糖尿病に伴う低アルドステロン症の成因に関する研究:副腎皮質各種ステロイドのアンジオテンシンIIまたはACTHに対する反応性によるアルドステロン生合成過程の検討
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This study was designed to clarify the cause of hyporeninemic hypoaldosteronism (HH) associated with diabetes mellitus. Fourty diabetic patients (DP) were divided into 3 groups; 12 patients without neuropathy or nephropathy, 13 with neuropathy and without nephropathy, and 15 with neuropathy and nephropathy; in the third group 3 HH patients were included. Fourteen normal subjects served as controls. In all DP and the normal sub(P<SUB>Ald</SUB>), jects, plasma concentration of aldosterone 18-hydroxycorticosterone (P<SUB>18-0H-B</SUB>), corticosterone (P<SUB>B</SUB>), 11-deoxycorticosterone (P<SUB>DOC</SUB>) and cortisol (P<SUB>F</SUB>) were measured before and after intravenous administration of angiotensin II (A II, 10 ng/kg/min, for 30 min) or ACTH (<SUP>1-24</SUP> ACTH, 0.25 mg). In 27 DP, plasma renin activity (PRA) increased from 0.8 ±0.6 SD to 2.4 ±2.2 ng/ml/h (normal : 1.2 ±0.7 to 3.2 ±1.7 ng/ml/h) 2 hours after intravenous administration of furosemide (1 mg/kg) and assumption of the upright posture. No significant difference in PRA was found between DP and controls, whereas the response to these stimuli decreased significantly in 9 DP with neuropathy and nephropathy (from 0.4 ±0.2 to 0.7 ±0.4 ng/ml/h). The major results were as follows : <BR>1) The mean of P<SUB>Ald</SUB> (5.9±2.4 ng/100 ml) in DP was significantly lower than that in controls (7.7 ±2.2 ng/100 ml). There was no significant difference of P <SUB>Ald</SUB> between DP without complications and controls. P<SUB>Ald</SUB> in DP with neuropathy alone (5.0 ±1.5 ng/100 ml, p<0.05) and that in DP with neuropathy and nephropathy (4.7 ±2.4 ng/100 ml, p<0.05) were lower than that in controls. The mean of P<SUB>18-0H-B</SUB> (12.3 ±4.3 ng/100 ml) in DP was similar to that (14.2 ±3.2 ng/100 ml) in controls. P<SUB>18-0H-B</SUB> in DP without complications and that in DP with neuropathy alone were similar to that in controls. However, P<SUB>18-OH-B</SUB> (8.8 ± 3.2 ng/100 ml) in DP with neuropathy and nephropathy was significantly lower than that in controls (p<0.001). No difference in P<SUB>B</SUB>, P<SUB>DOC</SUB> or P<SUB>F</SUB> was observed between DP and controls.<BR>2) P<SUB>Ald</SUB> increased from 6.0 ± 2.5 ng/100 ml in DP (p<0.001) and from 7.6 ± 2.2 to 15.7 ± 5.3 ng/100 ml in controls (p<0.001) 30 min after A II infusion. P<SUB>Ald</SUB> increased from 7.6 ± 2.5 ng/100 ml in DP without complications (p<0.001), from 5.9 ± 1.5 ng/100 ml to 7.0 ± 1.8 ng/100 ml in DP with neuropathy alone (p<0.001) and from 4.7 ± 2.4 ng/100 ml to 5.5 ± 2.5 ng/100 ml in DP with neuropathy and nephropathy (p<0.01). The increments in the 3 groups were significantly lower than that in controls (p<0.05, p<0.001, p<0.001). P<SUB>18-0H-B</SUB> increased from 12.1 ± 4.5 to 15.4 ± 6.8 ng/100 ml in DP (p<0.001) and from 14.1 ± 3.5 to 26.6 ± 5.0 ng/100 ml in controls (p<0.001) after A II infusion. P<SUB>18-0H-B</SUB> increased from 15.3 ± 4.2 to 22.3 ± 7.3 ng/100 ml in DP without complications (p<0.001), from 13.1 ± 2.8 to 14.7 ± 2.9 ng/100 ml in DP with neuropathy alone (p<0.001) and from 8.7 ± 3.7 to 10.6 ± 3.5 ng/100 ml in DP with neuropathy and nephropathy (p<0.01). The increments of P<SUB>18-0H-B</SUB> in DP with neuropathy alone (p<0.001) and in DP with neuropathy and nephropathy (p<0.001) were lower than that in controls. P<SUB>B</SUB>, B<SUB>Doc</SUB> and P<SUB>F</SUB> did not change significantly after A II infusion in either controls and DP.<BR>3) P<SUB>Ald</SUB> increased from 6.0 ± 2.3 to 16.2 ± 7.2 ng/100 ml in DP (p<0.001) and from 7.6 ± 2.2 to 24.6 ± 5.3 ng/100 ml in controls (p<0.001) 60 min after ACTH administration.
- 一般社団法人 日本内分泌学会の論文
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