No abstract

In patients with locally advanced or metastatic thyroid cancer, the tyrosine kinase inhibitor vandetanib has several endocrine effects. Thyroid hormone, calcium, and vitamin D analog requirements increased, but consequences of the biological alterations on phosphocalcic metabolism and gonadotrope and adrenal functions are unknown.

Variants in LMNA, encoding A-type lamins, are responsible for laminopathies including muscular dystrophies, lipodystrophies, and progeroid syndromes. Cardiovascular laminopathic involvement is classically described as cardiomyopathy in striated muscle laminopathies, and arterial wall dysfunction and/or valvulopathy in lipodystrophic and/or progeroid laminopathies. We report unexpected cardiovascular phenotypes in patients with LMNA-associated lipodystrophies, illustrating the complex multitissular pathophysiology of the disease and the need for specific cardiovascular investigations in affected patients. A 33-year-old woman was diagnosed with generalized lipodystrophy and atypical progeroid syndrome due to the newly identified heterozygous LMNA p.(Asp136Val) variant. Her complex cardiovascular phenotype was associated with atherosclerosis, aortic valvular disease and left ventricular hypertrophy with rhythm and conduction defects.A 29-year-old woman presented with a partial lipodystrophy syndrome and a severe coronary atherosclerosis which required a triple coronary artery bypass grafting. She carried the novel heterozygous p.(Arg60Pro) LMNA variant inherited from her mother, affected with partial lipodystrophy and dilated cardiomyopathy. Different lipodystrophy-associated LMNA pathogenic variants could target cardiac vasculature and/or muscle, leading to complex overlapping phenotypes. Unifying pathophysiological hypotheses should be explored in several cell models including adipocytes, cardiomyocytes and vascular cells. Patients with LMNA-associated lipodystrophy should be systematically investigated with 24-h ECG monitoring, echocardiography and non-invasive coronary function testing.

No abstract

Many drugs can induce hyperandrogenic symptoms, such as hirsutism, acne, seborrheic dermatitis, malepattern baldness, menstrual irregularities, clitoral hypertrophy, or deepening of voice. Anabolic-androgenic steroids, synthetic progestins, and antiepileptics are the most frequently implicated drugs in hyperandrogenism. The mechanisms of androgen excess are various: (1) intrinsic androgenic activity of the drug, (2) interaction with sex hormone-binding globulin, or (3) functional alterations of the hypothalamic-pituitary-ovary axis. Nevertheless, the physiology of these drugs remains generally unclear. Such is the case for valproate, which seems to induce a form of polycystic ovary syndrome (PCOS) by increasing ovarian androgen synthesis. It should be remembered that it is always necessary to rule out other causes of androgen excess, especially an ovarian or adrenal tumor or PCOS, before attributing the symptom(s) to a drug.