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)

In all, 55 eyes of 55 patients were examined prospectively in random order with the Humphrey field analyzer [central field 76 points, full threshold strategy, single-stimulus presentation, response-button control (HFA 1); central field 76 points, defect-depth strategy, response-button control (HFA 2)] and the Dicon TKS-4000 [central field 76 points, defect-depth strategy, multiple-stimulus presentation, response-button control (DIC 1); central field 76 points, defect-depth strategy, multiple-stimulus presentation, voice control (DIC 2)]. Some 26 patients (47%) had glaucomatous field defects, 7 patients (13%) had lesions of the visual pathway, 5 patients (9%) had normal fields. The other 17 patients (31%) had field defects due to vascular lesions of the retina or the optic nerve, retrobulbar neuritis, cataract, dysthyroid optic neuropathy, disorders of the macula, or human immunodeficiency virus (HIV) retinopathy. The mean testing time for the whole study population was 5.2 +/- 2.7 min for DIC 1. The difference from the mean testing time for HFA 2 (6.4 +/- 2.7 min) is statistically significant (p = 0.0013). DIC 2 reduces the mean testing time to 4.9 +/- 2.6 min. The difference from DIC 1 is not statistically significant (p = 0.8110). A multiple-stimulus presentation and voice control seem to be useful methods to reduce the testing time in automated perimetry without a loss of accuracy. Voice control, as used in the DICON TKS 4000, still has to be improved, however.
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PMID:Multiple-stimulus presentation and voice control in automated perimetry. 147 32

We report a case of a mixed sensorimotor, predominantly axonal mononeuritis multiplex that developed after a severe meningococcal septicemia and disseminated intravascular coagulation (DIC) with associated distal limb necrosis. Ischemia resulting from the DIC-induced multiple vascular occlusions is suggested as the leading cause of this neuropathy.
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PMID:Peripheral neuropathy in meningococcal septicemia. 299 4

A 3-year-old male Setter-type dog had a progressive distal sensorimotor polyneuropathy characterized by weakness, bilateral atrophy of distal appendicular musculature, and reduced response to tactile stimuli. The diagnosis of a distal axonopathy was supported by electromyographic findings of fibrillation potentials, positive sharp waves in distal limb muscles, and absence of evoked action potentials, myopathic changes of atrophic angular fibers, and myelinated nerve fiber depletion in distal parts of peripheral nerves. The neuropathy appeared 5 weeks after 38 days of heparin therapy for disseminated intravascular coagulation. The disseminated intravascular coagulation, a complication of thiacetarsamide therapy for heartworm disease, had resolved 40 days after the end of heparin therapy. The cause of the neuropathy was not determined.
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PMID:Distal polyneuropathy after canine heartworm disease therapy complicated by disseminated intravascular coagulation. 628 83

We reported a case of motor neuropathy with pyramidal sign following prolonged administration of a high dose of muscle relaxant, pancuronium bromide (Myoblock). A 40-year-old male was admitted to our hospital with acute episode of pancreatitis. He was treated with artificial ventilation and Myoblock to manage delirious state, disseminated intravascular coagulation and multiple organ failure. Total dose of 823 mg (24 mg/day) of Myoblock was given intravenously over 36 days. After Myoblock was discontinued, he regained his consciousness and marked muscle weakness with atrophy was noted in both limbs, more severe in distal lower limbs, without any noticeable sensory and sphincter disturbances. Motor nerve conduction studies showed normal nerve conduction velocities with markedly decreased amplitude of compound muscle action potentials. Repetitive nerve stimulation studies revealed decrement response after tetanic stimulation, which disappeared later. Needle EMG showed active denervation potentials and marked polyphasic motor unit potentials. Muscle biopsy revealed neurogenic muscle atrophy with fragmented acetylcholine esterase-positive postsynaptic sites. Sural nerve biopsy showed slight to moderate degree of axonal degeneration of myelinated fibers. Clinical, electrophysiological, and pathological studies above indicated that the main affected sites were neuromuscular junctions including the terminal twigs of motor neurones and postsynaptic membrane, and pyramidal tracts, predominant in lower limbs. About one month after the recognition of the muscle weakness, his muscle strength improved gradually, however, spasticity with hyperreflexia and pathologic reflexes of both legs were found, and became more prominent thereafter. Intensive physiotherapy and rehabilitation led improvement to the point that he became able to ambulate with walking-aids about 7 months later, but marked spasticity persisted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of motor neuropathy with pyramidal sign due to prolonged administration of high dose of pancuronium bromide (Myoblock)]. 840 81

We experienced a rare case of sinus histiocytosis with massive lymphoadenopathy (Rosai-Dorfman disease) accompanying hypertrophic cranial pachymeningitis. The patient is a 64-year-old woman with an early symptom of rt. peripheral facial palsy. She had a 4-month history of headache with a 5-week history of numbness in the rt. supraorbital nerve area, and lost her weight by 10 kg in 2 months. She developed rt. trochlea nerve palsy and numbness in the lt. mandibular nerve area. Laboratory findings showed that ALP, LDH and CRP were higher than normal. Of CT, MRI and MRA, the images of her head were normal. However, the Gd-enhanced MRI only showed a diffuse pachymeningeal enhancement. After about 3 months from the onset of rt. peripheral facial palsy, she died of DIC of unknown etiology. As a result of examinations in anatomical pathology, she was diagnosed as having sinus histiocytosis with massive lymphoadenopathy (Rosai-Dorfman disease). There were a large number of histiocytes on the pachymeninx. These findings suggest that hypertrophic cranial pachymeningitis caused multiple cranial neuropathy. We emphasize that use of Gd-enhanced MRI in the early stage is important for diagnosis.
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PMID:[Rosai-Dorfman disease accompanying hypertrophic cranial pachymeningitis with an early symptom of right peripheral facial palsy]. 1242 22

Protein C, protein S, and antithrombin III were measured in 35 patients with acute leukemia (13 with AML and 22 with ALL). Low levels of proteins C and S were present in 15 (42.9%) and 20 (57.1%) patients, respectively, and 6 patients had low levels of antithrombin (ATIII). Seven patients also had DIC at presentation. There were no significant differences in the levels of protein C, protein S, and ATIII in patients with or without DIC. Twenty patients were available for re-evaluation at the end of induction therapy. The low levels of protein C and ATIII found at diagnosis had risen to normal levels at the end of the induction therapy, while low =levels of protein S remained in 75% of the patients. One patient with low protein C at presentation developed myocardial infarction on day 15, and another patient died of progressive neuropathy. No other thrombotic manifestations were seen. Whether the low protein C, protein S, or antithrombin levels predispose patients with acute leukemia to thrombosis in the absence of DIC is not known.
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PMID:Roles of protein C, protein S, and antithrombin III in acute leukemia. 1649 9