Endocrine, Metabolic & Immune Disorders-Drug Targets (Formerly Current Drug Targets - Immune, Endocrine & Metabolic Disorders) - Volume 17, Issue 1, 2017

Context: Herpetic whitlow is caused by herpes virus (type1 or 2) during primary infection or as result of autoinoculation. Commonly, it is caused by HSV-2 in adults with positive history for genital infection. Case Description: We report the case of a 44-year-old woman that came to our attention with a 3- year history of recurrent cutaneous eruption on the ring finger of her left hand associated to lymphangitis of the homolateral arm. Laboratory exams including PCR on blood and cutaneous swab allowed to diagnosis it as a rare case of herpetic whitlow. Conclusion: The case here reported demonstrates that herpetic whitlow should be kept in mind by physicians in recurrent cases of fingers infection. Advanced diagnostic techniques as PCR are required to help clinicians to achieve a definite diagnosis and to choose the right treatment.

Background: Controversy persists regarding the effect of mixtures of conjugated linoleic acids (c9, t11- and t10, c12-CLA) in fasting blood glucose (FBG) and waist circumference (WC) in humans. Objective: The aim of this meta-analysis is to explore the effect of CLA on FBG and WC. Method: PubMed, Google Scholar, Cochrane Library, Science Direct, Pro-Quest and Ovid were searched up to January 2015. Studies that examined the effect of CLA supplementation or foods enriched with CLA on FBG and WC in healthy adults were included. Studies in animals or unhealthy individuals and studies other than clinical trials were excluded. Of the 3,095 articles initially retrieved, 32 eligible randomized clinical trials were included in this systematic review. The mean difference and standard deviation of changes in FBG and WC in the intervention and control groups were used as effect size measures for the meta-analysis. Results: Subgroup analysis showed that CLA supplement consumption did not significantly influence FBG (standardized mean differences [SMD] = 0.075 mg/dL; 95% confidence interval (CI) = −0.099 to 0.249; p = 0.399) or WC (SMD = -0.149 cm; 95% CI = −0.522 to 0.225; p = 0.435). Foods enriched in CLA also showed no significant effect on FBG (SMD = 0.126 mg/dL; 95% CI = −0.100 to 0.352; p = 0.274) or WC (SMD = -0.233 cm; 95% CI = −0.625 to 0.159; p = 0.244). Conclusion: We conclude that c9, t11- and t10, c12-CLA administered as a supplement or used to enrich foods does not affect FBG or WC in humans.

Type 2 diabetic patients are known to have a tendency to develop cardiovascular (CV) disease (CVD), and related unfavourable outcomes such as heart failure, myocardial infarction (MI), cerebrovascular events (e.g. stroke), and related mortality. Long- term clinical trials have revealed contradictory findings regarding the relationship between glycemic control and CV benefits due to variations in the key characteristics of the study population. During the last decade, number of pharmacological agents used for glucose- lowering in the treatment of type 2 diabetes mellitus (T2DM) has increased owing to the introduction of dipeptidyl peptidase- IV (DPP- IV) inhibitors, glucagon- like peptide- 1 (GLP- 1) receptor agonists, and sodium-glucose co-transporter 2 (SGLT- 2) inhibitors. This review aims to focus on the mechanisms of action of these drugs in the cardiovascular system and the trials evaluating their impact on CVD. Furthermore, trials in the last decade evaluating the impact of traditional glucose- lowering drugs on CVD are included. For this purpose, we searched PubMed for articles in English using the search terms “type 2 diabetes mellitus, glucose- lowering drugs, antidiabetic medications, cardiovascular, cardiovascular disease, cardiovascular system” between inception to September 2016. We also searched separately for each medication in addition to the keyword “cardiovascular disease” on PubMed. To identify further articles, we hand searched related citations in review articles and commentaries.

Food protein-induced proctocolitis (FPIP) is the most common colonic manifestation of food allergy in infants, accounting for up to 60% of exclusively breast-fed children. The causative foods derived from the mother's diet, which are then excreted in her milk. The suggested risk factors for the development of FPIP are an immature immune system, altered intestinal permeability and other factors that activate local immune function, such as genetic susceptibility in combination with particularly sensitizing foods. FPIP is an enhanced immune responsiveness of some infants to very small amounts of food antigens, inducing an inflammatory mucosal response, mediated by T cells.

Schizophrenia is one of the most severe psychiatric diseases with a significant impact on the psychosocial functioning of the patients. People with schizophrenia are at risk to die prematurely because of their illness with their poor lifestyle contributing to the excess morbidity and higher mortality rate. In particular, lifestyle (e.g. poor diet, low rates of physical activity and increased likelihood to smoke cigarettes) predisposes them to poor physical health and comorbid medical diseases. In addition, the treatment of schizophrenia usually involves the long-term administration of antipsychotic drugs and some of these medications are implicated in the increased risk of metabolic and cardiovascular effects. The antipsychotic-induced hyperprolactinemia was ascertained for the first time by Kleinberg in 1971 and was considered for this treatment. Antipsychotics are the most common pharmacological agents which cause hyperprolactinemia The aim of this review is to describe PRL physiology, PRL biological effects and pathway to the diagnosis, causes, consequences of HPRL focusing on the antipsychotic effects on the PRL. We conducted a review of studies published between 1974 and December 2014. The search was performed using the following PubMed search terms: “Hyperprolactinemia” and “antipsychotic” and 827 papers were detected. The articles were examined and the overlapping or insufficiently clear works were excluded. Finally we chose 104 titles. We added to the selected articles additional articles, including 28 articles regarding the latest international guidelines, the pathophysiology of hyperprolactinemia and the various therapeutic choices.

