The beneficial effects of lipid-lowering drugs beyond lipid-lowering effects: A comparative study with pravastatin, atorvastatin, and fenofibrate in patients with type IIa and type IIb hyperlipidemia

Hyperlipidemia is an important risk factor for atherosclerosis. Hemorheological factors contribute to morbidity and mortality in patients with dyslipidemia. We evaluated the effects of 3 antihyperlipidemic drugs (pravastatin, atorvastatin, and fenofibrate), which have different mechanisms of action and different patterns of action on lipid profiles, on erythrocyte deformability and fibrinogen levels in patients with type IIa and type IIb hyperlipidemia. Twenty-one patients (4 men and 17 women) with type IIa and IIb hyperlipidemia were randomized to 3 drugs (pravastatin 20 mg/d, atorvastatin 10 mg/d, fenofibrate 250 mg/d) for 8 weeks. Plasma glucose, total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) analysis were performed on a BM-Hitachi 747-200 autoanalyzer (Hitachi-Roche, Tokyo, Japan). Fibrinogen analysis was performed according to Clauss method. Erythrocyte deformability was assessed with cell transit analysis device. There was no significant difference in body mass index, lipid profile, fibrinogen level, and erythrocyte deformability index values among the groups before treatment (P > .05). In all groups, there were statistically significant reductions in total LDL-C levels (P .05). There was no significant change in HDL-C levels during the treatment with statins (P > .05), but there was a significant increase in the fenofibrate group (P .05), but in fenofibrate group, fibrinogen levels were significantly decreased (P < .05)

THE EFFECTS OF RALOXIFENE ON OSTEOCALCIN, AS A BONE TURNOVER MARKER IN ORCHIECTOMIZED RATS

WOS: 000339535700003Background. The aim of the present study was to measure the effects of raloxifene on bone metabolism and strength in orchiectomized male rats. Materials/Methods. Forty-three 4-month-old Wistar albino male rats were used and divided into 3 groups as orchiectomy (ORCX; n=23), sham (n=15), and control (n=5). Raloxifene (10 mg/kg/day) and methylcellulose (0.5 mL/day, as a vehicle treatment) treatments were initiated 2 months after ORCX for 2 months, then the rats were sacrificed. The left femur and fourth lumbar vertebrae (LV4) were measured to assess the effects of the orchiectomy and the raloxifene treatment and maintenance regimens. Bone strength was assessed using a compression test for the vertebrae and a three-point bending test for the femurs (N/mm). Results. Raloxifene increased femoral and vertebral bone strength in osteoporotic rats, but this increase was not statistically significant. Bone strength was found to be 267.44 +/- 18.03 in the femurs of the ORCX-raloxifene group and 246.32 +/- 49.37 in the femurs of the ORCX-C group (p>0.05). Vertebral bone strength was 147.78 +/- 09.51 in the ORCX-raloxifene group and 114.61 +/- 05.93 in ORCX-C group (p=0.488). Raloxifene also increased the femoral and vertebral bone density compared with the control group, but the change was not significant. While raloxifene significantly decreased the serum osteocalcin levels (p=0.007), it did not decrease the carboxyterminal cross-linking telopeptide of bone collagen (CTX) levels significantly (p=0.066). Conclusions. Raloxifene caused a statistically significant decrease in serum osteocalcin levels and a non-significant reduction in NTX levels in orchiectomized rats

The effects of raloxifene on osteocalcin, as a bone turnover marker in orchiectomized rats

