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)

Cerebellar infarcts have been neglected for a long time and are now shown well by CT and especially MRI. Some infarcts involve the full territory supplied by a cerebellar artery. They are frequently complicated by edema with brain stem compression and supratentorial hydrocephalus, requiring at times emergency surgery, and are often accompanied by other medullary, medial pontine, mesencephalic, thalamic and occipital infarcts. On the other hand, partial territory infarcts are usually confined to the cerebellum and have a benign outcome with total recovery or minimal disability. They are more common than full territory infarcts. However, clinical presentations are similar to those full territory infarcts, differing mainly by the lack of drowsiness or unconsciousness. The main symptoms are vertigo, headache, vomiting, unsteadiness of gait and dysarthria. Signs include ipsilateral limb dysmetria, ipsilateral axial lateropulsion, ataxia and dysarthria. Vertigo is more severe and rotary in posterior inferior cerebellar artery territory infarcts, whereas dysarthria and ataxia are prominent in superior cerebellar artery territory infarcts. A few brain stem signs are sometimes added. In these territorial cerebellar infarcts, cardioembolism is the most common cause. Atherosclerotic occlusion comes next, involving the intracranial part of the vertebral artery and, less frequently, the lower basilar artery, both locations inaccessible to surgery. Other causes are artery to artery embolism from a vertebral artery origin stenosis, or the aortic arch, in situ intracranial branch atherosclerotic occlusion, and vertebral artery dissection. Border zone cerebellar infarcts occur in one third of the cases. They are small cortical or deep infarcts. They have the same symptoms and signs as territorial infarcts except for more frequent postural symptoms occurring over days, weeks or months after the ischemic event. The infarcts mainly have a thromboembolic mechanism, and sometimes have a hemodynamic mechanism: 1) focal cerebellar hypoperfusion due to large artery occlusive disease in more than half the cases, 2) small or end (pial) artery disease due to hypercoagulable state (thrombocythemia, polycythemia, hypereosinophilia, disseminated intravascular coagulation), arteritis or intracranial atheroma, and 3) rarely systemic hypotension due to cardiac arrest.
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PMID:[Cerebellar infarctions and their mechanisms]. 809 Oct 85

We reported a family with dentato-rubro-pallido-luysian atrophy (DRPLA) and chronic renal failure. The proband was a 66-year-old woman who developed gait disturbance, limb ataxia, pyramidal tract signs, and dementia since age 54. T2-weighted brain MR images revealed symmetric high-signal lesions in the cerebral white matter, in addition to cerebellar, brainstem, and cerebral cortical atrophy. She suffered from renal failure and became dialysis-dependent at the age of 59, four years after the onset of chronic nephritic syndrome. At the age of 66, she was admitted to our hospital because of hyperthermia and disturbance of consciousness, and died of DIC. Her CAG repeats in the DRPLA gene were 58 and 12. An autopsy was performed. The brain weighed 910 g. Histological findings confirmed the diagnosis of DRPLA. Her mother died of chronic renal failure. All three siblings had cerebellar ataxia, and two siblings had chronic nephritic syndrome. Among them, only her younger brother was diagnosed as non-IgA glomerulonephritis based on kidney biopsy findings at the age of 48. Though the nature of the association between DRPLA and renal dysfunction remains obscure, the DRPLA gene abnormality may be correlated with chronic renal failure in this family.
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PMID:[A family with DRPLA and chronic renal failure]. 1096 59

Rocky Mountain spotted fever (RMSF) was diagnosed in 30 dogs examined at North Carolina State University, Veterinary Teaching Hospital between 1984 and 1997. Historical, physical examination, and laboratory abnormalities were reviewed. Diagnostic criteria included a four-fold rise in antibody titer to Rickettsia rickettsii (R. rickettsii) (n=15) or a single R. rickettsii antibody titer of 1:1,024 or greater (n=15; when this initial titer was determined one week or more after the onset of clinical signs). Fifteen (50%) dogs were greater than seven years of age, and 13 (43%) dogs were between two and seven years of age. There was no sex predilection. Only five (17%) dogs had a history of known tick exposure. Presumably due to delayed diagnosis, dogs with antibody titers of 1:1,024 or greater at the time of presentation had a higher incidence of more severe neurological dysfunction (e.g., ataxia, hyperesthesia, vestibular disease, and seizures) and cutaneous lesions (e.g., hyperemia, edema, petechiae, ecchymoses, and necrosis). Laboratory findings included anemia, leukocytosis accompanied by toxic granulation of neutrophils, hypoalbuminemia, and coagulation abnormalities; signs were generally more severe in the 15 dogs with R. rickettsii antibody titers of 1:1,024 or greater at the time of presentation. Twelve (40%) dogs in this study were severely thrombocytopenic (less than 75 x10(3) platelets/microl; reference range, 200 to 450 x 10(3)/microl), without clinical evidence of fulminant disseminated intravascular coagulation. In this study, the survival rate following R. rickettsii infection was 100%.
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PMID:Canine Rocky Mountain Spotted fever: a retrospective study of 30 cases. 1120 76

