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It would appear that all patients, especially young men, are at risk for the development of this syndrome and that the pathogenesis remains uncertain in many cases.

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Measuring testosterone levels became easier in the 1970s, and it wasn't long before levels were being checked in men across all age groups. At that time, several authors reported an age-associated decline of serum testosterone levels beginning in the fourth or fifth decades of life. Other studies found that the decline in testosterone with age might be more related to comorbidities that develop in many aging men. Aggressive marketing campaigns by pharmaceutical companies have led to increased awareness of this topic, and primary care physicians are seeing more patients who are concerned about "low T." Unfortunately, testosterone replacement therapy has not been straightforward. Many men with low testosterone levels have no symptoms, and many men with symptoms who receive treatment and reach goal testosterone levels have no improvement in their symptoms. The actual prevalence of hypogonadism has been estimated to be 39% in men aged 45 years or older presenting to primary care offices in the United States. As the US population ages, this number is likely to increase. This article, targeted to primary care physicians, reviews the concept of late-onset hypogonadism, describes how to determine the patients who might benefit from therapy, and offers recommendations regarding the workup and initiation of treatment.A 56-year-old overweight man with symptoms of low energy, daytime sleepiness, and decreased libido happens to be watching a golf tournament on TV from his favorite recliner and suddenly a commercial appears. Th is patient is in your offi ce the following Monday and asks you, "Is it low T?"Aggressive marketing campaigns by pharmaceutical companies have led to increased awareness of hypogonadism among men, who may then present to the clinic requesting testing or treatment (1). As a result, primary care physicians are seeing more patients like the one described above. Th e physiological age-related decrease in testosterone production should be differentiated from late-onset hypogonadism (LOH), defi ned as the presence of three sexual symptoms and low testosterone (low T) in aging men (2). Th is defi nition was proposed to help clinicians identify aging men with low testosterone who could potentially benefi t from hormonal replacement therapy. Th e purpose of this article is to review the data on LOH, also known as low T, and present the most recent evidence and recommendations regarding the approach to the patient from our case scenario. PHYSIOLOGY AND DEFINITIONSMale reproductive endocrine physiology involves the hypothalamic-pituitary-target organ and feedback model. Disruptions at diff erent levels of this pathway can lead to disturbed androgenic eff ects: primary disorders of the testes (primary hypogonadism), disorders of the pituitary or hypothalamus (secondary hypogonadism), and disorders of androgen action on target tissue or androgen resistance. Other less common entities that manifest as androgen defi ciency include chronic stress (by suppressing gonadotropin-releasing hormone secretion) and exogenous...

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We are reporting a case of familial thoracic aortic aneurysm and dissection in a 26-year-old man with no significant past medical history and a family history of dissecting aortic aneurysm in his mother at the age of 40. The patient presented with cough, shortness of breath, and chest pain. Chest X-ray showed bilateral pulmonary infiltrates. CT scan of the chest showed a dissection of the ascending aorta. The patient underwent aortic dissection repair and three months later he returned to our hospital with new complaints of back pain. CT angiography showed a new aortic dissection extending from the left carotid artery through the bifurcation and into the iliac arteries. The patient underwent replacement of the aortic root, ascending aorta, total aortic arch, and aortic valve. The patient recovered well postoperatively. Genetic studies of the patient and his children revealed no mutations in ACTA2, TGFBR1, TGFBR2, TGFB2, MYH11, MYLK, SMAD3, or FBN1. This case report focuses on a patient with familial TAAD and discusses the associated genetic loci and available screening methods. It is important to recognize potential cases of familial TAAD and understand the available screening methods since early diagnosis allows appropriate management of risk factors and treatment when necessary.

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