Bone mineral density and bone turnover in patients with psoriatic arthritis.

Psoriasis is a common inflammatory skin disease, and conflicting data have been published about osteoporosis and bone turnover markers in patients with psoriatic arthritis. The aim of this study was to assess bone mineral density (BMD) and bone turnover markers in psoriatic patients with and without peripheral arthritis and to investigate the relationship between clinical parameters and markers of bone turnover. Forty-seven patients (24 women, 23 men) with psoriasis were included to the study. Demographic data and clinical characteristics were recorded. Erythrocyte sedimentation rate and C-reactive protein were assessed as disease activity parameters. BMD was determined for lumbar spine and total hip by dual X-ray absorptiometry (DXA). Serum Ca, P, alkalen phosphatase (ALP), and serum type I collagen cross-linked C telopeptide (CTX) were measured as bone turnover markers in all patients. The patients were divided into two groups according to their peripheral arthritis status. The clinical and laboratory variables, as well as bone mass status of the groups, were compared with each other. Eighteen patients had peripheral arthritis. All the female patients were premenopausal. None of the patients had radiologically assessed axial involvement. There was no significant difference between the BMD levels of psoriatic patients with and without arthropathy. One patient (5%) had osteoporosis, and nine (50%) patients had osteopenia in arthritic group, while eight (27.5%) patients had osteopenia in patients without arthritis. Serum CTX, ALP, Ca, and P levels were not significantly different in arthritic than in non-arthritic patients (p > 0.05). In patients with psoriatic arthritis, the duration of arthritis was negatively correlated with BMD values of lumbar spine and total femur and serum CTX levels, suggesting an association of increased demineralization with the duration of joint disease. In conclusion, psoriatic patients with peripheral arthritis with longer duration of joint disease may be at a risk for osteoporosis, which can require preventative treatment efforts.

Plasma homocysteine concentrations and serum lipid profile as atherosclerotic risk factors in subclinical hypothyroidism.

BACKGROUND AND OBJECTIVES: Because subclinical thyroid dysfunction may be a risk factor for cardiovascular disease, we evaluated the atherosclerosis tendency in subclinical hypothyroid (SCH) patients. PATIENTS AND METHODS: Fifty-three subclinical hypothyroid patients (serum thyrotropin [TSH] concentrations >4.12 mU/L) were compared with a control group of 50 euthyroid subjects whose age, sex and body mass indices were similar to the patient group. We tested whether serum TSH concentrations were correlated with plasma total homocysteine concentration (tHcy), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC) and triglycerides (TG). RESULTS: There was a significant statistical difference between the patient and control groups for normal free T4 (1.02+/-0.17 vs. 0.86+/-0.13, P<.001), TSH (1.64+/-1.02 vs. 6.62+/-2.61, P<.001), TC (185+/-39 vs. 206 +/- 42, P=.01), TG (103+/-54 vs. 132+/-85, P=.04), LDL-C (114+/-33 vs. 127+/-36, P=.04), and TC/HDL-C (3.81+/-106 vs. 4.19+/-1.02, P=.04), respectively. No statistically significant difference was found between the two groups for HDL-C, VLDLC, LDL-C/HDL-C, and tHcy. Serum TSH was significantly correlated with plasma tHcy (r=0.55; P=.001), TC (r=0.52; P=.001), LDL-C (r=0.49; P=.001), TC/HDL-C (r=0.38; P=.002) and LDL-C/HDL-C (r=0.36; P=.004) across all participants. CONCLUSION: Our study suggests that the atherogenicity of SCH is not mediated by hyperhomocysteinemia. Associated hyperlipidemia may explain the observed increased risk of coronary artery disease in patients with SCH.

Plasma visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus and impaired glucose tolerance.

