甲状腺機能亢進症を伴う周期性四肢麻痺の臨床的並びに実験的研究
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概要
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A) Clinical Study<BR>Ten cases (9 males, 1 female) of periodic paralysis associated with hyperthyroidism and five cases (males) without any thyroid abnormality were studied.<BR>Their ages ranged from seventeen years old to forty-nine years old.<BR>Precipitating factors were high carbohydrate intake, alcohol, overwork etc., which seemed to be inherent to individual case.<BR>The onset of paralysis was observed exclusively at night and early morning, none in daytime. Only one case was of familial form.<BR>Plasma potassium in these patients without paralytic attack was found to be within the normal range. Ten cases showed clinical signs and symptoms of hyperthyroidism with incrersed BMR, PBI and thyroidal I<SUP>131</SUP> uptake. However in six cases the attacks of paralysis had followed the onset of hyperthyroidism.<BR>Three cases showed slight hyperglycemic curves following the glucose tolerance test.<BR>In most cases, urinary total 17-OHCS was slightly increased above the normal range.<BR>In two cases associated with hyperthyroidism, auricular fibrillation was observed.<BR>In order to provoke an episode of periodic paralysis, hypertonic glucose solution ranging from 150 g. to 200 g. in total amount was injected intravenously within 30-60 minutes. Complete paralysis was induced in five out of fifteen cases. The rest of them showed incomplete paralysis. Oral or intravenous administration of KCl resulted in complete improvement of paralysis in all cases within a few minutes to one hour. Blood chemical analysis was carried out in the patients during this provocative test.<BR>There were no significant differences in the changes of blood sugar, lactic acid, pyruvic acid and plasma PBI between the patients with periodic paralysis thyrotoxic and normal subjects.<BR>However, there was significant decrease of plasma potassium and inorgamic phosphorus in the patients with periodic paralysis as compared with thyrotoxic and also with normal subjects.<BR>The patients of periodic paralysis associated with hyperthyroidism were treated I<SUP>131</SUP> or Methyl-mercapto-imidazol.<BR>Attacks of periodic paralysis improved completely in all the case after their thyroid functions returned to the normal range. Parotin (Hormone of parotis gland) was administered to the patients with periodic paralysis without hyperthyroidism resulting in satisfactory effects.<BR>B) Experimental Study : <BR>Dogs were fed a low potassium (5 m.eq. per day) and high sodium (200 m.eq. per day) diet and also with thyroid extract 5 g per day for about one month in order to induce hyperthyroidism up to the 100% increased of oxygen consumption rate. In these hyperthyroid dogs, hypertonic glucose solution (100 g/250 ml) or glucose+ insulin (10 U) were administered intravenously within 30 minutes in order to provoke a paralytic attack.<BR>Two out of thirteen hyperthyroid dogs showed typical complete pararysis which was confirmed by electromyogram with quantitative electric stimulator to femoral nerves.<BR>The paralysis comyletely disappeared following administration of 1-2 g. of KCl.<BR>Potassium and Sodium in femoral artery and vein, in femoral muscles and in urine were determined before, during and after the provocative test. Plasma potassium decreased significantly in all the case, following administration of glucose irrespective of the attack of paralysis.<BR>There were little arterio-venous differences in plasma potassium in the dogs without paralytic attack.<BR>However in the dogs which showed typical paralytic attack, the arterio-venous differences in plasma potassium were significant during the attack of paralysis and even before the provocative test. However these arterio-venous differences were reversed by intravenous administration of KCl.<BR>Potassium contents in muscles decreased in most cases of euthyroid dogs after intravenous administration of glucose.<BR>On the contrary,
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