Metabolic syndrome is a clustering of various metabolic parameters, which include diabetes, low high-density lipoprotein cholesterol, elevated triglycerides, abdominal obesity, and hypertension. It has merged as a worldwide epidemic and a major public health care concern. However, due to the different criteria used for the assessment, the frequency of metabolic syndrome in the general population is variable but it is more common in the older people. Metabolic syndrome is closely linked to cardiovascular risk and increases cardiovascular outcomes and all-cause mortality. Recent evidences showed that alterations of the thyroid function could have an impact on the components of the metabolic syndrome, suggesting that thyroid hormones have a variety of effects on energy homeostasis, lipid and glucose metabolism, and blood pressure. In this review, we summarize available data on the action of thyroid hormone on the components of metabolic syndrome.

Background: Low dehydroepiandrosterone sulfate (DHEAS) levels and a high cortisol/ DHEAS ratio are associated with higher mortality in elderly, dialyzed, and immunocompromised patients. The role of these hormones in patients with hypoglycemia unawareness (hypo) or in pancreas or islet recipients treated by glucocorticoid-free immunosuppressive regimen (IS) has not been studied. Objective: The aim of this study was to determine the effects of IS and of recurrent hypoglycemia on DHEAS and adrenocorticotropic hormone (ACTH) levels in patients with type-1 diabetes (T1DM). Methods: A case control, cross-sectional analysis of patients in a prospective database enrolled 84 patients with T1DM. They were divided into 4 groups of 21 subjects each: 1) islet or pancreas recipients with hypoglycemia who are IS (hypo +, IS +); 2) pancreas and kidney transplant recipients without insulin or hypoglycemia (hypo – , IS +); 3) T1DM patients with hypoglycemia (hypo +, IS -); and 4) T1DM patients without hypoglycemia (hypo – , IS –). Results: DHEAS and ACTH levels were significantly decreased in patients with hypoglycemia (P = 0.0002 and P = 0.0001, respectively) as well as in those with IS (P = 0.0497 and P < 0.001, respectively) compared to those without hypoglycemia or IS. The influence of hypoglycemia unawareness on DHEAS levels was stronger than that of immunosuppression (P < 0.10). Conclusion: Low DHEAS and ACTH levels represent an additional component of hypoglycemia unawareness syndrome and they remain low in patients receiving glucocorticoid-free immunosuppression. DHEAS may serve as a marker, the importance of which remains unclear, but deserves attention.

Background: We recently identified a regulatory rheumatoid factor (regRF), the production of which is associated with autoimmune disease resistance and remission. In studies of regRF in the blood of healthy rats, spontaneous increases in the regRF level were noted. We suggest that in the normal state, a mechanism exists for maintaining the activity of the pool of regRF-producing lymphocytes at a level that makes it possible to control the expansion of autoreactive lymphocytes. Objective: The purpose of this study was to test the hypothesis that the endogenous stimulator of regRF production is Fc fragments of IgG that are formed upon exposure to the proteases of neutrophils. Results: Injection of Salmonella typhi LPS caused neutrophilic leukocytosis in the rats, followed by elevated level of regRF. Neutrophils were obtained from LPS-treated rats and then treated with LPS in vitro to degranulate them to form pre-split IgG that exposes antigenic determinants for regRF. A condition required for Fc fragments to be formed by neutrophils is that the pre-split IgG must be treated with a thiol reducing agent. Antigenic determinants for regRF were retained by Fc fragments of IgG. Conclusion: Thus, the pre-split IgG and Fc fragments of IgG formed by LPS-activated neutrophils are the potential physiological activators of regRF production.

Background: Although osteoarthritis (OA) has predominantly been considered a noninflammatory degenerative arthropathy, there is growing evidence that various inflammatory and immunological processes might contribute to the onset, progression, and burden of the disease. Objective: The purpose of the present investigation was to study the systemic inflammatory and stress responses and the innate response mediated by neutrophils in OA patients. Method: A group of patients diagnosed with primary OA according to the American College of Rheumatology criteria and a control group of age-matched healthy volunteers were enrolled in the study. Serum inflammatory cytokine levels (IL-1β, TNF-α, IL-8, IL-6, IL-10, and TGF-β) were evaluated using the Bio-Plex Luminex system. Circulating neuroendocrine-stress biomarkers, such as cortisol and extracellular 72 kDa heat shock protein (eHsp72), were measured by ELISA. The phagocytic and microbicide capacities of circulating neutrophils were evaluated by flow cytometry. All parameters were determined in all volunteers. Results: The OA patients showed an inflammatory state accompanied by an altered stress response. This was manifested in high circulating levels of the inflammatory cytokines IL-1β, TNF-α, IL-8, IL-6, and TGF-β and the stress protein eHsp72. There were also decreased systemic levels of cortisol, and a reduction in neutrophil phagocytic and microbicidal capacities. Conclusion: An immune-neuroendocrine dysregulation affecting both systemic inflammatory and stress mediators and the function of innate immune cells underlies OA. This reflects an altered feedback between the innate/inflammatory and stress responses in this pathology.