Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presentation deals with the enzymatic spectrum of the blood serum (aminotransferase-glutamino-pyruvic and glutamino-oxaloacetic acid, sera cholinesterase, histidase, acid alkaline phosphatase) in 100 patients with transient disorders of cerebral circulation in the form of ischemic and hemorrhagic strokes. These disorders of circulation appeared on the background [corrected] of atherosclerosis and hypertensive disease or in other combination along with vasculitis of a different etiology. The most significant were changes of histidase and acid phosphatase activity and an inhibition of cholinesterase activity in ischemic and hemorrhagic strokes with expressed focal disorders of cerebral circulation. In an improvement of the clinical state following medicative therapy there was a normalization of these indices. The only exclusion was histidase the content of which in some cases remained cunhanged.
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PMID:[Blood serum enzymatic spectrum in vascular diseases of the brain]. 62 45

Malignant rheumatoid arthritis (MRA) is a name for rheumatoid arthritis (RA) complicated with systemic vasculitis or other severe extra-articular manifestations, which can cause a fatal outcome. MRA is found in 4-5% of inpatients with RA. The male to female ratio is 1:1.45. Histologically, 3 main types are recognised in rheumatoid vasculitis; RA type (vasculitis with rheumatoid nodule-like appearance), PN type (fibrinoid vasculitis similar to PN), and EA type (endoarteritis obliterans). High titers of rheumatoid factor, immune complexes, hypocomplementemia, hypoproteinemia, decreased choline esterase activity, elevated alkaline phosphatase activity and leukocytosis are characteristic laboratory features of MRA. Recently, it appears that MRA is becoming less and the prognosis is getting better, perhaps due to the advancement in treatment.
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PMID:[Malignant rheumatoid arthritis]. 158 55

The organophosphate insecticide Diazinon has been reported to cause acute pancreatitis in dogs. Based on histochemical examination of the acinar tissue, it was suggested that pancreatic tissue-fixed butyrylcholinesterase (BuChE) is the target enzyme of organophosphate toxicity. To further evaluate this theory, we exposed dogs, cats, and guinea pigs to a single sublethal dose of the organophosphate insecticide Diazinon (75 mg/kg). In cats, which lack pancreatic BuChE, no pathological changes occurred after two, three, and six hours, whereas in the guinea pigs as in dogs, both having abundant pancreatic BuChE, vacuolization of the acinar cells, interstitial edema and vasculitis indicate acute edematous pancreatitis as early as two hours. Atropine pretreatment (0.2 mg/kg) gave complete protection against pancreatitis. It was concluded that inhibition of pancreatic BuChe leads to cholinergic hyperstimulation of the acinar cell, which results in acute pancreatitis, and that pancreatic BuChE is essential for dogs and guinea pigs to downregulate cholinergic excitation. The insecticide pancreatitis model is considered a simple, non-invasive, reproducible, and cheap and useful method to evaluate early changes and methods of treatment in acute pancreatitis. Pancreatitis in humans has also been reported after accidental insecticide exposure.
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PMID:Effects of insecticide, diazinon, on pancreas of dog, cat and guinea pig. 359 77

We reported a 63-year-old woman, suffered from myasthenia gravis with thymoma who later developed subacute motor neuronopathy after thymectomy. She noticed distally dominant muscle weakness and atrophy of bilateral upper extremities without sensory loss 4 month after thymomectomy. Her muscle weakness did not improve by intravenous administration of anti-cholinesterase (Tensilon test). Electrophysiological examinations showed no decremental response of examined muscles during repetitive nerve stimulation, nor motor nerve conduction block nor demyelination of affected peripheral nerves. Laboratory study demonstrated positive anti-acetylcholine receptor, anti-nuclear and SS-A antibodies. On immunohistochemistry, the patient's sera positively stained human and rat anterior horn cell cytoplasm as well as axoplasm of spinal white matter and root nerve axon, suggesting the presence of anti-axon antibody, possibly against neurofilament or tubulin components. The biopsied muscle specimen showed neurogenic muscle changes, but with no evidence of vasculitis nor cellular infiltration. Therapeutic trial of plasmapheresis was effective for her muscle weakness. Further recovery of weakness and muscle atrophy of hand muscles was obtained by combined therapy of intravenous and oral corticosteroid administration and plasmapheresis. These clinical, electrophysiological and histological findings suggested that antibodies against neuronal component might be responsible for her motor neuronopathy associated with myasthenia gravis. The findings of our case study may support the idea that some cases of motor neuron disease are caused by auto-immune mechanism.
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PMID:[Subacute motor neuronopathy associated with myasthenia gravis and thymoma]. 1054 13

Microscopic polyangiitis (MPA) is a pauci-immune, necrotising, small-vessel vasculitis with an incidence of 3.6 per million population that typically presents in adulthood. Myasthenia gravis (MG), the most common disorder of the neuromuscular junction is rare, with an incidence of four per million population. We present the case of an adolescent girl previously diagnosed with MPA at age 7 years who presented with breathlessness and respiratory failure aged 15 years. The respiratory symptoms were due to thymoma-MG, which was successfully treated with cholinesterase inhibitors and thymectomy. This case report illustrates that the well-established doctrines of Occam's razor and of 'common conditions occurring commonly' are not universally applicable, and that in the adolescent age group, one should still consider Hickam's dictum.
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PMID:Microscopic polyangiitis and myasthenia gravis: the battle of Occam and Hickam. 1741 7

There are many cause of cholinesterase deficiency, including drugs, liver disease, chronic anemia, malignant states, cardiac failure, severe acute infection, surgical shock, severe burn, collagen disease and vasculitis syndromes. Vasculitis syndromes are relatively rare, and among them, Churg-Strauss syndrome (CSS) is even rarer. We report here on a case of a patient with CSS who underwent endoscopic sinus surgery under general anesthesia.
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PMID:A patient with Churg-Strauss syndrome who underwent endoscopic sinus surgery under general anesthesia -A case report-. 2065 99