[A case of lithium intoxication with vertical nystagmus, tetraplegia and cerebellar ataxia as permanent sequelae].
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Biomedical subjects
Publications and source records attributed to J Kaneko.
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Electrophoretic screening of glucose-6-phosphate dehydrogenase (EC 1.1.1.49, G6PD) was conducted one sample of 9,260 children born to the atomic bomb survivors in Hiroshima (Honshu) and Nagasaki (Kyushu). The prevalence of electrophoretic variants was 0.11% in males and 0.42% in females in Hiroshima, and 0.16% in males and 0.31% in females in Nagasaki. Enzymologic characteristics of 10 variants obtained from three males and seven hemizygous fathers of heterozygous females were examined. As a result, three new types of G6PD variants were identified among five variants detected in Hiroshima, and three new types among five variants in Nagasaki. All the variants except one belonged to Class 3, as defined by Yoshida et al. (1971).
A total of 15,387 individuals living in Hiroshima and Nagasaki, of whom 10,864 are unrelated, were examined for erythrocyte triosephosphate isomerase (TPI) by starch gel electrophoresis using TEMM buffer, pH 7.4. Four kinds of new variants, one having a cathodal migration and three having anodal migrations, were encountered in this population. These variants were further characterized by starch gel electrophoresis using tris-EDTA buffer, pH 9.3, and isoelectric focusing. An anodally migrating allozyme TPI 2HR1 exhibited markedly decreased enzyme activity, as evaluated by the staining intensity of the variant bands. The level of TPI activity in erythrocytes from this individual with the phenotype TPI 1-2HR1 was about 60% of the normal mean. Family studies confirmed the genetic nature of all the variants.
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Plasmapheresis and irradiation of the tumor were performed in conjunction with prednisolone therapy to a severe case of polyneuropathy associated with a solitary sclerotic secreting myeloma and endocrinological abnormalities. The patient was 27-year-old male with progressive history of polyneuropathy of seven months duration. On admission, he was quadriplegic with cranial nerve involvements. Pitting type of generalized edema, skin pigmentation and sensory impairment were also present. Respiratory failure occurred soon after the admission. Plasmapheresis lowered the level of M protein but failed to improve clinical course in the short term. On the other hand, prompt amelioration of clinical symptoms followed the irradiation of the tumor. It is difficult to prove clinical effects of plasmapheresis upon symptoms of chronic polyneuropathy. It is suggested that some humoral factor of myeloma might attribute to this syndrome and secreted at higher rate than our plasmapheresis but easily suppressed by the irradiation of the tumor. We suppose that radiation therapy could be the treatment of the first choice for such a severe case like ours. However, further experiences of plasmapheresis of this syndrome are necessary to determine the effect of plasmapheresis. Some other etiological aspects are also discussed.
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