Risk factors for non-melanoma skin cancer development in renal transplant recipients: a 40 year retrospective study in Croatia.

AIM: To determine the prevalence of non-melanoma skin cancer (NMSC) and disease-specific risk factors in renal transplant recipients (RTRs). METHODS: This retrospective cohort study enrolled 1232 RTRs (736 men) treated in University Hospital Center Zagreb over 40 years. The effect of sex, age at transplantation, geographic residence, dialysis vintage, and the type of immunosuppressive therapy on NMSC occurrence was investigated. RESULTS: The prevalence of NMSC was 6.81%. Overall, 60.7% of patients developed basal cell carcinoma (BCC) and 30.9% of patients developed cutaneous squamous cell carcinoma (cSCC). Only 8.3% developed both tumors. The BCC:cSCC ratio was 1.76:1. The risk for NMSC was 50% higher in men. Patients older than 50 years at transplantation were at greater risk for NMSC development. Residence in an area with higher ultraviolaet radiation (UV) exposure and dialysis vintage before transplantation did not influence NMSC development. Cyclosporine and azathioprine treatment conferred a greater risk for NMSC than tacrolimus or mycophenolate mofetil treatment. CONCLUSION: RTRs are at high risk for NMSC development. Sex, age at transplantation, and type of immunosuppressive therapy play a role in tumor development.

Laugier-Hunziker syndrome in endocrine clinical practice.

Laugier-Hunziker syndrome (LHS) is a rare, benign and acquired disorder characterized by hyperpigmentation of the oral cavity and lips along with longitudinal melanonychia. No underlying systemic abnormalities or malignant predisposition is associated with it. In everyday clinical practice, an endocrinologist encounters certain endocrine conditions (e.g. Addison's disease, McCune-Albright syndrome) that present with, inter alia, mucocutaneous hyperpigmentation. Even though LHS is easily distinguished from endocrine entities mentioned earlier, diagnostic evaluation usually requires skilled and thorough practitioner. Since it is the diagnosis of exclusion, a number of systemic conditions must be ruled out prior to making the final diagnosis. However, its major differential diagnosis is primarily Peutz-Jeghers syndrome, which carries an increased risk of cancer. Here, we report a case of a young woman who was referred to the endocrinologist for diagnostic evaluation of dark-colored lesions of the oral cavity and nails. All performed laboratory tests were within reference range. Endoscopic gastrointestinal evaluation did not reveal neoplastic formations. Owing to an adult-onset, asymptomatic clinical course and negative diagnostic findings, we made a final diagnosis. In this case, target diagnostic evaluation notably reduced the need for additional expensive and invasive procedures and treatments. LEARNING POINTS: Laugier-Hunziker syndrome is a rare, acquired cause of asymptomatic, benign mucocutaneous hyperpigmentation.Prior to making a final diagnosis, certain medical entities with overlapping clinical features must be excluded.Endocrine conditions that usually present with the hyperpigmentation of the skin and mucous membranes (e.g. Addison's disease, McCune-Albright syndrome) can be easily ruled out based on clinical and laboratory findings.Its major differential diagnosis, Peutz-Jeghers syndrome is characterized by melanotic macules of the face and mouth, intestinal polyposis and significantly increased risk of different types of cancer, especially gastrointestinal.Anamnesis, physical examination and target diagnostic evaluation reduce the need for additional invasive and expensive procedures and treatment.

Preliminary report of hypoglycemic response in obese metabolic syndrome males treated with metformin after weight loss intervention.

We conducted this study to determine the degree of obesity influence on the hypoglycemic response of growth hormone and cortisol after weight loss of 5%. A total of 45 non-diabetic, male subjects followed in the outpatient endocrinological departments were divided into three groups comprising 15 subjects in each group, based upon body mass index (BMI) to healthy, overweight and obese group. Metformin was administered in the dose of 50 mg daily to the overweight and obese participants. Cortisol was measured at 0, 60 and 120 minutes. Growth hormone (GH) was measured at -15, 0, 30, 60, 90 and 120 minutes. Values of cortisol and GH were compared upon changes in hypothalamo-pituitary-adrenal (HPA) response to insulin induced hypoglycemia initially and after weight loss of 5% for overweight and obese participants. The BMI of the healthy group ranged 20.0-24.5 kg/m2 (median: 22.8); overweight group ranged 25.9-29.7 kg/m2 (median: 28.3); and obese group ranged 30.9-34.6 kg/m2 (median: 32.6). There were no significant differences of cortisol values among groups at 0 (chi2 = 2.0; p = 0.365); 60 (chi2 = 0.754; P = 0.686) and at 120 minutes (chi2 = 0.466; p = 0.792). The comparisons among groups were significant for differences of GH values at -15 (chi2 = 25.0; p < 0.01); 0 (chi2 = 16.2; p < 0.01); 30 (chi2 = 16.2; p < 0.01); 60 (chi2 = 32.8; p < 0.01); 90 (chi2 = 30.2; p < 0.01) and at 120 minutes (chi2 = 27.3; p < 0.01). Healthy and obese subjects significantly differed in growth hormone response at -15 (Z = 4.67; p < 0.01); 0 (Z = 3.83; p < 0.01); 60 (Z = 2.78; p = 0.05); 90 (Z = 4.67; p < 0.01) and at 120 minutes (Z = 4.23; p < 0.01). Changes on the various levels of HPA axis, when it is activated by a stress as it is the case in insulin-induced hypoglycemia correspond to the degree of obesity. Weight loss of 5% was not enough for restoration of a normal stimulated growth hormone release and did not influence on the level of cortisol.