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)

This is the first report of brachial plexus inflammation associated with clinical herpes zoster paresis. A 78-year-old female with a 3-week history of herpes zoster of the C4, C5, and C6 dermatomes developed left upper arm monoplegia. She died from an acute myocardial infarction. Post-mortem provided a rare opportunity to study the neuropathology of herpes zoster motor involvement. Histology of the brachial plexus showed extensive lymphocytic infiltration, myelin breakdown, and preservation of axons without vasculitis. The cervical spinal cord showed perivascular lymphocytic cuffing and no anterior horn necrosis. We suggest, the brachial plexus inflammation was a distal extension of a dorsal ganglionitis. Brachial plexus neuritis may be a direct cause of reversible upper limb paresis in herpes zoster. We demonstrate the motor neuropathy is an inflammatory demyelinative process consistent with the recovery observed in a number of patients. We postulate post-herpetic neuralgia may be related to an ongoing inflammatory process.
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PMID:Herpes zoster brachial plexus neuritis. 910 Nov 5

A 35-year-old patient with hemophilia A presented with rapidly progressive polyarteritis nodosa (PAN). He had been infected with hepatitis B virus (HBV) by repeated transfusion and was positive for hepatitis B surface antigen but negative for hepatitis B surface antibody. The patient presented symptoms of acute epididymitis followed by emergency admission because of acute appendicitis. On day 7 of admission, he complained of severe back pain, and computerized tomography (CT) showed massive perirenal hematoma. On day 49, mild monoplegia in the left arm suddenly developed, and CT and magnetic resonance imaging revealed multiple cerebral infarctions. Factor VIII replacement therapy was attenuated; however, cerebral infarction was progressive and extended throughout the cerebral hemispheres. He was diagnosed with classic polyarteritis nodosa (cPAN), and pulse methylprednisolone was continued. The patient died of supratentorial herniation, and autopsy revealed that vasculitis associated with intimal thickening was present in the liver, pancreas, intestine, kidneys, and larger-sized cerebral arteries. The development of cPAN appeared to have originated from chronic HBV infection, and this is the first report of cPAN in hemophilia patients. Concomitant hemorrhagic and thrombotic manifestations of cPAN are hardly treatable in patients with coagulation disorders, and the current case may represent a rare transfusion-related complication in hemophilia patients.
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PMID:Classic polyarteritis nodosa presenting rare clinical manifestations in a patient with hemophilia A. 1678 73