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 succeeded in developing a Wistar rat multiple organ failure (MOF) model by intraperitoneal injection of Zymosan. 80 rats were divided into the experimental and control groups. On alternative days (1, 2, 4-5 day), rats were killed after their blood specimens were examined. In the experimental group, changes in PaO2, GPT and Cr were apparently significant as compared with those in the control group. Symptoms included lethargy, hyporeaction, and alimentary tract hemorrhage. By combining function with pathology changes at the cellular and subcellular level and histochemical aspects, we listed MOF pathological features for the diagnosis of DIC at its different stages.
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PMID:[Rat multiple organ failure model caused by zymosan injections: a pathomorphological study]. 181 34

Histopathological study on 723 brains from routine necropsies was performed. Ten brains (1.38 percent) were found to have histological lesions of disseminated intravascular coagulation (DIC) with multiple fresh fibrin and/or platelet thrombi in the cerebral microcirculation. Among them, premortem diagnosis was made in only one case, and only two cases also showed evidence of visceral involvement. Microthrombi were found most frequently in the cerebral cortex and hypothalamic region and in the cerebral white matter, brain stem, and cerebellum, in descending order. Neurological symptoms and signs, including lethargy, coma and seizure, were detected in all cases. The abnormal body temperature and/or urinary output observed in most patients appeared to be related to the frequent hypothalamic involvement by DIC. The exclusive or predominant involvement of the brain by multiple microthrombi may be considered as a localized form of DIC. It is probably related to cerebral ischemia since severe acute neuronal ischemic changes also were noted in most brains.
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PMID:Disseminated intravascular coagulation involving the brain: a topographical study. 712 Apr 79

Two infants with fatal echovirus type 11 infections are described. Disseminated intravascular coagulation developed in both patients, and at postmortem examination, diffuse hemorrhagic necrosis of multiple organ systems was evident, most strikingly in the liver. A 3-month-old child is described, in whom lethargy, vomiting, pitting edema of the occipital scalp and neck, and subsequent diffuse echovirus disease developed. The clinical manifestation in this infant of focal myositis with histologic documentation at postmortem examination is unique to echovirus 11 disease. To our knowledge, this child represents the first described patient with nonparalytic, fatal echovirus type 11 infection occurring beyond the immediate neonatal period.
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PMID:Fatal echovirus type 11 infections. 729 6

Erythema multiforme major and disseminated intravascular coagulation developed in a dog 24 hours after exposure to a d-limonene-based insecticidal dip. Clinical signs included severe lethargy and weakness, ulceration of the oral mucosa, and erythematous serpiginous, annular, and arciform lesions on the head, trunk, and limbs. Clinicopathologic abnormalities included leukocytosis with neutrophilia, normocytic normochromic anemia, thrombocytopenia, prolongation of prothrombin and partial thromboplastin times, increased fibrin degradation products, hypoproteinemia, hyponatremia, hypochloremia, azotemia, high serum alanine aminotransferase and alkaline phosphatase activities, and high serum bilirubin concentration. Despite intensive supportive care, the dog developed severe intrathoracic and abdominal hemorrhage and died. Necropsy revealed severe diffuse epidermal necrosis and widespread hemorrhage within organs. Insecticidal dips containing d-limonene have the potential to induce various toxic effects, including, possibly, erythema multiforme major, and should be used cautiously.
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PMID:Erythema multiforme major and disseminated intravascular coagulation in a dog following application of a d-limonene-based insecticidal dip. 759 26

Extraneural manifestations of toxoplasmosis often are not recognized antemortem in patients with AIDS. We describe a patient who was seropositive for human immunodeficiency virus and presented with lethargy, abdominal tenderness, rapidly progressive ventilatory failure, rhabdomyolysis, myoglobinuria, and disseminated intravascular coagulation. Although the diagnosis of pancreatitis was not considered while the patient was alive, an autopsy demonstrated pancreatic necrosis associated with toxoplasmal cysts. No other infection was evident. This case suggests that Toxoplasma gondii can cause severe pancreatitis in patients with AIDS.
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PMID:Necrotizing pancreatitis and multisystem organ failure associated with toxoplasmosis in a patient with AIDS. 845 54

The pathogenesis of a newly recognized, molecularly and antigenically distinct human babesial isolate (WA1) and Babesia microti, the common cause of human babesiosis in the United States, were compared in a Syrian hamster model. A group of 33 adult female hamsters were inoculated intraperitoneally with either WA1-infected, B. microti-infected, or uninfected hamster erythrocytes. All WA1-infected animals became parasitemic by postinoculation (PI) day 3 or 4 and were severely lethargic and dyspneic by PI days 6 to 10. Death often occurred spontaneously by PI day 10, with parasitemia of 12 to 90%. Hamsters inoculated with B. microti became parasitemic by PI day 7 and developed peak parasitemia (42 to 60%) by PI day 14 that subsequently decreased to low or undetectable values. Although the B. microti-infected hamsters developed severe anemia, they generally remained asymptomatic. Postmortem examination of WA1-infected hamsters revealed intravascular aggregates of large mononuclear inflammatory cells that occasionally occluded small to medium veins, pulmonary leukoclastic phlebitis, thrombosis, and multifocal coagulative necrosis in the heart, spleen, lung, and liver. No vascular lesions or areas of coagulative necrosis were detected in any B. microti-infected or control hamsters. The results of this study suggest that marked leukocytosis followed by acute necrotizing phlebitis resulting in disseminated intravascular coagulation, thromboembolism, and infarction may be central to the pathogenesis of WA1 infections.
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PMID:Comparative pathogenesis of human WA1 and Babesia microti isolates in a Syrian hamster model. 890 83

