The effect of the content of the knowledge on adherence to medication in hypertensive patients.

OBJECTIVE: It was suggested that knowledge might influence the adherence to treatment in hypertension. Accordingly, in this study, we investigated the effects of content of knowledge on medication adherence and knowledge-based predictors of adherence to treatment in hypertensive patients. METHODS: This cross-sectional study included 227 hypertensive patients (70% female;mean age: 57+/-12 years), who were followed by cardiology and internal medicine clinics. The patients were asked to fulfill a questionnaire including 40 items. Besides the demographic and disease-related questions, the patients were also asked (1) the name of the drug, (2) the duration of the drug use;(3) the reason of using the drug;(4) the cause of hypertension;(5) the target level of hypertension;(6) the result of hypertension;(7) the side effects of antihypertensive medicines. Statistical analyses were performed using Chi-square, Fischer exact, Mann Whitney U tests and logistic regression analysis. RESULTS: It was found that 163 (72%) were adherent and 64 (28%) were nonadherent to the treatment. Angiotensin-II receptor antagonist use (OR=4.405;95%CI: 1.561-12.365, p=0.022) and hypertension duration > or =5 years (OR=0.446;95%CI: 0.246-0.811, p=0.006) was found to be independently related to adherence. Among the knowledge-based variables, knowing the duration of use of the medicine (OR=6.822;95% CI: 1.478-31.241, p=0.075), the reason of use of medicine (OR=2.828;95% CI: 1.445-5.543, p=0.018), the cause of the hypertension (OR=3.447;95% CI: 1.889-6.290, p=0.037) and the target level of blood pressure (OR=12.859;95% CI: 5.045-32.640, p<0.001) significantly increased the adherence rates. On the other hand, knowing the name of the medicine (p=0.112) or the results of hypertension (p=0.719) had no effect on adherence, while knowing the side effects of the medicine (OR=0.607;95% CI: 0.340-1.084, p=0.005) had negative effect. The total number of correct answers was also higher in patients with adherence to treatment (p=0.002). CONCLUSION: Patient knowledge about hypertension and medications is associated with higher adherence rates. However, it should be taken into consideration that the possible effects of knowledge may differ according to its content.

Maprotiline induced weight gain in depressive disorder: changes in circulating ghrelin and adiponectin levels and insulin sensitivity.

Agents such as clozapine, olanzapine and mirtazapine frequently trigger an increase in body weight. Though the mechanisms have not been thoroughly clarified, recent studies indicate a role for ghrelin in regulation of appetite and weight gain. We investigated the relation of maprotiline induced weight gain to serum ghrelin and adiponectin levels, as well as insulin resistance in lean subjects with depressive disorder. A total of 40 male lean subjects with depressive disorder were treated with maprotiline (150 mg/day) for 30-days. Clinical data, fasting plasma glucose, lipids, insulin levels, serum ghrelin and adiponectin concentrations were determined before and after treatment. Insulin resistance was estimated using the homeostasis model assessment (HOMA) formula. After 30 days of treatment with maprotiline, mean body mass index increased significantly. Blood ghrelin and insulin levels and HOMA indexes increased, and adiponectin concentration decreased (p<0.001, for all) after the treatment period. Changes in ghrelin levels correlated neither of the parameters tested; whereas decrease in plasma adiponectin was associated with an increase in BMI (r=-0.671, p<0.001). In conclusion, the results indicate that treatment of lean patients with depressive disorder with maprotiline results in an increase in serum ghrelin and reduction in adiponectin levels. Weight gain due to maprotiline treatment may be related to its negative effects on the metabolic variables.

Thorax deformity, joint hypermobility, and anxiety disorders.

OBJECTIVE: To evaluate the association between thorax deformities, panic disorder, and joint hypermobility METHODS: The study includes 52 males diagnosed with thorax deformity, and 40 healthy male controls without thorax deformity, in Tatvan Bitlis and Isparta, Turkey. The study was carried out from 2004 to 2006. The teleradiographic and thoracic lateral images of the subjects were evaluated to obtain the Beighton scores; subjects' psychiatric conditions were evaluated using the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-1), and the Hamilton Anxiety Scale (HAM-A) was applied in order to determine the anxiety levels. Both the subjects and controls were compared in sociodemographic, anxiety levels, and joint mobility levels. In addition, males with joint hypermobility and thorax deformity were compared to the group with thorax deformity without joint hypermobility. RESULTS: A significant difference in HAM-A scores was found between the groups with thorax deformity and without. In addition, 21 subjects with thorax deformity met the joint hypermobility criteria in the group with thorax deformity, and 7 subjects without thorax deformity met the joint hypermobility criteria in the group without thorax deformity, according to Beighton scoring. The Beighton scores of the subjects with thorax deformity were significantly different from those of the group without deformity. Additionally, anxiety scores of the males with thorax deformity and joint hypermobility were found higher than males with thorax deformity without joint hypermobility. CONCLUSION: Anxiety disorders, particularly panic disorder, have a significantly higher distribution in male subjects with thorax deformity compared to the healthy control group. In addition, the anxiety level of males with thorax deformity and joint hypermobility is higher than males with thorax deformity without joint hypermobility.

