Congenital adrenal hyperplasia (CAH) owing to 21-hydroxylase deficiency is a common disorder, and is characterised by a defect in cortisol biosynthesis with or without a defect in aldosterone synthesis and androgen excess. The classic form, also known as the severe form, occurs in 1:15,000 births worldwide, while the nonclassic or mild form occurs in approximately 1:1,000 births worldwide and is much more common (up to 1:20) in certain ethnic groups. In classic 21-hydroxylase deficiency, glucocorticoids are given in doses sufficient to suppress adrenal androgen secretion, and mineralocorticoids are given to normalise electrolytes and plasma renin activity. The management of CAH may be complicated by iatrogenic Cushing's syndrome, inadequately treated hyperandrogenism, or both. Prenatal treatment may decrease virilisation of the affected female foetus, but the efficacy and safety of treating CAH prenatally remains to be fully defined. Close clinical monitoring of growth and development is essential to optimise treatment outcome. New treatment approaches are currently under investigation in the most severely affected patients, while nonclassic CAH does not always require treatment.

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A 22-year-old man with hypogonadotropic hypogonadism was receiving monthly intramuscular injections of testosterone replacement therapy. The patient refused to self-administer the injections because of discomfort, so the therapy was switched to testosterone patches. He experienced a pruritic, macular, erythematous rash underneath the reservoir area of two different transdermal formulations, which did not improve after pretreatment with topical corticosteroids. Eventually, he tolerated application of a testosterone gel and his serum testosterone levels returned to normal after 1 month of therapy. Commercially available and investigational testosterone products and therapeutic monitoring guidelines for androgen replacement are reviewed.

Background: Takayasu arteritis (TA) is a large vessel vasculitis that affects the aorta and its primary branches. The coronary arteries are uncommonly involved. Case Presentation: A 52-year-old man, with a history of TA not on immune suppressants due to recurrent active miliary tuberculosis, was scheduled for open abdominal repair of a multilobulated saccular thoracoabdominal aneurysm. Cardiology was consulted for pre-operative evaluation. His physical exam and EKG were unremarkable. Imaging of his coronaries with CT angiography showed proximal and distal right coronary artery dilation (14 mm) and a intraluminal thrombus. Revascularization surgically or percutaneously was not advised. Additional vascular interventions were postponed until the patient received adequate treatment for his tuberculosis and uncontrolled TA. The patient was started on ASA and warfarin for the intraluminal thrombus and coronary aneurysm. Discussion: Coronary artery aneurysms are rare in TA. When coronaries are involved, ostial stenosis or occlusion is the most common lesion. Invasive coronary angiography is difficult due to diffuse vascular disease and involvement of the aorta. The imaging modality of choice remains a debate. CT angiograms remain a reasonable option for the assessment of coronary involvement. There is no established guideline for the treatment of coronary thrombus in patients with TA. Because coronary aneurysms promote thrombus formation by stasis and abnormal flow conditions, it is reasonable to treat with ASA combined with warfarin as they do in Kawasaki disease. Conclusion: Although rare in TA, coronary aneurysm formation is possible. A coronary angiogram is technically difficult in this group of patients, and CT angiograms remains a safe option to define coronary anatomy. The treatment guidelines are lacking, and ASA combined with warfarin is a reasonable option to reduce myocardial infarction and death.