A 26-year-old woman suffered disseminated intravascular coagulation (DIC) and a brief respiratory arrest following recreational use of 3,4-methylene-dioxymethamphetamine (MDMA; 'ecstasy'), together with amyl nitrate, lysergic acid (LSD), cannabis and alcohol. She was left with residual cognitive and physical deficits, particularly severe anterograde memory disorder, mental slowness, severe ataxia and dysarthria. Follow-up investigations have shown that these have persisted, although there has been some improvement in verbal recognition memory and in social functioning. Magnetic resonance imaging and quantified positron emission tomography investigations have revealed: (i) severe cerebellar atrophy and hypometabolism accounting for the ataxia and dysarthria; (ii) thalamic, retrosplenial and left medial temporal hypometabolism to which the anterograde amnesia can be attributed; and (iii) some degree of fronto-temporal-parietal hypometabolism, possibly accounting for the cognitive slowness. The putative relationship of these abnormalities to the direct and indirect effects of MDMA toxicity, hypoxia and ischaemia is considered.
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PMID:Amnesic syndrome and severe ataxia following the recreational use of 3,4-methylene-dioxymethamphetamine (MDMA, 'ecstasy') and other substances. 1174 84

We report a 58-year-old man with slowly progressive muscle atrophy and weakness in the four extremities, accompanying cerebellar ataxia and sensory impairment of all modalities. He was a product of consanguineous marriage. His neurological manifestations began in childhood. He was admitted to our hospital because of marked abdominal distension and pretibial edema with hypoalbuminemia and hyperlipidemia. Neuroimaging studies showed marked atrophy of the cerebellum and spinal cord. Nerve conduction studies presented with slowing and sural nerve biopsy revealed demyelination with onion-bulbs. Abdominal distension was interpreted to be caused by chronic idiopathic intestinal pseudo-obstruction (CIIP), leading to protein-losing gastroenteropathy and hypalbuminemia caused by the CIIP. He died of DIC by myelodysplasic syndrome and DIC, two years later. Postmortem study demonstrated with severe loss of anterior horn cells and gliosis in the spinal cord. The Clarke's column was also affected. There was symmetrical degeneration in the dorsal column and corticospinal tracts. The cerebellum showed atrophy of molecular layer, prominent loss of Purkinje's cells and sparse granular cell layer, but no obvious change in the dentate nucleus. Neuronal loss in the dorsal root ganglia was remarkable. There were no alternations in the cerebral cortex, striatum, thalamus, subthalamic nucleus, and pontine nucleus, except for mild changes in substantia nigra and inferior olivary nucleus. This case was clinically suspected either of variant of Friedreich's ataxia or an early onset ataxia associated with hypoalbuminemia (EOAHA), although marked autonomic dysfunction was atypical. But the postmortem study, demonstrated with marked neuronal loss in anterior horn cells and cerebellan cortex and rather suggested an independent category of this case.
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PMID:[An autopsy case of atypical Friedreich's ataxia with chronic idiopathic intestinal pseudo-obstruction]. 1180 52