Effect of testosterone on insulin sensitivity in men with idiopathic hypogonadotropic hypogonadism.

OBJECTIVE: To assess the presence of insulin resistance (IR) among a homogeneous cohort of male patients with idiopathic hypogonadotropic hypogonadism (IHH) and to investigate the effects of testosterone therapy on IR in this specific group. METHODS: Twenty-four male patients with untreated IHH and 20 age-, sex-, and weight-matched eugonadal healthy control subjects were recruited for the study. Plasma glucose, plasma insulin, total and free testosterone, follicle-stimulating hormone, luteinizing hormone, estradiol, and sex hormone-binding globulin levels were measured in fasting blood samples, and biochemical and hormonal analyses were performed for all study participants. IR was calculated by the homeostasis model assessment of insulin resistance (HOMA-IR) formula and the quantitative insulin sensitivity check index (QUICKI). Body mass index was calculated by weighing and measuring the heights of all study participants at the beginning of the investigation. Body fat mass and body lean mass were calculated as percentages of body weight by bioelectrical impedance analysis of body composition. Sustanon 250 (a combination of 4 testosterones) was administered intramuscularly once every 3 weeks for 6 months to male patients with IHH after a basal anthropometric, biochemical, and hormonal evaluation. The response to therapy was monitored by regular clinical examinations and serum testosterone measurements. After 6 months of testosterone treatment, the entire anthropometric, biochemical, and hormonal evaluation was repeated 14 days after the last injection of testosterone. RESULTS: Before treatment, male patients with IHH had higher fasting plasma glucose concentrations, higher fasting plasma insulin levels, a higher HOMA-IR score, and a lower QUICKI when compared with the control group. After testosterone treatment in the patient group, the HOMA-IR score decreased dramatically to the level in the control group. The high body fat mass of the male patients with IHH was reduced significantly after testosterone treatment, concomitant with significant increases in body mass index and body lean mass. CONCLUSION: Insulin sensitivity improves and body fat mass decreases with long-term testosterone replacement therapy.

Left ventricular function in male patients with secondary hypogonadism.

BACKGROUND: In addition to the effects on ventricular repolarization, testosterone could also affect left ventricular performance. The enhancement of left ventricular contractility in testosterone-deficient rats following testosterone replacement implies to the possible testosterone effect. OBJECTIVES: The aim of the current study is to reveal the alterations of left ventricular functions, if any, in secondary hypogonadal male patients. METHODS: Thirty-four males with secondary hypogonadism comprised the study group. The control group consisted of 30 healthy subjects. Echocardiographic measurements including left ventricular dimensions, ejection fraction, mitral inflow, and left ventricular outflow parameters were obtained from all subjects. Tissue Doppler parameters were also measured from left ventricular lateral wall and interventricular septum. RESULTS: Left ventricular diameters, wall thicknesses, and performance parameters were similar in both groups. Mitral inflow parameters showed a statistically insignificant difference. Pulse-wave tissue Doppler interpretation of hypogonadal and healthy subjects were similar in terms of lateral and septal basal segment Sm, Em, and Am wave velocities. CONCLUSIONS: Regarding the findings of previous studies that showed impaired myocardial contractility and lusitropy in testosterone deficient rats and our study results, further studies are needed for better understanding of testosterone's effects on human myocardium.

Psychotic disorder induced by oxybutynin: Presentation of two cases.

Anticholinergic agents are muscarinic receptor antagonists that suppress the activity of the acetylcholine system in the brain. Some of these agents also increase the concentration of dopamine in the synaptic cleft, which may result in psychotic symptoms. Oxybutynin is an antimuscarinic drug that may have adverse effects on the CNS, including memory impairment, confusion, delirium and hallucinations in elderly patients. To date, several case reports have been published about the association between oxybutynin and psychotic symptoms in elderly subjects, but we were unable to find any case reports describing oxybutynin-induced psychotic disorders in young people. Here we report on two patients, a 7-year-old boy and a 21-year-old man, who developed a brief psychotic disorder that may have been caused by oxybutynin. The first patient was kept under observation with vital functions supported but no medication. All his psychotic symptoms regressed and his general condition improved. The second patient was treated with olanzapine 10 mg/day. His psychotic symptoms resolved within 3 weeks. Our two case reports provide evidence that oxybutynin may induce psychotic disorders, and in younger 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.

The association of plasma adiponectin levels with hypertensive retinopathy.

