An Update on Addison's Disease.

Addison's disease - the traditional term for primary adrenal insufficiency (PAI) - is defined as the clinical manifestation of chronic glucocorticoid- and/or mineralocorticoid deficiency due to failure of the adrenal cortex which may result in an adrenal crisis with potentially life-threatening consequences. Even though efficient and safe pharmaceutical preparations for the substitution of endogenous gluco- and mineralocorticoids are established in therapy, the mortality in patients with PAI is still increased and the health-related quality of life (HRQoL) is often reduced.PAI is a rare disease but recent data report an increasing prevalence. In addition to the common "classical" causes of PAI like autoimmune, infectious, neoplastic and genetic disorders, other iatrogenic conditions - mostly pharmacological side effects (e. g., adrenal haemorrhage associated with anticoagulants, drugs affecting glucocorticoid synthesis, action or metabolism and some of the novel anti-cancer checkpoint inhibitors) are contributing factors to this phenomenon.Due to the rarity of the disease and often non-specific symptoms at least in the early stages, PAI is frequently not considered resulting in a delayed diagnosis. Successful therapy is mainly based on adequate patient education as a cornerstone in the prevention and management of adrenal crisis. A focus of current research is in the development of pharmacokinetically optimized glucocorticoid preparations as well as regenerative therapies.

Pilot study of serum inhibin B as a potential marker of testosterone doping in weight lifting men.

OBJECTIVE: The aim of this study was to explore effectors of the pituitary-testicular axis suitable as potential biochemical markers to screen for testosterone doping. DESIGN: Pilot study with male bodybuilding athletes with a self-reported history of testosterone doping (repeated intramuscular administration of testosterone preparations, last injection 8 weeks or less ago) compared with an equal sized control group matched for sex, age, and body mass index. SETTING: Endocrine outpatients. PARTICIPANTS: Fifteen healthy young men of white background. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Inhibin B, testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH). RESULTS: Although the levels of testosterone, LH, and FSH did not differ between the 2 groups, the serum concentrations of inhibin B in individuals with a history of testosterone doping were exclusively at or below the lower limit of the normal range for adult men (100-400 pg/mL). Inhibin B was significantly lower in those men who used testosterone for weight lifting (76.1 +/- 36.3 ng/L [mean +/- SD]) than in controls (182.1 +/- 35.4 ng/L). CONCLUSION: A low concentration of serum inhibin B may reflect the application of exogenous testosterone and appears to be a potential marker associated with anabolic androgenic steroid doping.

[Hypophosphatemic osteomalacia]. / Hypophosphatämische Osteomalazie.

Hypophosphatemic osteomalacia first presenting in adulthood is a rare disease. It is characterized by decreased serum phosphate, renal phosphate wasting, elevated alkaline phosphatase, and osteomalacia. The authors present a case with typical constellation of an oncogenic (tumor-induced) osteomalacia, the possible differential diagnosis, diagnostic evaluation, and complete healing after tumor resection. The new concepts of hereditary and acquired hypophosphatemic osteomalacia are discussed helping us understand this rare disease.