Increased blood cortisol in alcoholic patients with aseptic necrosis of the femoral head

Abstract

Although aseptic necrosis of the femoral head secondary to alcoholism is a very frequent entity, its etiology remains unknown. The same pathogenic mechanism is thought to be shared both by aseptic necrosis secondary to alcoholism and steroid therapy. Since alcohol stimulates adrenal steroid secretion, we have studied serum cortisol and urinary free-cortisol levels in 8 patients with aseptic necrosis of the femoral head due to alcoholism and compared them with those found in 8 age-matched patients with aseptic necrosis of idiopathic origin. Serum cortisol levels and urinary free-cortisol levels were significantly higher in the alcoholic than in the idiopathic group: serum 227 +/- 21.7 vs 154 +/- 22.1 ng/ml, P less than 0.001; urine 0.20 +/- 0.002 vs 0.13 +/- 0.04 micrograms/mg Cr/day, P less than 0.001. The data indicate that alcohol-induced aseptic necrosis of the femoral head results, at least in part, from increased circulating cortisol.

A mouse model for glucocorticoid‐induced osteonecrosis: Effect of a steroid holiday

“…These findings in our murine model are consistent with clinical reports that cortisol levels were lower in renal transplant recipients developing osteonecrosis after glucocorticoid use than in those who did not develop osteonecrosis 36. Thus, discontinuous dexamethasone may be less osteonecrotic than continuous dexamethasone (8% in the discontinuous vs 45% in the continuous dexamethasone group) by allowing partial recovery from adrenal suppression during the few days each week off dexamethasone.…”

Bilateral Preiser’s disease in a patient with hypercoagulability

“…[14] Patients with a diagnosis of avascular necrosis demonstrated significantly elevated serum and urinary free cortisol levels, which is thought to contribute to the inherent pathology. [15] Hyperlipidemia was also associated with osteonecrosis, as patients with AVN demonstrated significantly elevated levels of serum cholesterol compared to age-matched controls. [16] Coagulation abnormalities have been implicated in the pathogenesis of avascular necrosis and have come to the forefront of discussion.…”

Association between alcohol-induced osteonecrosis of femoral head and risk variants ofMMPSin Han population based on a case-control study

“…Rico et al reported that alcohol-induced ONFH induced by alcohol stimulate the excessive secretion of adrenal glucocorticoids, and found that alcohol and hormones may stimulate ONFH through a common pathway [ 29 , 30 ]. Alcohol caused lipid metabolism the abnormal increase of fatty substance in blood circulation which gathered into a ball of fat, lead to reduced blood flow speed, clogging capillaries and causing the femoral head microvascular thrombosis, eventually leading to ONFH [ 31 , 32 ].…”