Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present the case of a 67-year-old female patient with microscopic polyangiitis presented with polyneuropathy of lower extremities and rapidly progressive glomerulonephritis. Disease had started as a pain and weakening of muscular strength first in the left and than in the right leg. Electromiography has shown that a mainly dominant neurological affection was paresis of peroneal nerve in both lower extremities. In laboratory examination the titer of anti-myeloperoxidase anti-neutrophilic cytoplasmic antibodies (p-ANCA) was elevated. Due to renal involvement presented as a microscopic haematuria and decreasing of renal function, patient undergone kidney biopsy. It confirmed the immune vasculitis microscopic polyangiitis type with ANCA-associated glomerulonephritis. This is one of rare case of microscopic polyangiitis without lung simptomatology, first presented with asymmetrical polineuropathy of lower extremities. The patient was treated with methylprednisolone and cyclophosphamide in dosis adjusted to the level of disease severity and the renal function (methylprednisolone 1 mg/kg of body weight for two months with gradually tapering to the minimum effective dose and cyclophosphamide 1 mg/kg of body weight). This treatment lead to the partial remission of disease. In maintenance therapy azathioprin was introduced instead of cyclophosphamide.
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PMID:Microscopic polyangiitis presented with polyneuropathy of lower extremities and ANCA-associated glomerulonephritis: case report. 2236 5

A 42-year-old woman was admitted due to systemic lupus erythematosus complicated with glomerulonephritis and pulmonary hypertension. During the treatment for these complications, she presented motor paresis and sensory loss caused by transverse myelitis. In spite of methyl prednisolone pulse therapy, she further developed acute confusional state due to disseminated encephalitis and fell into respiratory arrest. On laboratory examination, elevation of anti-NR2 antibodies in serum as well as in cerebrospinal fluid was noted. Although she recovered from the disseminated encephalitis after extensive treatment with high doses of corticosteroid and intravenous cyclophosphamide, she suddenly died of pulmonary hypertension. Autopsy findings confirmed the presence of liquefaction necrosis in the entire circumference of the whole spinal cord along with intimal hyperplasia and obliteration of the small arteries, accompanied by mononuclear cell infiltration and disruption of internal elastic lamina. It is therefore most likely that our patient developed longitudinal transverse myelitis through spinal cord vasculitis, which extended to brainstem and brain parenchyma, leading to the development of disseminated encephalitis.
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PMID:Transverse myelitis extended to disseminated encephalitis in systemic lupus erythematosus: Histological evidence for vasculitis. 2511 57