T he objective of this study was to investigate whether patients with the metabolic syndrome (MetS) and an imbalance in cortisol metabolism express increased urinary albumin excretion compared to those patients with metabolic syndrome alone.Seventy-four patients with MetS were evaluated using a low-dose dexamethasone suppression test (LDDST) to identify disturbed cortisol balance (cortisol levels > 50 nmol/L after LDDST). The level of albumin in the urine was also evaluated.Disturbed cortisol balance was found in 8% of all evaluated patients with MetS. Microalbuminuria was present significantly more often (p<0.01) in those patients with MetS and an imbalance in cortisol metabolism compared with patients suffering MetS alone (urine albumin: 210 mg/L vs. 26 mg/L, respectively, p<0.01).A substantial percentage of patients with MetS had inappropriate cortisol homeostasis. Of importance, excretion of urinary albumin was increased in these patients. This observation may indicate that this subgroup within the MetS population has a higher cardiovascular risk and possible increased endothelial dysfunction, with a subsequent need for stricter control to prevent cardiovascular morbidity and mortality.

Abnormal thyroid function tests in this euthyroid patient were found to be false due to significant interference of supraphysiological levels of plasma biotin. Laboratory tests applying immunoassays using a biotin-containing reagent should be interpreted with caution in patients on biotin substitution.

A female hemodialysis patient with galactorrhea due to hyperprolactinemia was treated with different dialysis modalities to assess the effect on prolactin levels. A single session of both high-flux hemodialysis and hemodiafiltration resulted in decreased prolactin levels (16,6% and 77,2%, resp.). However, baseline prolactin levels measured immediately before the next dialysis session did not change markedly. After cabergoline treatment was started, prolactin levels normalized and galactorrhea disappeared. Thus, dopaminergic inhibition of prolactin secretion might be reduced in patients with end-stage renal disease. This dopaminergic resistance could be an important mechanism of hyperprolactinemia in hemodialysis patients and its subsequent treatment strategies.