Male hypogonadism is defined as low circulating testosterone level associated with signs and symptoms of testosterone deficiency. Although the bidirectional link between hypogonadism and cardiovascular disease has been clarified, the association between testosterone and chronic heart failure (HF) is more controversial. Herein, we critically review published studies relating to testosterone, hypogonadism, and HF and provide practical clinical information on proper diagnosis and treatment of male hypogonadism in patients with HF. In general, published studies are extremely heterogeneous, frequently have not adhered to hypogonadism guidelines, and suffer from many intrinsic methodological inaccuracies; therefore, data provide only low-quality evidence. Nevertheless, by selecting the few methodologically robust studies, we show the prevalence of testosterone deficiency (30%–50%) and symptomatic hypogonadism (15%) in men with HF is significant. Low testosterone correlates with HF severity, New York Heart Association class, exercise functional capacity, and a worse clinical prognosis and mortality. Interventional studies on testosterone treatment in men with HF are inconclusive but do suggest beneficial effects on exercise capacity, New York Heart Association class, metabolic health, and cardiac prognosis. We suggest that clinicians should measure testosterone levels in men with HF who have symptoms of a testosterone deficiency and conditions that predispose to hypogonadism, such as obesity and diabetes. These patients—if diagnosed as hypogonadal—may benefit from the short- and long-term effects of testosterone replacement therapy, which include improvements in both cardiac prognosis and systemic outcomes. Further collaborative studies involving both cardiologists and endocrinologists are warranted.

Introduction Thousands of genes are implicated in spermatogenesis, testicular development and endocrine regulation of testicular function. The genetic contribution to male infertility is therefore considerable, and basic and clinical research in last years found a number of genes that could potentially be used in clinical practice. Research has also been pushed by new technologies for genetic analysis. However, genetic analyses currently recommended in standard clinical practice are still relatively few. Areas covered We review the genetic causes of male infertility, distinguishing those already approved for routine clinical application from those that are still not supported by adequate clinical studies or those responsible for very rare cause of male infertility. Genetic causes of male infertility vary from chromosomal abnormalities to copy number variations (CNVs), to single-gene mutations. Expert opinion Clinically, the most important aspect is related to the correct identification of subjects to be tested and the right application of genetic tests based on clear clinical data. A correct application of available genetic tests in the different forms of male infertility allows receiving a better and defined diagnosis, has important role in clinical decision (treatment, prognosis), and allows appropriate genetic counselling especially in cases that should undergo assisted reproduction techniques.

Intriduction: The thyroid is an organ with one of the highest selenium concentrations, containing many selenoproteins implicated in thyroid hormone metabolism. Treatment with levothyroxine has been recommended for all subclinical hypothyroid patients with TSH levels > 10 mU/L, whereas for those with TSH< 10 mU/L treatment remains controversial. Aim: A randomised controlled prospective study was performed to investigate the effects of Se treatment on patients with autoimmune thyroiditis and mild sub-clinical hypothyroidism (TSH < 10 mU/L). Material and methods: A total of 196 patients with autoimmune thyroiditis were recruited in the study. Patients were assigned to receive (case) or not receive (control) an oral selenomethionine treatment. Cases received 83 mcg selenomethionine/day orally for four months. All the patient’s charts were submitted to thyroid hormonal profile (TSH, fT4) and TPOAb evaluation upon enrolment and at the end of the study. Results: In total 192 patients completed the study. Cases and controls were superimposable for age, gender, thyroid hormonal profile, and TPOAb levels. At the end of the study, 33/192 (17.2%) participants restored euthyroidism (Responders). Responders were significantly more frequent among Cases than Controls (30/96 [31.3%] vs. 3/96 [3.1%], p < 0.0001). Conclusion: Selenium supplementation could restore euthyroidism in one third of subclinical hypothyroidism patients with autoimmune thyroiditis. (Endokrynol Pol 2016; 67 (6): 567–571) Intriduction: The thyroid is an organ with one of the highest selenium concentrations, containing many selenoproteins implicated in thyroid hormone metabolism. Treatment with levothyroxine has been recommended for all subclinical hypothyroid patients with TSH levels > 10 mU/L, whereas for those with TSH< 10 mU/L treatment remains controversial. Aim: A randomised controlled prospective study was performed to investigate the effects of Se treatment on patients with autoimmune thyroiditis and mild sub-clinical hypothyroidism (TSH < 10 mU/L). Material and methods: A total of 196 patients with autoimmune thyroiditis were recruited in the study. Patients were assigned to receive (case) or not receive (control) an oral selenomethionine treatment. Cases received 83 mcg selenomethionine/day orally for four months. All the patient’s charts were submitted to thyroid hormonal profile (TSH, fT4) and TPOAb evaluation upon enrolment and at the end of the study. Results: In total 192 patients completed the study. Cases and controls were superimposable for age, gender, thyroid hormonal profile, and TPOAb levels. At the end of the study, 33/192 (17.2%) participants restored euthyroidism (Responders). Responders were significantly more frequent among Cases than Controls (30/96 [31.3%] vs. 3/96 [3.1%], p < 0.0001). Conclusion: Selenium supplementation could restore euthyroidism in one third of subclinical hypothyroidism patients with autoimmune thyroiditis. (Endokrynol Pol 2016; 67 (6): 567–571)

Background: A significant number of patients show sub-optimal adherence to levothyroxine (LT4) therapy, mainly because they have to postpone their breakfast by at least 30 min. The aim of this observational cross-sectional study was to assess the therapeutic compliance of patients on LT4 treatment and to verify the preference of a lifetime treatment in tablet or liquid form. Patients and Methods: Ambulatory care patients aged 18 years or older, affected by hypothyroidism and on LT4 treatment (in tablet or liquid form) were administered the eight-item Morisky Medication Adherence Scale (MMAS-8). The MMAS-8 questionnaire was supplemented with 3 further items to specifically evaluate preference between tablet and liquid forms of LT4 for lifetime treatment. Results: A total of 320 patients (272 female), median age 47.9 ± 15.6 years (range, 20–78 years), completed the MMAS-8 questionnaire. Eighty-seven percent of the participants were adhering to their treatment for both tablet and liquid LT4 formulations, although significant differences emerged. Patients on LT4 tablets forgot to take their medication more frequently (p < 0.001), felt hassled about sticking to their treatment plan (p < 0.001), and had difficulty remembering to take all their medication(s) (p < 0.001) than those on liquid LT4 treatment. Conclusions: Adherence to LT4 treatment was high for both tablet and liquid formulations. Taking LT4 at breakfast was the most convenient option for most patients.