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Biomedical subjects

Fatih Tanriverdi

Publications and source records attributed to Fatih Tanriverdi.

7 recordsLinked to original sources
PubMed2006

High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma.

CONTEXT: Recent data have demonstrated that traumatic brain injury (TBI)-mediated hypopituitarism could be more frequent than previously known. However, most previous data were obtained from retrospective studies. OBJECTIVES: The aim of this study was to determine 1) the prevalence of anterior pituitary hormone deficiencies in the acute phase of TBI and after 12 months, 2) whether severity of trauma correlated with basal hormone levels, and 3) whether initial hormone deficiencies predicted medium-term hormonal status. DESIGN AND PATIENTS: Fifty-two TBI patients (43 men and nine women) were included in the prospective study. Pituitary function was evaluated within 24 h of admission and after 1 yr. RESULTS: Some 5.8% of the patients had TSH deficiency, 41.6% had gonadotropin deficiency, 9.8% had ACTH deficiency, and 20.4% had GH deficiency (GHD). Twelve months after TBI, 5.8% had TSH deficiency, 7.7% had gonadotropin deficiency, 19.2% had ACTH deficiency, and 37.7% had GHD. Twenty-six patients (50.9%) had at least one anterior pituitary hormone deficiency, 21 patients (41.2%) had isolated hormone deficiencies, and five patients (9.7%) had combined hormone deficiencies. Overall, the pituitary hormone deficiencies recovered in 30 (57.7%) patients after 1 yr, and new pituitary hormone deficiencies were present in 27 (51.9%) patients after 1 yr. CONCLUSIONS: GHD is the most common pituitary deficit 12 months after TBI, and 50.9% of the patients had at least one anterior pituitary hormone deficiency. Pituitary function may improve or worsen in a considerable number of patients over 12 months.

Adolescent↗
PubMed2006

Investigation of the skin characteristics in patients with severe GH deficiency and the effects of 6 months of GH replacement therapy: a randomized placebo controlled study.

OBJECTIVE: The presence of GH receptor in human skin and its appendages suggests a direct effect of GH on skin characteristics. The skin is usually thin and dry in patients with GH deficiency (GHD). Sheehan's syndrome classically refers to postpartum hypopituitarism and GH is one of the earliest pituitary hormones lost. While severe GHD is a well-established feature of Sheehan's Syndrome, skin characteristics and the effects of GH replacement therapy (GHRT) have been investigated neither in Sheehan's syndrome nor in other disorders of GHD. The aim of this study was to investigate the skin characteristics, including the sebum content, hydration (skin capacitance), transepidermal water loss (TEWL), pH and skin temperature, and particularly the effects of 6 months of GHRT on these parameters in GH deficient patients with Sheehan's syndrome. PATIENTS AND DESIGN: Sixteen severely GH deficient women with Sheehan's syndrome (48.1 +/- 10.9 years), and 20 age and menopausal status similar women as control subjects were included. Ten patients received recombinant GH for 6 months (treatment group) and 6 patients received placebo (placebo group) during this period. Skin properties were measured at baseline and after 6 months of GHRT using noninvasive and well-established measuring methods. RESULTS: At baseline the skin capacitance was significantly decreased on the forehead and forearm, and sebum content was significantly decreased on forehead in patients with Sheehan's syndrome compared to control subjects (P < 0.05). In the treatment group there was a significant increase in sebum content on forehead after 6 months of GHRT compared to the baseline value (P < 0.05). However there were no significant changes in other parameters including sebum content on the forearm, TEWL, Ph, skin capacitance and temperature of both the forearm and forehead. In the placebo group there were no changes in any of the evaluated parameters after 6 months of treatment compared to baseline values. CONCLUSIONS: The present study clearly shows that the sebum content on the forehead and skin hydration of the forehead and forearm are significantly decreased in GH deficient patients with Sheehan's syndrome. However 6 months of GHRT significantly increased only the sebum content on the forehead. These data suggest that GH and/or IGF-I may have a modulatory role on several skin characteristics.

Adult↗
PubMed2006

Effects of 3 years of intravenous pamidronate treatment on bone markers and bone mineral density in a patient with osteoporosis-pseudoglioma syndrome (OPPG).

We present a 21 year-old woman with osteoporosis-pseudoglioma syndrome (OPPG) suffering from bone pain and frequent long bone fractures (approximately 1 or 2 fractures/year) who was treated with i.v. pamidronate for 3 years. OPPG is a rare autosomal recessive disorder characterized by severe widespread osteoporosis leading to pathological fractures and congenital or early onset blindness. Bone mineral density (BMD) (g/cm2) was determined at lumbar spine and femur neck by dual energy X-ray absorptiometry. BMD studies were also performed in her parents and 18 year-old brother who were phenotypically normal. Within 2 months of the first pamidronate treatment the patient reported considerable decrease in bone pain and improved mobility. During the treatment period no important side effects and no recurrent bone fracture were reported. There were substantial increases in BMD, T score and z-score at both lumbar spine and femoral neck during therapy. Baseline lumbar spine BMD increased from 0.416 to 0.489 g/cm2 and femoral neck BMD increased from 0.455 to 0.532 g/cm2 after 3 years. Although her parents and brother did not have any history of fracture, BMD measurements revealed that her parents were osteopenic and her brother was osteoporotic. We demonstrated that pamidronate therapy seems to be safe and beneficial in both spinal and peripheral skeleton osteoporosis in patients with OPPG. Moreover, the present study clearly indicates that bone density studies and LRPS gene screening for mutations should be performed in phenotypically normal family members of patients with OPPG.