Visfatin, a new adipokine, facilitates adipogenesis and has insulin-mimetic properties. We aimed to investigate the plasma visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus (T2DM) and impaired glucose tolerance (IGT), who had no obesity or hypertension. Twenty-two patients with T2DM, 18 subjects with IGT and 40 healthy controls were enrolled. Visfatin levels were measured along with the BMI, blood pressure, lipids, glucose, insulin, adiponectin and hsCRP levels, and HOMA-IR indexes. Age, sex and BMI were similar in all groups. Visfatin levels were higher in the diabetic group than the controls (p=0.01). There was no significant difference in the visfatin levels between the T2DM and IGT groups as well as IGT group and healthy controls. Plasma visfatin concentrations did not differ between men and women. Visfatin levels did not correlate with BMI, blood pressure, plasma adiponectin, insulin, hsCRP, glucose and lipid levels or HOMA-IR indexes in the three groups. These results indicate that hyperglycemia causes an increase in plasma visfatin levels and, as in people with T2DM but not with IGT, this increase gets more prominent as the glucose intolerance worsens.

Blockade of the renin-angiotensin system increases plasma adiponectin levels in type-2 diabetic patients with proteinuria.

BACKGROUND/AIMS: Adiponectin seems to be an important modulator for metabolic and vascular diseases. A case study was designed to measure plasma adiponectin levels and to investigate the effects of angiotensin-converting enzyme inhibitors on adiponectin levels in type-2 diabetic patients with proteinuria. METHODS: Forty-nine patients (28 males, 21 females) and 23 healthy volunteers (13 males, 10 females) were included in the case study. Patients with proteinuria were treated with 5 mg/day ramipril (n = 21) for 4 weeks. RESULTS: Adiponectin levels of patients were significantly lower than those of healthy volunteers (p < 0.001). There were significant negative correlations between adiponectin concentrations and insulin levels as well as the homeostasis model assessment (HOMA) index in the patient group (r = -0.655, p < 0.001; r = -0.469, p = 0.001, respectively). There was also a significant negative correlation between plasma adiponectin concentrations and the degree of proteinuria (r = -0.912, p < 0.001). Plasma adiponectin levels in patients with proteinuria (n = 21; 4.81 +/- 3.17 microg/ml) were significantly lower than those without proteinuria (n = 28; 10.25 +/- 2.03 microg/ml; p < 0.001). After the treatment period, adiponectin levels significantly increased (p < 0.001) and proteinuria, plasma insulin, and HOMA indexes significantly decreased in the treatment group (p < 0.001, p < 0.001, p = 0.002, respectively). CONCLUSIONS: The results suggest that adiponectin is inversely correlated with proteinuria and treatment with ramipril both corrects proteinuria and increases the low adiponectin levels in diabetic patients.

Plasma homocysteine level is elevated in patients on isotretinoin therapy for cystic acne: a prospective controlled study.

PURPOSE: Isotretinoin (Iso) has marked side effects. Homocysteine (Hcy) metabolizes in the liver, requiring folate and vitamin B12. Elevated blood levels of Hcy have been linked to an increased risk of premature coronary artery disease (CAD). In this study, we evaluated Hcy levels, vitamin B12, and folate in patients on Iso treatment for cystic acne (CA). METHODS: Seventy-four patients with CA were included to the study group. Blood levels of Hcy, vitamin B12, and folate were assessed before and after 45 days of Iso therapy. The control group consisting of 80 individuals were tested once. RESULTS: Hcy levels were statistically significantly increased in patients on Iso treatment. Vitamins were unaltered, while lipids and liver enzymes increased statistically significantly. CONCLUSION: Hcy levels are elevated in patients on Iso treatment for CA. It may be due to either the inhibition of cystathionine-beta-synthase, an enzyme required in the metabolism of Hcy, by the drug and/or the liver dysfunction. Daily supplementation with vitamin B12 and folate, which are the cofactors of the enzymatic reactions involved in Hcy metabolism, can lower plasma levels of Hcy, so it is recommended to take these vitamins in case of deficiency along with Iso to prevent premature occlusive vascular disease.