Background. The aim of the present study was to measure the effects of raloxifene on bone metabolism and strength in orchiectomized male rats. Materials/Methods. Forty-three 4-month-old Wistar albino male rats were used and divided into 3 groups as orchiectomy (ORCX; n=23), sham (n=15), and control (n=5). Raloxifene (10 mg/kg/day) and methylcellulose (0.5 mL/day, as a vehicle treatment) treatments were initiated 2 months after ORCX for 2 months, then the rats were sacrificed. The left femur and fourth lumbar vertebrae (LV4) were measured to assess the effects of the orchiectomy and the raloxifene treatment and maintenance regimens. Bone strength was assessed using a compression test for the vertebrae and a three-point bending test for the femurs (N/mm). Results. Raloxifene increased femoral and vertebral bone strength in osteoporotic rats, but this increase was not statistically significant. Bone strength was found to be 267.44±18.03 in the femurs of the ORCXraloxifene group and 246.32±49.37 in the femurs of the ORCX-C group (p>0.05). Vertebral bone strength was 147.78±09.51 in the ORCX-raloxifene group and 114.61±05.93 in ORCX-C group (p=0.488). Raloxifene also increased the femoral and vertebral bone density compared with the control group, but the change was not significant. While raloxifene significantly decreased the serum osteocalcin levels (p=0.007), it did not decrease the carboxyterminal cross-linking telopeptide of bone collagen (CTX) levels significantly (p=0.066). Conclusions. Raloxifene caused a statistically significant decrease in serum osteocalcin levels and a non-significant reduction in NTX levels in orchiectomized rats

Low transforming growth factor-beta 1 serum levels in idiopathic male osteoporosis

Introduction: Although the etiology of osteoporosis is different between men and women, the underlying pathophysiological mechanism is similar, namely an absolute or relative increase in bone resorption, leading to progressive bone loss. Transforming growth factor (TGF)-beta 1 is a growth factor in human bone, which is produced by osteoblasts, and which has various effects on osteoclasts and osteoblasts. The aim of our study was to determine serum TGF-beta 1 levels in male patients with idiopathic osteoporosis. Methods: Twenty five males with idiopathic osteoporosis and 25 age-matched controls were studied. Osteoporosis was defined by a T score of <-2.5 in the lumbar spine or at the femoral neck. We measured levels of TGF-beta 1, estradiol, total and bioactive testosterone. Various markers of bone remodeling were also, measured. Results: TGF-beta 1 was significantly lower in osteoporotic patients than in controls (3.706 ng/dl, 25-75 percentiles: 2.81-5.33 vs 8.659 ng/dl, 25-75 percentiles: 4.837-11.835; p=0.000). Moreover, TGF-beta 1 levels were positively correlated with bone mineral density (BMD) at the femoral neck (r=0.439, p=0.028), and at the lumbar spine (r=0.41, p=0.042). No correlation was found between serum estradiol, testosterone and TGF-beta 1 levels. Discussion: Serum TGF-beta 1 levels are depressed in osteoporotic men and are positively, correlated with hip and spine BMD. The results of our study suggest that TGF-beta 1 may play a role in the pathogenesis of idiopathic male osteoporosis

Cushing's syndrome due to ectopic CRH secretion by adrenal pheochromocytoma accompanied by renal infarction.

Ectopic production of corticotropin-releasing hormone (CRH) by a pheochromocytoma is an infrequent cause of Cushing's syndrome. We report the case of a 43-year-old man with Cushing's syndrome due to a CRH-producing adrenal pheochromocytoma. The patient had clinical and biochemical evidence of hypercortisolism in conjunction with high ACTH levels and non-suppressible serum cortisol levels on low-dose and high-dose dexamethasone suppression testing. In addition to these clinical features of one month's duration, the patient developed symptoms of pheochromocytoma including headache, hypertension that was resistant to conventional therapy and excessive sweating. Biochemical testing confirmed elevated 24-hour urinary catecholamines and metabolites. Abdominal CT revealed a 4.5 x 4 x 3.5 cm mass in the left adrenal gland. He underwent elective left adrenalectomy. Light microscopic and immunochemical studies revealed a pheochromocytoma that contained immunoreactive CRH and was negative for ACTH. Plasma ACTH and dexamethasone supression tests normalized after surgery. This is an unusual case of a CRH-secreting pheochromocytorna. This was complicated by renal infarction, illustrating further the complexity of Cushing's syndrome in a patient with pheochromocytoma caused by CRH hypersecretion