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Tumor necrosis factor (TNF)-α is a pro-inflammatory cytokine associated with psoriasis pathogenesis. Anti-TNF-α therapies are effective in psoriasis. A significant weight gain has been reported in patients treated with anti-TNF-α agents. The aim of the present study was to evaluate the body composition changes in psoriatic patients receiving anti-TNF-α therapies according with disease phenotype. Forty patients affected with psoriasis were followed up for 24 weeks and divided into two groups: psoriasis vulgaris (PsO) and psoriatic arthritis (PsA). Anthropometric, blood biochemical, body composition parameters, resting metabolic rate, and disease activity indexes were measured at baseline and at week 24. After 24 weeks of anti-TNF-α administration, the disease activity indexes and concentration of inflammatory markers were significantly decreased. Seventy-five percent of PsO and 60% of PsA patients had an increase in body weight. Weight changes correlated with fat mass gain in the PsO group, and with fat and lean mass gain in the PsA group. In the present study, we demonstrated that a blockage of TNF-α bioactivity is related with fat and lean mass gain in both PsO and PsA subjects. The anti-TNF-α therapies could play a key role in the cross talk between adipose tissue and skeletal muscle, mediated by the reduction of TNF-α and interleukin-6 production.

The objective was to evaluate HLA DR/DQ alleles and their risk factor for type 1 diabetes in the Abruzzo region (central Italy). Sixty incident cases from the Abruzzo region were studied together with 120 unrelated control subjects living in the same administrative areas. The relative risk of diabetes associated with the alleles under study was calculated by deriving the odds ratio (OR) maximum likelihood estimates and their 95% confidence intervals (CI) by the exponentiation of the logistic regression beta-parameter. The combination DRB1*03/DQA1*0501/DQB1*0201 was found in 20.0% of patients and 7.1% of the control subjects, conferring an OR of 4.04 and a CI of 1.97-8.49. The combination DRB1*04/DQA1*0301/DQB1*0302 was found in 23.3% of diabetic patients and 6.7% of controls, giving an OR of 5.69 and a CI of 2.77-12.05. DRB1*11/DQA1*0505/DQB1*0301 and DQA1*0505/DQB1*0301 were negatively associated with type 1 diabetes (OR=0.27, CI 0.11-0.57; OR=0.07, CI 0.02-0.19). The DQA1 genotype at risk was found to be DQA1*0301/DQA1*0501: OR=23.80, CI 2.97-190.89, as it occurred with the highest frequency in the patient group. The DQB1 genotype at risk was found to be DQB1*0201/DQB1*0302, which occurred in 13.3% of patients but in only 1.1% of the control group (OR=29.75, CI 5.36-549.25). Our results shed further light on the risk of development of this disease during a specific time period in an area where the overall incidence of type 1 diabetes is known.

Angiotensin converting enzyme inhibitors (ACE-I) are known to affect the endothelial function decreasing the formation of the potent vasoconstrictor angiotensin II and increasing the bioavailability of the vasodilators bradykinin and nitric oxide. In order to test the potential differences among the class of ACE-I, we have evaluated their effects on endothelin-1 and nitric oxide availability, and on reactive oxygen species generation in human vascular endothelial cells (HUVECs) obtained from umbilical cord veins. HUVECs were cultured in the presence of either sulfhydryl-containing ACE-I (zofenoprilat or captopril) or nonsulfhydryl-containing ACE-I (enalaprilat or lisinopril). After 24 hours, all ACE-I reduced endothelin-1 secretion and increased nitric oxide production. However, zofenoprilat ( − 42% after 8 hours of incubation) was more effective ( 𝑃 < . 0 5 ) than enalaprilat ( − 25%), lisinopril ( − 21%), and captopril ( − 30%) in reducing endothelin-1 secretion. Similarly, zofenoprilat (+110% after 8 hours of incubation) was more effective ( 𝑃 < . 0 5 ) than enalaprilat (+64%), lisinopril (+63%), and captopril (+65%) in increasing nitrite plus nitrate production. The effect of ACE-I on the nitric oxide availability and on endothelin-1 secretion is mediated by the activation of bradykinin B 2 receptor being reverted, at least in part, by a specific antagonist. Zofenoprilat and, to a lesser extent, captopril also blunted tumour necrosis factor (TNF) 𝛼 -stimulated production of reactive oxygen species and decreased TNF 𝛼 -stimulated glutathione consumption in endothelial cells. In conclusion, structural differences among the class of ACE-I play a role in their interaction with mediators that influence the homeostasis of the endothelium. The marked antioxidant effects exerted by zofenoprilat due to its sulphydryl group and lipophilia seem to be responsible for its greater endothelium protective activity.

Left ventricular hypertrophy (LVH) detected by ECG has been shown to be associated with a higher prevalence of ventricular arrhythmias in members of the general population, in a case-control series of hypertensive patients and in never-treated hypertensive patients. In-keeping with this, it has been observed that hypertension-induced LVH increases the risk of sudden cardiac death. Furthermore, a consistent bulk of data suggests antihypertensive therapy targeted at regression or prevention of electrocardiographic LVH may reduce the incidence of arrhythmias. In this regard, recent clinical trials showed that antihypertensive therapy may delay or prevent the occurrence of cardiac arrhythmias and sudden cardiac death in patients with hypertension. Porthan et al. hypothesized that an antihypertensive therapy might also rapidly affect ventricular repolarization and sought to investigate the short-term electrophysiological effects of four common antihypertensive drugs, represented by an angiotensin II receptor blocker (losartan), a beta-blocker (bisoprolol), a calcium channel blocker (amlodipine) and a thiazide diuretic (hydrochlorothiazide) in hypertensive men. Porthan et al. showed that losartan and bisoprolol favorably affected ventricular repolarization, with beneficial effects on ECG parameters of ventricular repolarization duration and heterogeneity. On the contrary, hydrochlorothiazide significantly increased repolarization heterogeneity, while amlodipine administration did not affect ECG repolarization measures. Thus, the observed findings suggest an intriguing hypothesis on the possible role of antihypertensive therapy in favouring or preventing cardiac arrhythmias.

The main objectives of type 1 diabetes mellitus (DM) management include keeping glycemia levels within the euglycemic range to prevent complications. Daily self-monitoring is an important problem for many diabetic patients, particularly for adolescents. The aim of this study was to evaluate the determinants of poor daily self-monitoring, focusing on the patients' parents' perception of the problem. In order to evaluate parents' awareness of their children's disease-monitoring status, we carried out a cross-sectional investigation of a sample of children and adolescents from a population-based register, with the corresponding population of parents. To collect our data, we used a 33-item questionnaire, separately administered by diabetologists to both parents and children. We estimated the concordance with respect to patients' and parents' answers. Adolescents followed their overall medical prescriptions more regularly (48.8%) than children (29.7%), but most frequently they forgot to use glycemic tests (adolescents 42.4%, children 29.7%). A major duration of disease affected HbA1c levels (values > 8%) of patients younger than 14 years (pFisher = 0.016). Our results indicate a worse compliance of adolescents with respect to children in attending to daily self-monitoring, not just regarding daily glycemic levels but also the course of daily activities such as going to school, studying, working, and simulating symptoms and signs of hypo-hyperglycemia. Parents mostly ignored their child's self-monitoring status and the related motivations.