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)

We present a case of a 11/2-year-old boy with toxic enteritis, consecutive consumption coagulopathy, and sever brain damage. During the acute phase we found high activity of the BB isoenzyme of creatine kinase in cerebrospinal fluid, but not in the serum. Isoenzyme MM could also be found in the spinal fluid (37.9% of the total activity). We conclude that analysis for creatine kinase isoenzymes in spinal fluid is of clinical importance.
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PMID:Creatine kinase isoenzymes in cerebrospinal fluid in a case of brain damage. 94 52

Venom from newborn Bothrops asper snakes has higher lethal, hemorrhagic, edema-forming, proteolytic and defibrinating activities than venom from adult B. asper specimens. Electrophoretic analysis confirmed the variation between these venoms. Intramuscular injection of 100 micrograms of venom from newborn specimens in mice induced defibrination, together with moderate increments of serum levels of lactate dehydrogenase, creatine kinase, hemoglobin and total proteins. A conspicuous hemorrhage developed in injected muscle rapidly after envenomation, probably due to a drastic alteration in capillaries and larger blood vessels. Other histological alterations included moderate myonecrosis, lung collapse and prominent renal damage, characterized by tubular necrosis and hyalinization. Polyvalent antivenom effectively neutralized lethal, hemorrhagic and indirect hemolytic activities of newborn B. asper venom, although requiring higher antivenom doses than neutralization of venom from adult B. asper.
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PMID:Pathological and biochemical changes induced in mice after intramuscular injection of venom from newborn specimens of the snake Bothrops asper (Terciopelo). 144 Jun 47

We describe a 19-year-old Japanese man with severe extensive necrotizing fasciitis that started as Fournier's gangrene to involve the external genitalia, thigh and lower abdomen. High creatine phosphokinase, transient immunosuppression (reduced serum IgG level and negative tuberculin skin test reaction) and disseminated intravascular coagulation occurred during the necrotizing fasciitis.
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PMID:Extremely extended Fournier's gangrene. 226 83

Because an increasing number of patients were arriving at our emergency room with cocaine intoxication and rhabdomyolysis, we reviewed our experience with such patients. We identified 39 patients seen at our institution over an eight-year period with acute rhabdomyolysis after cocaine use. The patients' mean creatine kinase level was 12,187 U per liter (range, 1756 to 85,000). Thirteen of the 39 patients (33 percent) had acute renal failure; 6 of them died. In comparison to the patients with normal renal function, those with renal failure were more often admitted with profound hypotension (46 vs. 4 percent; P less than 0.001), hyperpyrexia (69 vs. 15 percent; P less than 0.001), and markedly elevated serum creatine kinase levels (mean, 28,084 vs. 7931 U per liter; P less than 0.01). Disseminated intravascular coagulation developed in seven patients with renal failure. All six deaths were in this group. Severe hepatic dysfunction was found in 11 patients with renal failure. We conclude that cocaine intoxication can cause acute rhabdomyolysis with acute renal failure, severe liver dysfunction, and disseminated intravascular coagulation and that the mortality rate among patients with this syndrome is high.
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PMID:Acute rhabdomyolysis associated with cocaine intoxication. 341 85

A rare isozyme of serum creatine kinase (CK) migrating cathodic to CK-MM on electrophoresis was found in a 30-year-old male with stomach cancer complicated by disseminated intravascular coagulation leading to massive upper gastrointestinal bleeding and marked anemia. Serum CK activity rose to a maximum of 374 U/l without detectable CK-MB isoenzyme. The patient was also characterized by a marked increase in serum lactate dehydrogenase (all isozymes elevated) and by preferential leakage of mitochondrial aspartate aminotransferase and glutamate dehydrogenase, indicating the presence of extensive tissue damage involving mitochondria. Skeletal muscle mitochondria were considered the most likely source of the additional CK isozyme.
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PMID:Cathodic isozyme of serum creatine kinase in a case of stomach cancer complicated by disseminated intravascular coagulation. 744 49

Acute exertional rhabdomyolysis is caused by a skeletal muscle injury that results in the release of myoglobin and other cellular contents into the circulatory system. Recent reports suggest that acute exertional rhabdomyolysis is more common and more serious than previously realized. Mild to moderate acute exertional rhabdomyolysis can result in hyperkalemia, hypernatremia, lactic acidosis and hyperphosphatemia. Disseminated intravascular coagulation, renal failure and compartmental syndrome may also occur. The physician should maintain a high index of suspicion for acute exertional rhabdomyolysis in patients who present with symptoms of an overexertion injury, most commonly pain and swelling in the affected muscles. Special attention should be given to evaluating the history for occupational, recreational, environmental and medical risk factors for rhabdomyolysis. Screening may be performed with a simple urine dipstick test; if the urine is orthotoluidine-positive, the diagnosis should be confirmed with measurement of the serum creatine kinase level. Early intervention with aggressive hydration and close monitoring for metabolic, renal or hematologic complications may prevent serious injury or death.
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PMID:Acute exertional rhabdomyolysis. 762 24

