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)

A case of multiple myeloma forming an intracranial mass which invaded the skull base was reported. A 72-year-old woman was admitted to the hospital because of left oculomotor paresis. Plain craniograms showed multiple punched out lesions. A CT scan demonstrated a mass lesion, which was homogeneously slightly enhanced with contrast medium, in the middle cranial fossa. MRI, both T1 and T2 weighted images, showed an isodensity mass. In the carotid angiograms the tumor was fed by the right branches of the cavernous portion of the internal carotid artery and the maxillary artery. Laboratory data were as follows: ESR: 132mm/30min, serum TP: 9.0g/dl, IgG: 4670mg/dl, IgA: 430mg/dl, and urinary Bence-Jones protein was detected. Bone marrow biopsy of the illiac bone demonstrated myeloma cells. During hospitalization oculomotor paresis disappeared, and the patient was treated with intramuscular interferon-alpha. Multiple myeloma which invades the skull base is rare, and only 10 cases have been reported since 1977. Moreover, the biclonal type is only 0.5% of all multiple myelomas.
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PMID:[A case of multiple myeloma (biclonal type) associated with an intracranial mass invading the skull base and oculomotor palsy]. 176 45

Hypokalaemic thyrotoxic periodic paralysis is an enigmatic and uncommon condition which occurs exclusively in males of Asian descent. The underlying causes of thyrotoxicosis may be any of the well-recognized etiologies including a toxic multinodular goiter, Graves' disease or iodine excess. Beside thyrotoxicosis, a number of other hormonal factors have been hypothesized to contribute to hypokalaemic thyrotoxic periodic paralysis, particularly postprandial hyperinsulinaemia and testosterone. We hereby present a case of a 48-year-old hepatitis C positive gender-assigned man in whom all of these factors are proposed to interact, lending further support to these hypotheses. The patient presented with interferon-induced thyroiditis causing acute generalized weakness whilst undergoing combination interferon-alpha-2beta and ribavirin therapy. As part of his hepatitis C infection, marked insulin resistance with hyperinsulinaemia was also present, exacerbating the paresis. Initial treatment with beta-blocker failed to normalize his serum potassium concentration, requiring the novel use of spironolactone, despite euthyroidism. This continued to be required until his testosterone supplement dissipated.
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PMID:Hepatitis C infection and thyrotoxic periodic paralysis--a novel use of an old drug. 1909 28