Abnormalities, Multiple↗
PubMed2006

Investigation of adrenal functions in patients with idiopathic hyperandrogenemia.

OBJECTIVE: Some patients with hyperandrogenemia had no identifiable cause, which was named as idiopathic hyperandrogenemia (IHA). The role of the adrenal glands in these patients was investigated. DESIGN: Clinical study in patients with IHA at the Endocrinology Department of a University Hospital. PATIENT(S): In this study, 26 pre-menopausal women with IHA and 20 healthy women were included. Basal hormonal investigations, ACTH test and a 75 g oral glucose tolerance test (OGTT) were performed. Basal levels of total testosterone, free testosterone, androstenedione (A4), sex hormone-binding globulin, DHEA sulfate (DHEAS), cortisol, 17-hydroxyprogesterone (17-OHP), 11-deoxycortisol (11-S) and ACTH-stimulated levels of cortisol, A4, DHEAS, 17-OHP, and 11-S were measured. Additionally, glucose and insulin responses to OGTT were obtained. RESULTS: The patients and the control subjects had similar age and body mass index. Peak and area under the curve (AUC) responses of 11-S (P<0.05), DHEAS (P<0.005), and A4 (peak, P<0.005; AUC, P<0.001) to ACTH test were significantly higher in the patients with IHA than in the control subjects. There was a significant correlation between the basal DHEAS levels, peak 11-S, and AUC11-S, in response to ACTH-stimulation test in patients with IHA (P<0.005, r, 0.6). Four (16.6%) patients with IHA had glucose intolerance. CONCLUSION: Our data suggest that adrenal androgen excess may playanimportant role in patients with IHA and these patients exhibit increased prevalence of glucose intolerance.

Adolescent↗
PubMed2005

Massive cardiac thrombosis in a patient with Sheehan's syndrome.

Growth hormone deficiency (GHD) is a risk factor for increased cardiovascular disease, and it has been recently demonstrated that abnormalities in coagulation system might contribute to the increased cardiovascular morbidity and mortality. However, there is not enough data related to the major thrombotic events in GH-deficient patients. We describe the case of a 62-year-old woman with Sheehan's syndrome who developed massive cardiac thrombosis. She was hospitalized with acute pulmonary edema. ECG revealed high ventricular responsive atrial fibrillation (AF) and T-wave inversion on precordial leads. The ejection fraction of left ventricle (LVEF) was measured as 60% by transthoracic echocardiography (TTE) and there was 2nd degree mitral regurgitation with concentric hypertrophic LV walls. Transesophagial echocardiography (TEE) established thrombi both at right atrium and left atrial appendix. Before anticoagulant therapy several hemostatic and fibrinolytic markers were measured. Except increased D-dimer concentration (763.14 mug/L (0-325)) we did not observe any pathological finding in these parameters. After 14 days of discharge, the patient was admitted to the intensive care unit with upper gastrointestinal bleeding. The warfarin and salicylate were stopped for two months. At the end of two months, the patient was again hospitalized with congestive heart failure and there was a high ventricular responsive AF on ECG. TEE was performed and three thrombi were demonstrated at right atrium (RA), left atrium (LA) and left ventricle (LV). There was no active bleeding on upper GIS endoscopy and anticoagulant therapy was restarted. In this particular case massive cardiac thrombi involving three chambers (LA, RA, LV) were more extensive than expected in AF. Moreover, there was a 2nd degree mitral regurgitation in the patient, and based on previous studies mitral regurgitation has been associated with less prevalent LA spontaneous echo contrast and fewer thromboembolic events. Therefore we hypothesized that severe GHD in the present case might be the major contributing factor in massive cardiac thrombosis. In summary, based on previous data there is increased risk of thromboembolic events in GHD although the mechanism is unclear yet. Our case is the first case showing massive cardiac thrombosis in a severe GH-deficient patient with Sheehan's syndrome. Therefore, patients with GHD should be screened carefully for thrombus in clinical practice, and further studies need to be done to understand the relation between GHD and coagulation system.

Atrial Function↗
PubMed2003

Kallmann's syndrome: molecular pathogenesis.

Kallmann's syndrome (KS) is a genetic condition characterised by hypogonadotrophic hypogonadism (HH) and anosmia; although these are the defining features of the condition, additional neurological and non-neurological sequel may also occur depending on the specific mode of inheritance. KS affects about 1 in 8000 males and 1 in 40,000 females, with most presentations being of the 'sporadic' type. Of the inherited forms, hitherto, only the gene responsible for the X-linked form (X-KS), namely KAL-1, has been identified and the encoded protein, anosmin-1, consists primarily of a whey acidic protein (WAP) and fibronectin-like type III (FnIII) domains which appear to mediate distinctly different protein functions. The WAP/FnIII combination is conserved in anosmins across species and recent studies in rodents and in Caenorhabditis elegans demonstrate that anosmin functions in both axonal targeting and branching. Screening for loci that modify these phenotypes in C. elegans has identified heparan-6-O-sulphotransferase as a key interactor mediating anosmin-1 function. Furthermore, over-expression and loss of function of the C. elegans Kal-1 gene disrupt epidermal morphogenesis, resulting in ventral enclosure and male tail formation defects. These findings provide novel insights into the molecular pathogenesis of X-KS.

Amino Acid Sequence↗