In a retrospective study we analyzed the clinical and blood chemical data of 12 patients with severe tropical malaria in the intensive care units of the University Hospital Zurich and the Stadtspital Triemli, Zurich, between 1991 and 1994. None of the 12 patients had been exposed to malaria before or had taken drugs for chemoprophylaxis. 7 patients survived, 5 died from complications of malaria. According to the criteria of severe tropical malaria defined by the WHO, the following pathological clinical and blood chemical parameters were noted on admission: cerebral coma (2/12); blood hemoglobin < 5 g/dl (0/12), < 8 g/dl (2/12); serum creatinine > 265 mumol/l (3/12); blood glucose < 2.2 mmol/l (0.12); circulatory collapse/shock (0/12); bleeding/signs of disseminated intravascular coagulation in laboratory tests (4/12); acidosis with pH < 7.25 (1/12). Further signs of severe tropical malaria were: hyperparasitemia > 5% (9/12); qualitative and quantitative disturbances of consciousness (6/12); thrombocytopenia < 30 x 10(9)/l (9/12); hyponatremia 125-135 mmol/l (9/12), < 125 mmol/l (2/12); rhabdomyolysis with creatine kinase > 1000 U/l (4/12). The basic treatment consisted of parenteral quinine hydrochloride in all patients; doxycycline was added in 8 cases, clindamycin in 3. Adjuvant therapy with desferrioxamin was given in 3 cases. 6 patients had exchange transfusions. Parasitemia cleared in all patients within 5 to 6 days. Later in the course, 5 patients developed acute respiratory distress syndrome, 6 required hemofiltration due to oliguria, and one became comatose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intensive care aspects in severe tropical malaria: clinical aspects, therapy and prognostic factors]. 777 Jul 59

A 43-year-old, bisexual, black man with acquired immunodeficiency syndrome (AIDS), detected by CD4 lymphocyte criteria alone, presented with low-grade fever, chills, malaise, and watery diarrhea of 2 days' duration. Over the next 5 days, he developed a fulminant septicemia-like illness with progressive hypotension, disseminated intravascular coagulation, and very high serum lactic acid dehydrogenase (2,150 U/L) and serum creatine phosphokinase (5,395 U/L) levels, and died. The cause of this illness was not clinically apparent. A bone marrow biopsy performed on the day of his death revealed intracytoplasmic clusters of 3 microns long, oval, basophilic organisms, the exact nature of which was not evident by light microscopy. The diagnosis of disseminated toxoplasmosis (DT) was made only after electron microscopic study of the bone marrow revealed organisms with features typical of Toxoplasma gondii tachyzoites. These features included a multilayered pellicle, a pointed anterior end containing a conoid, up to nine rhoptries, sparse micronemes, and a posterior end containing a nucleus. Some of the organisms had divided by internal budding or endodyogeny. This case illustrates the value of transmission electron microscopy in making the diagnosis of DT.
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PMID:Disseminated toxoplasmosis and acquired immunodeficiency syndrome: diagnosis by transmission electron microscopy. 779 54

The author studied the clinical and laboratory effects of early parenteral nutrition (EPN) in patients who were comatose as a result of acute drug poisoning. All patients were unconscious at the time of admission and entry into the study and received our usual conservative therapy for the first 24 hours. Alternate patients received an EPN solution containing amino acids and glucose. Volume, composition, and caloric content of the EPN solution were calculated separately for each patient according to weight and height nomograms. It was found that the group receiving EPN (n = 46) normalized their nitrogen balance sooner and demonstrated a consistent decrease in their creatine phosphokinase level. Serum amino acid values in patients treated with EPN did not change significantly during the treatment trial. The control group (n = 40) demonstrated a significantly lower serum amino acid concentration on the third day of treatment (p < .001), had significantly more pneumonias (p < .05), and their hospitalization time was significantly longer (.01 < p < .05) than the EPN group. There were significantly fewer instances of disseminated intravascular coagulation in the group receiving EPN (p < .05).
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PMID:Early parenteral nutrition in patients unconscious because of acute drug poisoning. 843 19

Although rare, exertional collapse and sudden death are the most serious potential complications of sickle cell trait. Studies suggest that this condition may occur in susceptible persons when poor physical conditioning, dehydration, heat stress or hypoxic states precipitate sickling of the abnormal erythrocytes. Sickling leads to endothelial damage, which can cause vasoconstriction, disseminated intravascular coagulation and local tissue damage. Cardiac effects include acute ischemia and arrhythmias. Muscle damage results in acute compartment syndromes and release of myoglobin into the circulation. Acute renal failure is possible. Diagnosis is based on a high index of suspicion, and characteristic presentation and laboratory findings, including myoglobinuria, hyperkalemia, hypocalcemia, hyperphosphatemia and elevated creatine kinase levels. The differential diagnosis includes pulmonary embolism, acute cardiac events, anaphylaxis and heat stroke. Management is based on stabilization, rehydration, and the treatment and prevention of complications.
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PMID:Exertional collapse and sudden death associated with sickle cell trait. 904 99


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