Objective: To assess serum levels of carbohydrate antigen 125 (CA125) in patients with chronic congestive heart failure (CHF) and to assess any correlation with clinical symptoms and echocardiographic indices. Patients and methods: We enrolled 77 male patients (mean age: 73F10 years) admitted to the Cardiology Emergency Department (ED) with cardiac symptoms requiring hospitalization. Diagnosis of CHF was based upon medical history or initial echocardiographic evaluation on current admission. Serum CA125 was measured by an enzyme immunoradiometric assay, on admission and before discharge. Results: The median overall CA125 value was 22.4 (11.5-48.9) U/ml. Serum CA125 levels were related to the severity of CHF [New York Heart Association (NYHA) class I: 19.2 (7.2-31) U/ml, NYHA class II: 17.6 (10-23) U/ml, NYHA class III: 32 (25-77) U/ml and NYHA class IV: 34.3 (18.6-77) U/ml ( pb0.04)]. Patients in NYHA classes III and IV had significantly higher mean values of CA125, than patients in class II ( pb0.005 and pb0.05, respectively). Moreover, patients with fluid congestion (pulmonary congestion, ankle edema) had higher levels of serum CA125 than patients without congestion ( p=0.002 and pb0.03, respectively). Finally, levels of serum CA125 correlated weakly with right ventricular systolic pressure (RVSP) and renal function, while no significant correlation was found between CA125 and E wave deceleration time on Doppler echocardiography, left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), liver function and the medical treatment prescribed. Conclusion: Serum CA125 is associated with the clinical severity of CHF and the symptoms and signs of fluid congestion and therefore may be a useful additional tool for the evaluation and clinical staging of these patients.

Acne is a disorder of the pilosebaceous unit, common among adolescents, which may be extended to adulthood. The aim of this study was to assess the prevalence of hormonal disorders in women with acne resistance to conventional therapy. We included 72 women aged between 15 and 36 years (divided in two age groups) who presented to our clinic between May and October 2014, suffering from moderate and severe forms of papulopustular and nodulocystic acne. The subjects were non-responsive to classic dermatological treatment or had clinical manifestation of hyperandrogenism. Based on age, we divided the women into two groups, group I with 40 patients aged 15–22years and group II with 32 patients aged 23–36 years. Using ELISA, a hormonal profile was performed for each patient in days 1–3 of the menstrual cycle including, total testosterone, dehydroepiandrosterone sulfate (DHEA-S), follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol, prolactin, and plasma cortisol. For statistical analysis we used Stata 13 software. We compared the hormonal profile of the two groups and identified significant differences for: testosterone levels (mean value, 0.64±0.35 vs. 0.97±0.50 ng/ml; p<0.0001), DHEA-S levels (mean value, 0.85±0.27 vs. 1.05±0.33 mg/24 h; p=0.001), prolactin levels (mean value, 281.85±91.113 vs. 353.969±102.841 mIU/ml; p=0.002) and LH levels (14.8±6.7 vs. 20.1±8.2 mIU/ml; p=0.002) were higher in group II. No statistically significant differences were found for estradiol (p=0.588) and cortisol (p=0.182) levels. In conclusion, refractory acne can be the first sign of systemic illness including polycystic ovary syndrome. Thus, for a correct therapeutic approach it is necessary to interpret the clinical and biochemical elements in correlation with the medical history.

Neurohormonal activation with increased plasma renin activity and norepinephrine and vasopressin levels is characteristic of congestive heart failure and contributes to further decompensation and poor prognosis. We treated 20 such patients with the centrally acting sympathoinhibitory drug clonidine 0.15 mg BID and obtained hemodynamic measurements by cardiac catheterization and plasma neurohormone levels before and 2 to 3 hours after the first dose; in 7 patients, these measurements were taken again after 1 week of therapy. The initial dose produced significant decreases of 8% in mean arterial pressure, 23% in right atrial pressure, 21% in pulmonary capillary wedge pressure, 19% in mean pulmonary artery pressure, and 12% in heart rate, a 17% increase in stroke volume; and no significant changes in cardiac output and systemic vascular resistance. All changes remained virtually constant after 1 week. Plasma norepinephrine decreased by 28% after the initial dose and 62% after 1 week (P < 0.1), whereas plasma renin activity remained essentially unchanged. Plasma vasopressin tended to increase, its levels being inversely correlated with those of posttreatment norepinephrine (r = -.48 P < .03). Patients with baseline norepinephrine levels > 0.400 ng/mL has significantly poorer baseline hemodynamic parameters and tended to show more improvement with clonidine, although their data remained significantly worse than patients whose baseline norepinephrine was within the normal range. Sympathetic suppression with clonidine in congestive heart failure reduces preload, heart rate, and arterial pressure, all indexes of myocardial energy demand; the lack of significant reduction in systemic vascular resistance and increase in cardiac output might be attributable in part to enhanced release of vasopressin.2+ f2p4

Research shows that paternal psychological distress is associated with child emotional and behavioural difficulties. However, little is known about the direction of this association including whether it is bidirectional. The aim of this study was to explore the reciprocal relationships between paternal psychological distress and child emotional and behavioural problems longitudinally (at ages 3, 5, 7, 11 and 14 years) in a sample of 13,105 children (49% girls) who participated in the UK’s Millennium Cohort Study (MCS), a large-scale, nationally representative, longitudinal survey. Four domains of child problems (emotional symptoms, peer relations, conduct problems and hyperactivity/inattention) were measured with the Strengths and Difficulties Questionnaire and paternal psychological distress was measured with the Kessler K-6 scale. Data were analysed using cross-lagged path models. At all ages, paternal psychological distress predicted both subsequent child emotional symptoms as well as peer problems. Paternal psychological distress at child’s age 3 was related to more hyperactivity at age 5 and, at age 5, paternal psychological distress was associated with more conduct problems at age 7. At age 11, paternal distress was also related to age 14 conduct problems and hyperactivity. Child effects were fewer and were found mainly for behavioural problems. Notably, we found bidirectional links between paternal psychological distress and child peer difficulties, from 11 to 14 years. Paternal psychological distress appears to influence child behaviour more consistently than the converse. However, in early adolescence, there appears to be a reciprocal relationship between fathers’ mental health problems and children’s peer problems.

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