OBJECTIVE: Previous studies have demonstrated that low plasma adiponectin concentrations are associated with essential hypertension. It has also recently been shown that adiponectin plays an essential role in the modulation of angiogenesis. These data led us to hypothesize that adiponectin might contribute to end-organ damage in hypertension. METHODS: In the present study we have evaluated the relationship between plasma adiponectin concentrations and hypertensive retinopathy. One hundred and ten patients newly diagnosed with essential hypertension (EHT) (mean age, 46.79+/-5.0 years; body mass index (BMI), 26.47+/-2.23 kg/m(2); male/female ratio, 58/52) and 57 healthy normotensive control subjects (NT) (mean age, 46.84+/-5.4 years; BMI, 26.66+/-2.65 kg/m(2); male/female ratio, 33/24) were enrolled. RESULTS: Plasma adiponectin levels were significantly lower in EHT than in NT (P < 0.001). In addition, adiponectin concentrations were strongly correlated with systolic and diastolic blood pressures in EHT (r = -0.757, P < 0.001; r = -0.761, P < 0.001) while there was no correlation in the NT group. Plasma adiponectin in patients with grade 0 hypertensive retinopathy (n = 52) was significantly higher than that of the patients with grade 1 (n = 30) and 2 (n = 28) hypertensive retinopathy (P < 0.001 for each). Plasma adiponectin in patients with grade 0 hypertensive retinopathy was also significantly lower than that in the NT group (P < 0.001). The estimated threshold of plasma adiponectin concentration for hypertensive retinopathy was 17 microg/ml. This critical adiponectin level served largely to separate patients with retinopathy from those without. CONCLUSION: Our results have shown that plasma adiponectin concentrations decrease progressively with higher grades of hypertensive retinopathy even after correction for other atherogenic risk factors, suggesting that a critical adiponectin level is needed for the development of retinopathy.

Being well-informed about statin is associated with continuous adherence and reaching targets.

BACKGROUND: Statins are life saving drugs in cardiovascular practice. However, they still are underprescribed in many situations despite their well-established benefits. Adherence may be improved by increased comprehension of the patients. METHODS: Patients enrolled into a previous survey were randomized into two groups as those, who were informed comprehensively (Group 1) and those not (Group 2). 202 patients, all of whom were on secondary prevention, were contacted after median 15 months of follow up and evaluated whether they continued the statins, and reached targets. RESULTS: 102 out of 202 patients were those enrolled into Group 1, and 100 of them were those enrolled into Group 2. In Group 1, 62.7% of patients were on continuous statin therapy during period between initial and secondary contact, whereas, only 46% of patients in Group 2 were on continuous statin therapy (p = 0.017). Being well-informed about statin increased the likelihood of being on continuous statin therapy after median of 15 months by 1.977 folds. Concerning targets, 64.7% of those in Group 1 reached the targets, whereas, 43% of those in Group 2 reached the targets (p = 0.002). Being well-informed about statin increased the likelihood of having suggested targets by ATP III after median of 15 months by 2.430 folds. CONCLUSION: Providing patients with comprehensive knowledge about statins, even in patients, who were already on statin therapy, seems not only to improve adherence but also increase the percentage of those reaching targets.

Adiponectin may play a part in the pathogenesis of diabetic retinopathy.

OBJECTIVES: To measure plasma adiponectin concentrations in patients with type 2 diabetes and to investigate any association with the severity of diabetic retinopathy, because adiponectin seems to be an important modulator for metabolic and vascular diseases. METHODS: Seventy-four patients (mean age 46.8+/-5.1 years; body mass index (BMI), 26.8+/-2.10 kg/m(2)) and 54 healthy volunteers (mean age 46.8+/-5.4 years; BMI 26.47+/-2.33 kg/m(2)) were included. RESULTS: Adiponectin concentrations in the patients were significantly lower than those in controls (4.71+/-2.11 microg/ml for patients, n=74; 15.95+/-3.72 microg/ml for controls, n=54; P<0.001). In the patients group there was a significant negative correlation between adiponectin and homeostasis model assessment index (r=-0.318, P=0.006 respectively). Plasma adiponectin concentrations in patients with proliferative diabetic retinopathy (n=20; 3.16+/-1.83 microg/ml) or non-proliferative diabetic retinopathy (n=24; 3.97+/-1.47 microg/ml, P=0.014) were significantly lower than those in patients without diabetic retinopathy (n=30; 6.30+/-1.57 microg/ml, P=0.001). When the presence of diabetes was defined as the final variable in the conditional logistic regression model with the adiponectin concentration as the continuous variable, adiponectin was significantly involved in the model. CONCLUSION: The results show that adiponectin concentrations are lower in patients with type 2 diabetes and that the concentrations are associated with the severity of diabetic retinopathy. Our findings suggest that adiponectin may take part in the pathogenesis of diabetic retinopathy.