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  • ISSN: 2333-6692
    Special Issue on Low T or True Male Hypogonadism
    Ranjodh Gill
    Associate Professor
    Department of Internal Medicine
    Virginia Commonwealth University
    Research Article
    Eric Chung1,3*, Osama S Al-Bermani1, Ross P Fowler1 and Michael P Gillman2,3
    Abstract: Testosterone deficiency syndrome (TDS) is a clinical and biochemical syndrome frequently associated with age and co-morbidities and is characterized by deficiency in testosterone and relevant androgen-deficiency symptoms. The main physiological action of testosterone in male sexual function is in sexual desire by regulating the timing of the penile erectile with sex. However sexual dysfunction associated with TDS also includes erectile dysfunction (ED) and delayed ejaculation. The link between ED, testosterone deficiency and cardiovascular disorders is well documented. The recommended tests for men with ED include fasting glucose, cholesterol, lipids and testosterone level. Both ED and TDS are treatable conditions. A range of testosterone preparations are available for supplementation, and the combination of testosterone replacement therapy and phosphodiesterase type 5 inhibitors might improve outcomes in some cases. The selection of the testosterone replacement therapy should be a joint decision between an informed patient and his primary care physician, and regular follow-up should be conducted to assess treatment efficacy and surveillance for adverse events.
    Bruno Lopes Cançado1*, Luiz Carlos Miranda1, Maria Lucia Fleiuss2 and Miguel Madeira2
    Abstract: Bone loss in patients with prostate cancer undergoing anti-androgen therapy is underestimated by physicians. Osteoporosis is a silent condition that can lead to major fracture events. The osteoporosis’s fractures has as consequence a decrease in a patient’s general health and quality of life, an increase in morbidity and mortality, and an increase in the cost to the health care system. The application of preventive measures to avoid osteoporosis results in a simpler and more cost-effective solution, with few drawbacks to the patient, compared with the cost of treatment for osteoporosis-related fractures.
    Srinath Reshmi1, Nauder Faraday2 and Adrian Dobs1*
    Abstract: Epidemiologic studies suggest that cardiovascular disease affects men at an earlier age and may contribute to greater mortality. Cross sectional and prospective studies have considered the role of endogenous testosterone levels in cardiovascular disease and mortality but few prospective or randomized trials have looked at supplemental testosterone therapy and long term cardiovascular outcomes. Recent retrospective studies suggest that testosterone therapy increases the risk of cardiovascular disease and associated mortality, however it is still unclear by what mechanism. In this review we begin with a case report and attempt to summarize the mechanisms by which testosterone may promote arterial thrombosis and hemostasis. Overall testosterone plays a complex role in the thrombotic pathway, and may have different effects when given acutely or long term, especially in those with other modifiable and non-modifiable risk factors for cardiovascular disease.
    Review Article
    Kristin Lichti-Kaiser, Gary ZeRuth and Anton M Jetten*
    Abstract: Congenital hypothyroidism (CH) is the most frequent endocrine disorder in neonates. While several genetic mutations have been identified that result in developmental defects of the thyroid gland or thyroid hormone synthesis, genetic factors have yet to be identified in many CH patients along with the mechanisms underlying their pathophysiology. Mutations in the gene encoding the Krüppel-like transcription factor, GLI-similar 3 (GLIS3) have been associated with the development of a syndrome characterized by congenital hypothyroidism and neonatal diabetes and similar phenotypes were observed in mouse knockout models of Glis3. Patients with GLIS3-mediated CH exhibit diminished serum levels of thyroxine (T4) and triiodothyronine (T3) and elevated thyroid stimulating hormone (TSH) and thyroglobulin (TG). However, the inconsistent presentation of clinical features associated with this CH has made it difficult to ascertain a causative mechanism. Future elucidation of the biological functions of GLIS3 in the thyroid will be crucial to the discovery of new therapeutic opportunities for the treatment of CH.
    Antonio Mancini1*, Sebastiano Raimondo1, Chantal Di Segni1, Giovanni Gadotti1, Elena Giacchi2, Marcella Zollino3, Giovanni Neri3, Marco Bonomi4, Luca Persani4,5 and Alfredo Pontecorvi1
    Abstract: Hypogonadism is frequently associated with metabolic syndrome and testosterone levels correlate with parameters which are part of the cluster defining the syndrome itself. Different studies suggest a positive role of testosterone replacement therapy, but different aspects (including the definition of hypogonadism, especially in aging male, and the modality of treatment) still require confirmation. A model to explore the role of testosterone in influencing the beginning and course of the syndrome is early hypogonadism, due to genetic causes (both primary or secondary hypogonadism); moreover, few data are reported in transsexuals, despite the debate on biological bases of gender indentity, and the influence of pharmacological treatment before and after surgical sex reversal. We present here a review of literature and some paradigmatic cases, that seem to reinforce the concept of hypogonadism as a causative factor of metabolic syndrome.
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