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)

Twenty cases of toxic epidermal necrolysis were studied. 14 male and 6 female. The peak incidence by age was in the first two decades. All of them were related to drugs. Twelve of the cases had received antibiotics and, therefore an infection existed. The remaining 8 cases did not receive antibiotics and had no concomitant infection. We emphasise the clinical observation that in 11 cases the first symptom was an increase in cutaneous sensitivity, and then a rise in temperature, malaise, and extensive cutaneous sloughing resembling extensive burns. As for complications, only in 4 patients could we demonstrate disseminated intravascular coagulation (haematological tests were carried out in only 14 patients). The commonest complication observed was glomerular nephritis. Blood counts, blood chemistry and urine tests were altered more in relation to complications than to TEN. Protein electrophoresis, conversely, showed an increase of gamma globulin in 53.3% of cases, and inverted A/G ratio in 80%. S. aureus was cultured in 12 cases (not all of them children). E.S.R. was increased in 18 cases. Pathological findings with those already described: "in toto" epidermal necrolysis, intra and subepidermal blisters, and occasional inflamatory reaction at the level of the papillae, and the non-uniform presence of melanin in basal cells and Lyell cells. Prognosis was excellent, since we only had one death and one case of blindness due to bilateral ocular perforation. This could be due to the general medical care of the patient, nursing them with D.I.C., which in certain cases substituted by heparin with excellent results. Antibiotics were used in those infected.
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PMID:[Toxic epidermal necrosis. Review of the theme and presentation of 20 cases]. 39 34

Two patients are presented in whom cerebral angiography was complicated by bioccipital infarcts resulting in cortical blindness with persisting severe restriction of the visual field (case 1) and persisting cortical blindness (case 2). One patient (case 1) demonstrated a compensated, protracted disseminated intravascular coagulation (Table 1), which disappeared after treatment with phenprocoumon (Marcoumar). The other patient (case 2) demonstrated increasee spontaneous platelet aggregability (Table 2), which was treated sucessfully with acetylsalicylic acid (Magnyl) and dipyridamole (Persantine). We presume that the coagulation disturbances demonstrated after the angiography may be pathogenetic to the complications. We propose that patients with transient cerebral ischemia and apoplexy who are undergoing cerebral angiography should be studied with regard to coagulation before and after the cerebral angiography so that coagulation disturbances demonstrated may be treated before, or corrected after the angiography.
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PMID:Possible increased tendency to thrombosis after cerebral angiography. 45 38

A 76-year-old man with liver cirrhosis and diabetes mellitus was admitted to our hospital because of bacterial meningoencephalitis. He had eaten raw fish 2 days before onset. He also developed septic shock, disseminated intravascular coagulation, adult respiratory distress syndrome and panophthalmitis of the right eye. Vibrio vulnificus was isolated from the blood culture. Extensive therapy including antibiotics and nafamostat methylate, resulted in full recovery except for right blindness. The necrotizing fasciitis, which is common with Vibrio vulnificus infection, had not been complicated in this patient.
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PMID:[A patient with Vibrio vulnificus meningoencephalitis]. 1571 95

A 36-year-old woman, who had given birth once before, had an eclamptic epileptic seizure eight days after caesarean delivery of healthy premature twins. Severe headache and loss of vision, leading to blindness, had not been recognised as prodromal signs by the healthcare professionals involved. Thereafter, she suffered a generalised epileptic seizure with tongue bite. She recovered fully after treatment with magnesium sulphate and nifedipine. Eclampsia is a severe condition with high rates of maternal complications, such as abruptio placentae, disseminated intravascular coagulation, neurological problems, pulmonary oedema, acute renal insufficiency and even death. Recognition of prodromal symptoms like headache, visual disturbances and upper abdominal pain is of the utmost importance. Magnesium sulphate intravenously is the treatment of choice. About 25% of the cases of postpartum eclampsia develop 2-28 days after delivery. A history of pre-eclampsia before or during the delivery is often absent. There is a relative increase in the incidence of late postpartum eclampsia, possibly because of misinterpretation ofprodromal symptoms, as illustrated by this case report. Every physician should be able to recognise the symptoms of pre-eclampsia and be aware of the possible consequences.
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PMID:[Late postpartum eclampsia]. 1750 Mar 49

We present a patient with Posterior Reversible Encephalopathy Syndrome (PRES). A 74-year-old woman was admitted with sepsis, which originated from erysipelas on her neck the following day. She developed respiratory obstruction due to oedema, septic shock, disseminated intravascular coagulation (DIC), acute renal failure and atrial fibrillation. She responded well to treatment and improved rapidly, despite of her serious condition. When she had almost fully recovered after 15 days, her general condition worsened, and she developed confusion, blindness and pareses. MRI showed vasogenic oedema in the parietooccipital regions of the brain and in the cerebellum, consistent with PRES. PRES is a clinical and radiological diagnosis consisting of headache, confusion, cortical blindness, convulsions and sometimes pareses. MRI of the cerebrum with diffusion-weighted imaging (DWI) and Apparent Diffusion Coefficient (ADC) map are decisive to the diagnosis, and usually shows a characteristic bilateral vasogenic oedema in the parietooccipital region. This can distinguish PRES from brain infarction, which shows a cytotoxic oedema on MRI. We discuss our patient in the light of different conditions leading to PRES, possible pathophysiological factors and treatment options.
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PMID:[An old woman with sudden pareses and blindness]. 1735 25

Quinine is a common cause of drug-induced thrombocytopenia and the most common cause of drug-induced thrombotic microangiopathy. Other quinine-induced systemic disorders have been described. To understand the complete clinical spectrum of adverse reactions to quinine we searched 11 databases for articles that provided sufficient data to allow evaluation of levels of evidence supporting a causal association with quinine. Three reviewers independently determined the levels of evidence, including both immune-mediated and toxic adverse reactions. The principal focus of this review was on acute, immune-mediated reactions. The source of quinine exposure, the involved organ systems, the severity of the adverse reactions, and patient outcomes were documented. One hundred-fourteen articles described 142 patients with definite or probable evidence for a causal association of quinine with acute, immune-mediated reactions. These reactions included chills, fever, hypotension, painful acral cyanosis, disseminated intravascular coagulation, hemolytic anemia, thrombocytopenia, neutropenia, acute kidney injury, rhabdomyolysis, liver toxicity, cardiac ischemia, respiratory failure, hypoglycemia, blindness, and toxic epidermal necrolysis. One hundred-two (72%) reactions were caused by quinine pills; 28 (20%) by quinine-containing beverages; 12 (8%) by five other types of exposures. Excluding 41 patients who had only dermatologic reactions, 92 (91%) of 101 patients had required hospitalization for severe illness; 30 required renal replacement therapy; three died. Quinine, even with only minute exposure from common beverages, can cause severe adverse reactions involving multiple organ systems. In patients with acute, multi-system disorders of unknown origin, an adverse reaction to quinine should be considered.
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PMID:Diversity and severity of adverse reactions to quinine: A systematic review. 2682 44