly followed by coryza, sore throat, conjunctivitis, photophobia, nonproductive cough, and pleuritic pain. The characteristic rash was erythematous, maculopapular, and progressed frequently to vesicular, petechial, or purpuric lesions. It initially involved palms and soles with subsequent spread to proximal extremities and the trunk, sparing the face. Six of six chest roentgenograms showed infiltrates. Findings not previously described in atypical measles included liver enzyme elevations, thrombocytopenia, disseminated intravascular coagulation, possible transmission among three siblings, and suspected cardiac involvement. Measles complement fixation titers compatible with recent infection were seen in all patients. All patients had previously received killed measles vaccine. A substantial number of persons who are older adolescents or young adults may be at risk of developing atypical measles.
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PMID:Atypical measles in adolescents and young adults. 44 83

The first recognised outbreak of Marburg virus disease in Africa, and the first since the original epidemic in West Germany and Yugoslavia in 1967, occurred in South Africa in February 1975. The primary case was in a young Australian man , who was admitted to the Johannesburg Hospital after having toured Rhodesia. Two secondary cases occurred, one being in the first patient's travelling companion, and the other in a nurse. Features of the illness included high fever, myalgia, vomiting and diarrhoea, hepatitis, a characteristic maculopapular rash, leucopenia, thrombocytopenia, and a bleeding tendency. The first patient died on the seventh day from haemorrhage resulting from a combination of disseminated intravascular coagulation and hepatic failure. The other two patients were given vigorous supportive treatment and prophylactic heparin and recovered after an acute phase lasting about seven days. During this period on developed pancreatitis, the serum amylase remaining raised until the 32nd day after the onset of the illness. The other developed unilateral uveitis after having been asymptomatic for two months. This persisted for several weeks and Marburg virus was cultured from the anterior chamber of the eye.
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PMID:Outbreake of Marburg virus disease in Johannesburg. 81 15

With improving standards of antenatal care, severe pre-eclampsia dn eclampsia are becoming less common and experience in the management of these conditions is lessening. Co-ordinated plans for the care of patients should be established by obstetricians and anaesthetists working as a team. A suitable regime for drug therapy in severe pre-eclampsia or eclampsia is the following: Initial management Diazepam 10 mg slowly i.v. Pethidine 100-150 mg i.m. or i.v. in incremental dosage, or extradural blocks, if analgesia is also required. Hydrallazine 20 mg i.v. initially, followed by 5 mg at intervals of 20 min until the diastolic pressure is less than 110 mm Hg. Then, preferably by syringe pump in a concentration of 2 mg/ml, at a rate of 2-20 mg/h. If vomiting occurs this can be controlled by administration of atropine. Subsequent management Sedation and anticonvulsant therapy. Continue diazepam and, in severe cases, institute chlormethiazole infusion. Continue analgesia with pethidine or extradural block. Control of hypertension by adjusting the dose of hydrallazine. If tachycardia exceeds 120 beat/min give propanolol 2-4 mg i.v. Plasma protein depletion with groww oedema is treated by administration of salt-free albumin or plasma protein fraction. Diuretic therapy is indicated if there is gross oedema or signs suggestive of acute renal failure. Oliguria associated with increased blood urea may be a result of renal failure or dehydration. The latter should be evident from the patient's condition and central venous pressure, but i.v. fluids and frusemide 20-40 mg can be used as a therapeutic test. Mannitol reduces cerebral oedema and may be given if diuresis has been first produced with frusemide. Potassium chloride is given if the plasma potassium decreases to less than 3 mmol/litre. Heparin therapy is considered if there is clinical evidence of disseminated intravascular coagulation.
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PMID:The management of severe pre-eclampsia and eclampsia. 83 44

Five patients who had injected intravenous (i.v.) phenmetrazine or methamphetamine developed marked prostration resembling septic shock, disseminated intravascular coagulation, rhabdomyolysis with myoglobinuria, and azotemia. Soon after injection, four noted chills, fever, sweats, nausea, and abdominal cramps. Within hours, they developed vomiting, myalgias, paresthesias, headache, and orthostasis. Cardiorespiratory arrest, accelerated bleeding, and noncardiac pulmonary edema were observed in one patient. From 4 to 11 litres of saline were required in the first 24 h to maintain blood pressure and urine output, suggesting that shock resulted from massive loss of intravascular volume into necrotic muscle. Recognition of this syndrome and treatment by aggressive volume replacement led to the recovery of all five patients.
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PMID:Rhabdomyolysis and shock after intravenous amphetamine administration. 84 98

