Diabetes research and clinical practice · 2019
Increased parathyroid hormone is associated with higher fasting glucose in individuals with normocalcemic primary hyperparathyroidism and prediabetes: A pilot study.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Karras Spyridon N, Koufakis Theocharis, Tsekmekidou Xanthippi, Antonopoulou Vassiliki, Zebekakis Pantelis, Kotsa Kalliopi
Аннотация
AIMS: This pilot study aimed to evaluate differences in glycemic parameters between patients with prediabetes and normocalcemic primary hyperparathyroidism (NPHPT) and controls with prediabetes and normal parathyroid hormone (PTH) and calcium concentrations.
METHODS: 20 patients with NPHPT and prediabetes and 42 age-, gender-, and body mass index-matched controls with prediabetes were included. Glycemic parameters [fasting glucose (fGlu), glycosylated hemoglobin (HbA1c), fasting insulin (fIns)] were evaluated. Homeostasis Model Assessment was used for estimating insulin secretion (HOMA-B) and resistance (HOMA-IR). Participants underwent a 75-g oral glucose tolerance test.
RESULTS: HbA1c (5.9 ± 0.0 vs 5.9 ± 0.0%, p = 0.44), HOMA-IR (3.7 ± 1.2 vs 2.9 ± 0.2, p = 0.48), HOMA-B (117.8 ± 31.8 vs 146.9 ± 22.0%, p = 0.14), fIns (14.0 ± 4.3 vs 12.2 ± 1.1 μIU/ml, p = 0.53) and 2-hour post-load glucose concentrations (157.2 ± 2.2 vs 152.2 ± 2.0 mg/dl, p = 0.07), were nondifferent in the two groups. Higher fGlu levels were evident in the NPHPT, compared to the control group (105.6 ± 2.8 vs 98.2 ± 1.8 mg/dl, p = 0.01). fGlu demonstrated a positive correlation with PTH concentrations (rho = 0.374, p = 0.005).
CONCLUSIONS: Individuals with NPHPT and prediabetes present an unfavorable glycemic profile compared to age-matched people with prediabetes, suggesting a direct adverse effect of elevated PTH on glucose homeostasis.
METHODS: 20 patients with NPHPT and prediabetes and 42 age-, gender-, and body mass index-matched controls with prediabetes were included. Glycemic parameters [fasting glucose (fGlu), glycosylated hemoglobin (HbA1c), fasting insulin (fIns)] were evaluated. Homeostasis Model Assessment was used for estimating insulin secretion (HOMA-B) and resistance (HOMA-IR). Participants underwent a 75-g oral glucose tolerance test.
RESULTS: HbA1c (5.9 ± 0.0 vs 5.9 ± 0.0%, p = 0.44), HOMA-IR (3.7 ± 1.2 vs 2.9 ± 0.2, p = 0.48), HOMA-B (117.8 ± 31.8 vs 146.9 ± 22.0%, p = 0.14), fIns (14.0 ± 4.3 vs 12.2 ± 1.1 μIU/ml, p = 0.53) and 2-hour post-load glucose concentrations (157.2 ± 2.2 vs 152.2 ± 2.0 mg/dl, p = 0.07), were nondifferent in the two groups. Higher fGlu levels were evident in the NPHPT, compared to the control group (105.6 ± 2.8 vs 98.2 ± 1.8 mg/dl, p = 0.01). fGlu demonstrated a positive correlation with PTH concentrations (rho = 0.374, p = 0.005).
CONCLUSIONS: Individuals with NPHPT and prediabetes present an unfavorable glycemic profile compared to age-matched people with prediabetes, suggesting a direct adverse effect of elevated PTH on glucose homeostasis.