Coronary artery bypass grafting ameliorates the decreased plasma adiponectin level in atherosclerotic patients.

Adiponectin functions as an anti-inflammatory and anti-atherogenic factor, and the decreased plasma adiponectin is a risk factor for coronary disease. The aim of this study was to determine the changes in plasma levels of adiponectin, a potential parameter for atherosclerosis, in patients underwent surgical revascularization. We included forty patients with atherosclerosis (age, 58 +/- 9 years; body mass index [BMI] 26.93 +/- 2.3 kg/m(2)) undergoing coronary artery bypass grafting (CABG). Control group consisted of 40 healthy volunteers, matched for age, gender and BMI (age, 56 +/- 6 years; BMI, 26.78 +/- 2.3 kg/m(2)). We measured various parameters, including high sensitive C-reactive protein (hsCRP), homeostasis model assessment-insulin resistance (HOMA-IR) indexes, and adiponectin. The baseline profile of the patients before CABG showed higher levels of serum hsCRP (13.15 +/- 2.40 mg/l vs 3.97 +/- 1.07 mg/l) and HOMA-IR (1.86 +/- 0.30 vs 1.26 +/- 0.33) and lower plasma adiponectin levels (7.02 +/- 2.01 microg/ml vs 25.46 +/- 3.9 microg/ml), compared to controls (p < 0.001 for each parameter). Plasma adiponectin level was increased one month after CABG from the baseline level to 8.67 +/- 2.05 microg/ml(p < 0.001), although the level was still lower than the control value. Thus, postoperative adiponectin level might be helpful for evaluating the progression of atherosclerosis. Moreover, CABG significantly decreased hsCRP to 7.25 +/- 1.89 mg/l and HOMA-IR to 1.59 +/- 0.33, although these levels were higher than the controls. These results suggest that CABG decreases the cardiac risk factors in atherosclerotic patients.

The effect of fluvastatin on plasma adiponectin levels in dyslipidaemia.

OBJECTIVE: There is controversy about the effects of statins on insulin resistance and plasma adiponectin. The aim of this study was to investigate the effects of fluvastatin treatment on these parameters in a group of dyslipidaemic patients who had no confounding factors for insulin resistance or alterations in plasma adiponectin. DESIGN AND PATIENTS: Forty-nine patients [27 males, 22 females; mean age 47.2 +/- 10.3 years; body mass index (BMI) 29.64 +/- 3.2 kg/m2] with dyslipidaemia and 20 controls (six males, 14 females; mean age 45.3 +/- 9.31 years; BMI 30.07 +/- 4.04 kg/m2) were enrolled. All patients were treated initially with therapeutic lifestyle changes (TLC) for 6 weeks. Six out of 49 subjects were excluded from the study. Then, 24 out of 43 patients with high blood cholesterol despite TLC were allocated to fluvastatin 80 mg daily plus TLC, and the remaining 19 patients with normal cholesterol were subjected to TLC alone for additional 12 weeks. MEASUREMENTS: Plasma adiponectin, immunoreactive insulin levels, BMI, waist circumference, blood pressure, lipids, and glucose were determined. The insulin sensitivity index was quantified using the homeostasis model assessment (HOMA). RESULTS: TLC caused significant improvement in plasma insulin (P = 0.02) and elevation in plasma adiponectin (P = 0.02). Fluvastatin treatment decreased total cholesterol and low density lipoprotein (LDL)-cholesterol significantly (P = 0.01 and P = 0.02, respectively). No significant effect of fluvastatin was observed on plasma insulin or adiponectin or on the HOMA index. CONCLUSIONS: Fluvastatin does not improve plasma adiponectin levels and insulin sensitivity, despite its beneficial effects on lipid levels. Our data, however, were limited by the fact that a more accurate method of assessing insulin sensitivity, the euglycaemic-hyperinsulinaemic glucose clamp technique, was not used.