A patient with chronic active hepatitis developed vomiting, dyspnoea, tachycardia, diarrhoea and diffuse pains. For several years she had been treated with azathioprine and for a few weeks before admission with phenformin for mild diabetes. Laboratory examination revealed acute disseminated intravascular coagulation and lactacidaemia. Despite intensive treatment the patient died a few hours after admission, the post-mortem examination revealing diffuse pulmonary haemorrhages. The present case report and those published in the literature suggest that phenformin should not be given to diabetics who also have renal or hepatic disease. In any case, if phenformin is given, it should be stopped if hepatic, renal, infectious or thrombotic complications occur. In these cases and those of sudden unexplained deterioration in diabetics, hospitalisation is essential and lactic acid levels should be determined and coagulation tests performed.
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PMID:[Lactacidaemia and disseminated intravascular coagulation associated with phenformin medication (author's transl)]. 114 86

A case of life-threatening adverse effects following intravenous administration of a non-ionic contrast medium is reported. The patient, a 68-year-old diabetic hypertensive male with dyspnoea and cough had an abnormal chest radiograph, revealing congestive heart failure and an enlarged right hilum. Computed tomography (CT) of the chest was performed using 100 cm3 of intravenous iopamidol. Within half an hour the patient developed abdominal cramping, vomiting, and diarrhoea, followed by hypotension, tachycardia, fever to 40 degrees C, and delirium. His course was complicated by disseminated intravascular coagulation, rhabdomyolysis, renal failure, respiratory arrest, and atrial fibrillation. There was no evidence of infection, neoplastic disease, or myocardial infarction. Over the next month the patient slowly recovered. One other case report implicates a contrast agent with a similar syndrome. The features of this case fulfil the criteria for a probable adverse drug reaction of a type and severity rarely encountered.
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PMID:Case report: multisystem failure following intravenous iopamidol. 139 88

The authors report six patients with acute endosulfan intoxication. The symptoms of nausea, vomiting, headache, and dizziness began 2.7 +/- 0.5 h after ingestion; in four cases the patients had been hospitalized but were asymptomatic. All had severe metabolic acidosis with high anion gap and hyperglycemia; five of six had decreased blood platelets. Three patients had pulmonary aspiration, and five required mechanical ventilation. The one fatality followed acute renal failure, disseminated intravascular coagulation, thrombi in the pulmonary arteries and aorta, and cardiogenic shock. In this patient the blood endosulfan was 2.85 mg/L versus a mean of 0.48 mg/L in the survivors.
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PMID:Acute intoxication by endosulfan. 143 28

In 1989-90 in India, physicians used 4 different methods to induce second trimester abortion (14-20 weeks gestation) in 200 women at the Lokmanya Tilak Municipal General Hospital in Sion in Bombay. In 50 women each, they introduced 200 ml of 20% hypertonic saline into the amniotic sac, after removing 35-200 ml of amniotic fluid; 150 ml of ethacridine lactate extraovularly; prostaglandin F2 intramuscularly at regular intervals; and a cupful of 5% povidone-iodine topical solution in 150 ml of sterile normal saline extraamniotically. Intravenous oxytocin drip was started the morning after induction in all but those women receiving prostaglandin F2 to reduce the induction-abortion interval. 5% povidone-iodine solution successfully induced abortion in 100% of cases. The success rates for ethacridine lactate, hypertonic solution, and prostaglandin F2 were 98, 96 and 90%, respectively. Ethacridine lactate had the highest complete abortion rate (42%) followed closely by 5% povidone-iodine (39%). Prostaglandin F2 resulted in the shortest mean induction-abortion interval (20 hours vs. 38 hours for hypertonic solution, 30 hours for ethacridine lactate, and 32 hours for 5% povidone-iodine solution. 4 (8%) of the 50 women who underwent an abortion induced by hypertonic solution required a blood transfusion. Another woman undergoing hypertonic solution abortion developed disseminated intravascular coagulation and died. The only women who experienced vomiting and loose stools were women receiving prostaglandin F2 (30 women [60%]). The most cost-effective abortion method was 5% povidone-iodine solution in normal saline, indicating that this is the preferred method for poor patients.
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PMID:Comparative study of midtrimester termination of pregnancy using hypertonic saline, ethacridine lactate, prostaglandin analogue and iodine-saline. 146 Mar 14


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