Effect of tadalafil on erectile dysfunction in male patients with diabetes mellitus.

BACKGROUND/AIM: [corrected] During the first 10 years over 50% of diabetes patients develop erectile dysfunction (ED). It is more severe and resistant to therapy than in male patients with normal glucoregulation. The purpose of this pilot study was to estimate the tadalafil (Cialis) efficacy and safety in male patients with diabetes mellitus (DM), together with moderate to severe ED. METHODS: The study included 30 male patients with diagnozed type 1 or type 2 DM together with ED. ED was estimated through the International Index of Erectile Function (IIEF-6), Sexual Encounter Profile (SEP) questionnaire and prostaglandin test, at the beginning of the research and three months after the 20 mg tadalafil therapy initiation, once a week (on Fridays). Glycosylated haemoglobin in blood (HbAlc) values were also monitored. According to the ED severity (IIEF values at the beginning of the therapy) the patients were divided into 2 groups. The previous experience with sildenafil citrate (Viagra) and prostaglandin E1 intracavernous therapy was recorded. RESULTS: Tadalafil significantly improved ED (p < 0.001) for 7.40 points of the IIEF score, i.e. for 58% and 60% towards SEP2 and SEP3 questionnaire, respectively. Compared to the previous ED therapy subjectively better tadalafil experience was recorded. Each group experienced a significant improvement in IIEF score (p < 0.001), more significantly in the group 2 (8.26+/-1.49 points) compared with the medium improvement in the group 1 (6.27+/-1.35 points). After three months HbA1c values decreased for 2.26+/-1.62 (p < 0.001). CONCLUSION: Tadalafil is an effective tool for treating ED in diabetes patients. In some situations tadalafil application could replace prostaglandin test. The sexual sphere motivation leads to the improvement of glucoregulation in DM patients.

[Sarcoidosis localized in endocrine glands].

INTRODUCTION: There is a relationship between sarcoidosis and endocrine diseases: hypothalamus, hypophysis, thyroid gland, parathyroid gland, adrenal gland and calcium metabolism disorder. DISCUSSION: Neurological disorders, obesity, secondary hypogonadism, and thirst as a result of diabetes insipidus, dominate the clinical picture of hypothalanmic sarcoidosis. Diseases of adenohypophysis present with gonadotropic insufficiency and prolactin increase. They may cause disorders in menstruation and ovulation. Disorders of neurohypophysis manifest with moderate polyuria and polydipsia. Disorders of thyroid gland function in systemic sarcoidosis present with hyperthyroidism, hypothyroidism or thyroiditis. Sarcoidosis of the parathyroid gland is rare. Sarcoidosis of adrenal cortex may cause primary insufficiency of the suprarenal gland The secondary insufficiency of the suprarenal gland is caused by hypothalamic and pituitary sarcoidosis. In sarcoidosis, calcium metabolism disorder and hypercalcemia are frequent. Vitamin 1.25(OH)2D has an important role since it is increasingly produced in renal and extra renal regions. Hypercalcemia leads to hypercalciuria and nephrolithiasis, while the level of parathyroid hormone usually decreases. Increased levels of serum angiotensin converting enzyme (ACE) are also important markers in the diagnosis of sarcoidosis. CONCLUSION: Clinical manifestations of endocrine disorders depend on the localization of sarcoid lesions. The treatment of disorders is directed to the treatment of structure and functional disorders of glands involved, as well as to sarcoidosis. Successful treatment of sarcoidosis may cause regression of granulomatous lesions in the involved glands.

[Sarcoidosis and diabetes: therapeutic aspects].

FIRST CASE: A 45-year-old female patient with diabetes was on corticosteroid therapy for a year due to pulmonary sarcoidosis. During the last six years she was treated with oral antidiabetic drugs, but during the last couple of months, she required insulin therapy due to impaired glycoregulation. After corticosteroid therapy was discontinued, glycoregulation improved and insulin therapy was discontinued as well. SECOND CASE: a 32-year-old male patient was on prednisolone therapy due to pulmonary and extrapulmonary sarcoidosis. A few weeks later diabetes mellitus (de novo) was established. During the treatment of sarcoidosis with corticosteroids, short-term insulin therapy was due to impaired glycoregulation. Insulin therapy has improved the glycoregulation. DISCUSSION: There is no certain evidence about the incidence of diabetes mellitus under the influence of corticosteroids, due to increase of hepatic glucose production, insulin resistance and exhaustion of pancreatic beta-cells because of stimulated endogenous secretion. During treatment of sarcoidosis, corticosteroid therapy may cause deterioration of glycoregulation and occurrence of clinically manifested diabetes mellitus in patients with impaired glycose tolerance or predisposition to diabetes. CONCLUSION: Diabetic patients with sarcoidosis who need corticosteroid therapy, should control glycoregulation Patients with sorcoidosis, treated with corticosteroid therapy need regular control in order to diagnose early diabetes.