Pituitary · 2026
The effect of hypoprolactinemia on cardiometabolic effects of rosuvastatin in men: A matched Cohort Pilot Study.
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Krysiak Robert, Kowalcze Karolina, Szkróbka Witold, Ott Johannes, Zaami Simona, Okopień Bogusław
Аннотация
PURPOSE: Low prolactin levels are associated with an increased risk of vascular and metabolic diseases. Women with prolactin deficiency appear to have attenuated responses to lipid-lowering and insulin-sensitizing medications. This study aimed to evaluate the impact of hypoprolactinemia on the cardiometabolic effects of rosuvastatin in men.
METHODS: Three groups of men with indications for statin therapy were included. Group 1 comprised 16 individuals with prolactin levels below 3 ng/mL, while groups 2 (n = 23) and 3 (n = 37) included patients with levels between 3 and 20 ng/mL. Participants in groups 1 and 2 were chronically treated with cabergoline. Throughout the six-month study period, all patients received rosuvastatin. In addition to lipid profile and prolactin levels, assessed parameters included high-sensitivity C-reactive protein (hs-CRP), fibrinogen, homocysteine, uric acid, urinary albumin-to-creatinine ratio (UACR), carbohydrate metabolism markers, testosterone, and carotid intima-media thickness (CIMT).
RESULTS: At baseline, men with hypoprolactinemia showed higher hs-CRP, fibrinogen, homocysteine, UACR, HbA1c, and HOMA-IR, and lower testosterone than those with normal prolactin levels. Rosuvastatin reduced total and LDL cholesterol in all groups, with a greater effect in groups 2 and 3. Reductions in hs-CRP, fibrinogen, uric acid, homocysteine, and UACR occurred only in groups with normal prolactin. Group 1 exhibited increases in HbA1c and HOMA-IR. At study end, CIMT was greater in group 1 than in groups 2 and 3, whereas the latter two groups had comparable values. In men with hypoprolactinemia, the effects of rosuvastatin on total and LDL cholesterol, hs-CRP, fibrinogen, uric acid, homocysteine, UACR, HbA1c, HOMA-IR, and CIMT correlated with baseline and posttreatment prolactin concentrations.
CONCLUSION: These findings suggest that hypoprolactinemia may worsen cardiometabolic outcomes in men receiving rosuvastatin therapy.
METHODS: Three groups of men with indications for statin therapy were included. Group 1 comprised 16 individuals with prolactin levels below 3 ng/mL, while groups 2 (n = 23) and 3 (n = 37) included patients with levels between 3 and 20 ng/mL. Participants in groups 1 and 2 were chronically treated with cabergoline. Throughout the six-month study period, all patients received rosuvastatin. In addition to lipid profile and prolactin levels, assessed parameters included high-sensitivity C-reactive protein (hs-CRP), fibrinogen, homocysteine, uric acid, urinary albumin-to-creatinine ratio (UACR), carbohydrate metabolism markers, testosterone, and carotid intima-media thickness (CIMT).
RESULTS: At baseline, men with hypoprolactinemia showed higher hs-CRP, fibrinogen, homocysteine, UACR, HbA1c, and HOMA-IR, and lower testosterone than those with normal prolactin levels. Rosuvastatin reduced total and LDL cholesterol in all groups, with a greater effect in groups 2 and 3. Reductions in hs-CRP, fibrinogen, uric acid, homocysteine, and UACR occurred only in groups with normal prolactin. Group 1 exhibited increases in HbA1c and HOMA-IR. At study end, CIMT was greater in group 1 than in groups 2 and 3, whereas the latter two groups had comparable values. In men with hypoprolactinemia, the effects of rosuvastatin on total and LDL cholesterol, hs-CRP, fibrinogen, uric acid, homocysteine, UACR, HbA1c, HOMA-IR, and CIMT correlated with baseline and posttreatment prolactin concentrations.
CONCLUSION: These findings suggest that hypoprolactinemia may worsen cardiometabolic outcomes in men receiving rosuvastatin therapy.