Kumar S, Olukoga A O, Gordon C, Mawer E B, France M, Hosker J P, Davies M, Boulton A J
Department of Medicine, Manchester Royal Infirmary, UK.
Clin Endocrinol (Oxf). 1994 Jan;40(1):47-53. doi: 10.1111/j.1365-2265.1994.tb02442.x.
A high prevalence of diabetes mellitus has been shown in patients with primary hyperparathyroidism (PHPT). However, it is unclear whether this is related to the metabolic abnormalities in PHPT or to the presence of other risk factors for glucose intolerance in these patients. The aim of our study was to determine whether glucose intolerance and insulin insensitivity occur in subjects with PHPT who do not have other risk factors for diabetes mellitus.
Cross-sectional study of glucose metabolism in PHPT patients without other risk factors for diabetes mellitus, compared to age and body mass index (BMI) matched healthy subjects.
Nineteen non-obese, non-diabetic, normotensive patients with PHPT and 11 age and BMI matched healthy subjects.
The continuous infusion of glucose test was used to assess glucose tolerance. Plasma glucose and insulin were measured during a 1-hour continuous infusion of glucose (5 mg/kg ideal body weight/min); insulin sensitivity and beta-cell function were derived from the glucose and insulin data by mathematical modelling. Fasting serum concentrations of parathyroid hormone, ionized calcium and 1,25-dihydroxyvitamin D (1,25(OH)2D) were measured in all subjects.
PHPT patients attained higher plasma glucose levels at the end of the glucose infusion (median 9.0 (interquartile range 8.1-9.8) mmol/l) than did controls (7.9 (7.1-8.9) mmol/l, P < 0.05), and 8 (42%) PHPT patients had impaired glucose tolerance. Insulin sensitivity was lower in PHPT (60.3% (49.8-85.4)) than in controls (113.7% (89.3-149.2), P < 0.001); beta-cell function was not different in PHPT subjects. PHPT subjects with impaired glucose tolerance had reduced beta-cell function compared to PHPT subjects with normal glucose tolerance (89.9% (70.5-106.4) vs 120% (98.8-156.6) respectively, P < 0.05). No significant correlations were found between insulin sensitivity and PTH (rs = -0.21), 1,25(OH)2D (rs = -0.14), ionized calcium (rs = -0.11) and inorganic phosphate (rs = 0.34). Beta-cell function did not correlate with PTH (rs = 0.15), 1,25(OH)2D (rs = 0.04), ionized calcium (rs = 0.23) or inorganic phosphate (rs = -0.35).
Insulin insensitivity is present in PHPT even in the absence of hypertension and obesity, and may be the cause of glucose intolerance and diabetes. PHPT subjects with reduced beta-cell function are more likely to develop glucose intolerance.
原发性甲状旁腺功能亢进症（PHPT）患者中糖尿病患病率较高。然而，尚不清楚这是与PHPT的代谢异常有关，还是与这些患者中存在的其他葡萄糖不耐受风险因素有关。我们研究的目的是确定在没有其他糖尿病风险因素的PHPT患者中是否存在葡萄糖不耐受和胰岛素抵抗。
对没有其他糖尿病风险因素的PHPT患者的葡萄糖代谢进行横断面研究，并与年龄和体重指数（BMI）相匹配的健康受试者进行比较。
19名非肥胖、非糖尿病、血压正常的PHPT患者以及11名年龄和BMI相匹配的健康受试者。
采用持续葡萄糖输注试验评估葡萄糖耐量。在1小时持续输注葡萄糖（5mg/kg理想体重/分钟）期间测量血浆葡萄糖和胰岛素；通过数学建模从葡萄糖和胰岛素数据中得出胰岛素敏感性和β细胞功能。测量所有受试者空腹血清甲状旁腺激素、离子钙和1,25-二羟维生素D（1,25(OH)2D）浓度。
PHPT患者在葡萄糖输注结束时的血浆葡萄糖水平（中位数9.0（四分位间距8.1 - 9.8）mmol/L）高于对照组（7.9（7.1 - 8.9）mmol/L，P < 0.05），8名（42%）PHPT患者存在葡萄糖耐量受损。PHPT患者的胰岛素敏感性（60.3%（49.8 - 85.4））低于对照组（113.7%（89.3 - 149.2），P < 0.001）；PHPT受试者的β细胞功能无差异。与葡萄糖耐量正常的PHPT受试者相比，葡萄糖耐量受损的PHPT受试者的β细胞功能降低（分别为89.9%（70.5 - 106.4）和120%（98.8 - 156.6），P < 0.05）。未发现胰岛素敏感性与甲状旁腺激素（rs = -0.21）、1,25(OH)2D（rs = -0.14）、离子钙（rs = -0.11）和无机磷（rs = 0.34）之间存在显著相关性。β细胞功能与甲状旁腺激素（rs = 0.15）、1,25(OH)2D（rs = 0.04）、离子钙（rs = 0.23）或无机磷（rs = -0.35）均无相关性。
即使在没有高血压和肥胖的情况下，PHPT患者也存在胰岛素抵抗，这可能是葡萄糖不耐受和糖尿病的原因。β细胞功能降低的PHPT受试者更有可能发生葡萄糖不耐受。
