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PubMed1975

Cortisol metabolism in chronic liver disease.

Impairment of cortisol metabolism, evidence of endogenous hypercortism and sensitivity to oral corticosteroids are known to occur in patients with chronic liver disease. Measurements were made of plasma 11-OHCS and urinary cortisol levels and other parameters of adrenal function in a group of such patients. The mean plasma total 11-OHCS was lower in patients than in control subjects, although this difference was not statistically significant and the normal circadian rhythm was maintained. However, in patients with chronic liver disease a greater proportion of the 11-OHCS was in the non-protein bound state resulting in an elevation of this fraction. This elevation of non-protein bound 11-OHCS must represent a resetting of the pituitary-adrenal feedback mechanism in these patients. Corticosteroid binding globulin was lower in patients than in control subjects, although the difference was not statistically significant. Urinary cortisol excretion was significantly reduced as was excretion of 17-ketosteroids. Cortisol secretion rate was found to be normal. It is suggested that elevation of plasma non-protein bound 11-OHCS, resulting from impaired metabolism and reduced protein binding of cortisol in patients with hepatic disease, may explain the features of endogenous hypercorticism seen in such patients. Moreover, in the presence of impaired steroid metabolism and reduced protein binding, these patients may exhibit an increased sensitivity to corticosteroid therapy, and therefore administration of a reduced dosage may be advisable.

11-Hydroxycorticosteroids↗
PubMed1975

Cushing's syndrome with fluctuation due to adrenal adenoma.

A case of fluctuating Cushing's syndrome due to an adrenal adenoma is described. Plasma corticosteroids were frequently low and urinary steroids fluctuated markedly over a 15-month period. Only the response to dexamethasone was consistently abnormal and indicative of Cushings's syndrome.

11-Hydroxycorticosteroids↗
PubMed1985

Adrenal rest tumor of the liver causing Cushing's syndrome: treatment with ketoconazole preceding an apparent surgical cure.

Ketoconazole, an imidazole derivative known to inhibit cytochrome P450-dependent adrenal enzymes was given to a patient with a functioning adrenal rest tumor of the liver in preparation for surgery. The drug was administered in a stepwise manner for 42 days starting with 400 mg and reaching 1 g the last 4 weeks of the trial. Clear clinical improvement was evident early in the trial and was associated with evidence of amelioration of her hypercortisolism and striking changes in serum and urinary levels of steroid hormones and metabolites. Sex steroids in serum and urine fell dramatically from the first day to the end of the trial. Urinary 17-ketosteroid excretion fell from a basal average of 139 mg/24 h to near normal levels within a week of therapy; serum testosterone fell from a basal level of 2.4 to 0.18 ng/ml; serum 17 beta-estradiol fell likewise from 1096 to 150 pg/ml. In contrast, cortisol levels in serum and urine increased in the first 2 weeks of the trial and subsequently fell to values below the basal levels. Similarly, serum 17 alpha-OH-progesterone levels increased 63% above the basal levels by day 6 of the trial and declined afterwards. Nine months after successful tumor resection the patient is apparently cured as judged by steroid hormone levels and physical appearance. We conclude that ketoconazole was effective in blocking tumoral steroidogenesis which resulted in clinical benefit.

11-Hydroxycorticosteroids↗