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

We report a case of serotonin syndrome that occurred in a patient with chronic heart failure associated with a panic disorder. The 39-year-old Japanese man had been treated with paroxetine at 20 mg/d for 1 1/2 years. He presented with rhabdomyolysis, renal failure, fulminant liver failure, cardiac conduction disturbance, and disseminated intravascular coagulation, as well as conventional symptoms of serotonin syndrome including alterations in cognition (disorientation, confusion) and behavior (restlessness), autonomic nervous system dysfunction (fever, shivering), and abnormal neuromuscular activity (ataxia, hyperreflexia, myoclonus). All medications prescribed before hospital admission were discontinued. After 24 hours of continuous venovenous hemofiltration, diuresis resumed and renal and liver function improved rapidly. Disorientation, restlessness, hyperreflexia, and myoclonus abated slowly over the next 72 hours. The patient's anxiety subsided more slowly, and he recovered completely 1 week later. The plasma concentration of paroxetine was elevated far above the upper limit of the therapeutic range. The patient had cytochrome P-450 (CYP) 2D6*1/*5, a heterozygosity of an inactivated allele of CYP2D6, which metabolizes paroxetine. The patient was determined to be an intermediate metabolizer who was potentially vulnerable to paroxetine, a major inhibitor of CYP2D6. Heart failure is often accompanied by psychiatric disorders. A wide range of drugs commonly prescribed for these conditions, including beta-blockers, antiarrhythmics, and antidepressants, are metabolized by CYP2D6. Genetic screening for CYP2D6 in patients with these conditions may prevent life-threatening drug intoxication.
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PMID:Life-threatening serotonin syndrome in a patient with chronic heart failure and CYP2D6*1/*5. 1554 25

A 2-year-old, male, red-necked (Bennett's) wallaby (Macropus rufogriseus) from a zoological facility was presented for peracute onset of severe depression, unresponsiveness, ataxia, and loose feces. Serum biochemical abnormalities included azotemia, hypoalbuminemia, increased alanine aminotransferase activity, hyperbilirubinemia, hyperphosphatemia, and hyperkalemia, consistent with multi-organ system failure. Severe thrombocytopenia suggested possible disseminated intravascular coagulation. Peripheral blood smear examination revealed numerous ovoid, protozoal inclusions within monocytes and occasionally within neutrophils. Despite aggressive supportive therapy, the patent died within 5 hours of presentation. Gross necropsy and histopathologic findings included severe multifocal necrotizing lesions in multiple organs. Numerous intralesional protozoal organisms were observed and were identified as Toxoplasma gondii by immunohistochemistry. Macropods (wallabies and kangaroos) are known to be highly susceptible to toxoplasmosis, with high mortality rates; diagnosis most often is obtained at necropsy. Detection of protozoal organisms in peripheral blood leukocytes is reported rarely and has not been documented previously in a macropod. Parasitemia in this case was attributed to severe, disseminated disease. Careful examination of peripheral blood smears in macropods suspected of toxoplasmosis may be warranted.
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PMID:Toxoplasma gondii inclusions in peripheral blood leukocytes of a red-necked wallaby (Macropus rufogriseus). 1731 Dec 3

Children with acute encephalopathy (AEP) or acute encephalitis(AE) show variable findings in the clinical manifestations and on the neuroimaging. Patients with AE present variable symptoms: disturbance of consciousness, seizure, ataxia, dystonia, abnormal behavior, apnea, and others. This variability depends on the location of lesions including basal ganglia, brain stem, cerebellum, or cerebral gray/white matter. In AEP, MRI findings can be categorized into (1) severe brain edema, (2) acute necrotizing encephalopathy, (3) cortical necrosis that appears 4-5 days after the onset, and (4) others. Serum AST elevates in approximately 50% of AEP patients, and among them around 60% develops DIC. The high AST group includes Reye syndrome(RS), mimic RS and AEP with shock syndrome.
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PMID:[Clinical variability in viral infection related acute encephalitis or encephalopathy]. 2140 Aug 54

In the type of heat illness, several medical terms such as heat syncope, heat cramp, heat exhaustion, heat stroke are included. But their Japanese medical terms are neither unified nor clearly defined. To eliminate this problem, the new classification for heat illness is proposed. By the severity of heat illness, they are divided into three grades. Grade I is corresponded to heat cramp and heat syncope. Grade III is corresponded to heat stroke, and used for any one of the three following clinical findings, (1) Central nervous system dysfunction, i.e., consciousness disturbance, seizure, ataxia. (2) Liver and kidney dysfunction. (3) Clotting disorder, i.e., DIC. This classification can be beneficial not only to the diagnosis in the hospital, but also to the early detection and management of heat illness in the field.
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PMID:[Classification of heat illness]. 2269 May 95


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