Necrotizing enterocolitis (NEC) is the most serious and frequently acquired gastrointestinal disorder in neonates. The pathogenesis of NEC is unknown, but it may result from a disturbance of the delicate balance among gastrointestinal perfusion, enteric organisms, and enteral feeding. Risk factors for NEC include prematurity, hypoxic-ischemic insult, and formula or breast milk feedings. The clinical spectrum of NEC is multifactoral and ranges from temperature instability, apnea, lethargy, abdominal distention, bilious residuals, and guaiac-positive stools to septic shock, disseminated intravascular coagulation, and death. Medical management is usually adequate treatment for NEC. Surgical treatment is considered if medical management is inadequate to control the spread of the disease. Health care team members must be constantly alert to the presentation of NEC. Expeditious treatment will positively influence the outcome of the disease.
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PMID:Necrotizing enterocolitis. 1037 56

Background Cerebral venous thrombosis is an inusual disease in neonatal age. Increasing reports of this disorder had described since magnetic resonance angiography is used. Case report Newborn of apropriate seze for gestational age was delivered at 35 weeks of gestation. Refered a severe hipoxic-isquemic disease with multisistemic afectation. The second day of life presented disseminated intravascular coagulation with pulmonary bleeding. The third day, the infant developed seizures that required treatment with diazepam in continuous perfussion. MR angiography visualized superior sagital and transvers sinus thrombosis. Coagulation study detected factor V Leiden. Comments Frecuently venous cerebral thrombosis is presenting with lethargy and seizures. The most common vessels involved are sagital and transvers sinus. It is described in association with exogenous risk factors that increasing blood hyperviscosity and additional inhered coagulation dissorders such as defects on antihrombina III, protein C and S and activate protein C resistance. The last defect has a hight prevalence in subjects with trombosis events.
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PMID:[Neonatal cerebral thrombosis and deficit of factor V leiden]. 1100 60

A 22-year-old man developed unconsciousness, severe quadriplegia and muscle atrophy, and had markedly elevated serum creatine kinase levels after using the high-dose steroid and nondepolarizing neuromuscular blocking agents during the course of sepsis and DIC. On neurological examination, he was lethargic. The patient had generalized muscle weakness and wasting, and diminished deep tendon reflexes. He weakly responsed to painful stimuli on the legs. The motor nerve conduction study demonstrated decreased CMAP (compound muscle action potential) amplitudes. Motor and sensory nerve conduction velocities and their distal latencies were normal. Muscle biopsy revealed marked muscle fiber atrophy predominantly in type 2 fibers and numerous basophilic and a few necrotic fibers. Some atrophic fibers had decreased to absent myosin adenosine triphosphatase activity in their center. Accordingly, he was diagnosed as having acute quadriplegic myopathy (AQM), which has been reported mainly in Western countries. The mechanism of muscle fiber degradation in this myopathy is still unknown. On immunohistochemical analysis to our patient, enzyme activities of various proteases such as calpain, cathepsin B, and proteasomes were increased in the sarcoplasm, especially in the atrophic fibers. We suggest that lysosomal cathepsin, nonlysosomal calpain, and ATP-ubiquitin-proteasome proteolytic pathways participate in muscle fiber degradation in AQM.
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PMID:[A case of acute quadriplegic myopathy]. 1108 98

A 2-year-old female spayed domestic shorthair cat was examined because of lethargy, inappetance, vocalization, and abnormal aggressive behavior of 1 day's duration. The cat had been groomed the previous day with a d-limonene-based insecticidal shampoo. Skin lesions consisted of coalescing erythematous patches. Despite supportive care, the cat's condition deteriorated. Dermatohistopathologic changes included multifocal areas of acute coagulative epidermal necrosis. The dermis was infiltrated by a dense population of bacilli. d-Limonene toxicosis has been rarely described in dogs and cats. Toxic effects such as hypersalivation, ataxia, shivering, hypothermia, scrotal irritation, hypotension, and erythema multiforme major have been reported. Treatment for septicemia and disseminated intravascular coagulation, along with intensive supportive care, may be necessary.
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PMID:Acute necrotizing dermatitis and septicemia after application of a d-limonene-based insecticidal shampoo in a cat. 1236 86


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