Several clinical and experimental studies have demonstrated gender dimorphism in immune and organ responsiveness and in the susceptibility to and morbidity from shock, trauma, and sepsis. In this respect, cell-mediated immune responses have been shown to be depressed in males following trauma-hemorrhage, whereas they were aintained/enhanced in proestrus females. Furthermore, sex hormones have been shown to be responsible for this gender-specific immune response following adverse circulatory conditions. More specifically, studies indicate that androgens produce immunodepression following trauma-hemorrhage in males. In contrast, female sex steroids appear to exhibit immunoprotective properties following trauma and severe blood loss. With regard to the underlying mechanisms, receptors for sex hormones have been identified on various immune cells suggesting direct effects of these hormones on the immune cells. Alternatively, indirect effects of sex hormones, ie, modulation of cardiovascular responses or androgen-and estrogen-synthesizing enzymes, might contribute to gender-specific immune responses. Recent studies indicate that sex hormones, eg, dehydroepiandrosterone (DHEA), also modulate the function of peripheral blood mononuclear cells in surgical patients. Thus, the immunomodulatory properties of sex hormones/receptor antagonists/sex steroid synthesizing enzymes following trauma-hemorrhage suggests novel therapeutic strategies for the treatment of immunodepression in surgical patients.

DHEA stimulates proinflammatory cytokine release capacities of human PBMCs following major abdominal surgery. The estrogen receptor appears to be involved in mediating the immunomodulatory effect of DHEA. Thus, DHEA might be a useful adjunct for preventing immunosuppression in surgical patients.

In an unusual course of Wegener's granulomatosis (WG), a 71-year-old woman presented a 3-week history of unilateral painful parotid swelling unresponsive to antiphlogistic and antibiotic treatment. Following lateral parotidectomy with unspecific inflammatory histopathological findings, the patient developed disturbance of wound healing and high recurrent fever. Control chest X-ray showed several pulmonary round lesions. Immunologic testing for antinuclear cytoplasmatic antibodies (ANCA) was positive and CT navigated puncture revealed pronounced necrotic vasculitis of small arteries and veins. Consequently, systemic WG was diagnosed and specific immunosuppressive therapy was started. Long-term follow-up of 6 months showed a decline in the ANCA course, full remission of the presented symptoms and prevention of renal manifestations. Isolated inflammatory parotid enlargement can be the initial symptom of systemic WG and should be considered as differential diagnosis, especially when nondiagnostic histopathological results are obtained. Early testing for c-ANCA supplies valuable information and therefore should be prompted when additional symptoms occur. Once diagnosed as WG, appropriate therapy is able to prevent progression to severe clinical courses.

Fabry disease is an X-linked inherited disorder of glycosphingolipid metabolism due to the deficient activity of a lysosomal enzyme, α-galactosidase A. The resultant systemic accumulation of sphingolipids can lead to progressive and sudden hearing loss alongside renal, cardiac and cerebrovascular complications. Although replacement therapy seems to be beneficial for cochlear function, few data are available regarding treatment of sudden hearing loss. This case report describes the course of a unilateral sudden hearing loss in a young (15-year-old) male patient and its improvement following hyperbaric oxygen treatment.