Acute adrenal failure is a potentially fatal condition if overlooked. Occasionally, acute adrenal insufficiency may ensue from bilateral adrenal haemorrhage in patients with known antiphospholipid syndrome (APS). APS is characterized by recurrent arterial and venous thrombosis, pregnancy complications and detection of autoantibodies to phospholipids. This syndrome may be associated with non-organ specific diseases (e.g. connective tissue disorders) or with malignancies, but it may also appear in isolated form (primary APS). In a very few cases the heralding manifestation is given by adrenal failure. We report here a 63-year-old man presenting with acute adrenal insufficiency as the opening clinical manifestation of an APS. We also carried out a computer-aided search of the literature to identify all cases of primary adrenal failure as the first-recognized expression of a primary APS, a condition that not so infrequently may be tackled by endocrinologists. 20 patients fulfilled the inclusion criteria. The great majority of them were males (75%) with a mean age of 42 years. Abdominal pain was present in 14 patients, followed by fever (13 patients) and hypotension (12 patients). The main morphological findings by computed tomography or magnetic resonance were consistent with bilateral adrenal haemorrhage in 11 patients. Lupus anticoagulant was present in all of the 19 tested patients. Our observations emphasize the importance in the assessment of clotting times, and possibly of antiphospholipid antibodies, in all patients with diagnosis of rapidly progressive adrenal failure and concurrent abdominal pain.
Fabio Presotto, Francesca Fornasini, Corrado Betterle, Giovanni Federspil and Marco Rossato
Claudio Pagano, Giorgio Soardo, Walter Esposito, Francesco Fallo, Lorenza Basan, Debora Donnini, Giovanni Federspil, Leonardo A Sechi and Roberto Vettor
Objectives: Nonalcoholic fatty liver disease (NAFLD) is a major cause of liver-related morbidity and is frequently associated with obesity and metabolic syndrome. The recently discovered hormone adiponectin is produced by adipose tissue, and low plasma adiponectin is considered a key factor in the development of the insulin resistance underlying metabolic syndrome. Animal studies suggest that adiponectin may protect against non-alcoholic steatohepatitis, but direct evidence in humans is lacking. We therefore conducted this study to assess the relationship between plasma adiponectin and nonalcoholic fatty liver disease to explore its role in the pathogenesis of this disease.
Design and methods: We measured plasma adiponectin and anthropometric, biochemical, hormonal and metabolic correlates in a group of 17 NAFLD patients with diagnosis confirmed by biopsy, and 20 controls with comparable age, body-mass index and sex. Furthermore we compared plasma adiponectin in patients with simple steatosis and steatohepatitis.
Results: Plasma adiponectin was significantly lower in NAFLD patients than controls (5.93±0.45 vs 15.67±1.60 ng/ml). Moreover, NAFLD patients were significantly more insulin resistant while having similar serum leptin. Adiponectin was similar in simple steatosis and in steatohepatitis (6.16±0.78 vs 5.69±0.49 ng/ml). An inverse correlation was observed between adiponectin and homeostatic model assessment (HOMA) of insulin resistance (P = 0.008), while adiponectin did not correlate with serum transaminases and lipid values.
Conclusions: These data support a role for low circulating adiponectin in the pathogenesis of NAFLD and confirm the strict association between reduced adiponectin production by adipose tissue, NAFLD and insulin resistance.