Purpose: Expression of recently identified growth hormone-releasing peptide, ghrelin, and its receptor has been demonstrated in prostate cancer (PCA) cell lines. It was also shown that ghrelin has increased cell proliferation in vitro when added to PCA cell lines. The aim of this study was to evaluate the diagnostic value of serum ghrelin levels in detection of PCA. Material and Method: 30 patients with PCA and 50 patients with benign prostate hyperplasia (BPH) were enrolled in the study. The serum ghrelin levels of PCA and BPH patients were compared. The correlations between ghrelin and age groups, body mass index, total prostate-specific antigen (PSA) levels, free/total PSA ratio, Gleason score, and prostate volume were also studied. Results: There were no statistically significant differences between the two groups and parameters mentioned above in terms of serum ghrelin levels (p > 0.05). Conclusion: Although ghrelin has been shown to induce PCA cell proliferation by in vitro studies, its role in the diagnosis of PCA was not demonstrated in our clinical study. Insufficient secretion of ghrelin into serum or the effect of other sources of ghrelin to serum ghrelin levels could be responsible for this discrepancy.

Prostate Specific Antigen (PSA), a member of kallikrein family, is a specific serine protease of prostatic tissue. In some case reports, changes in PSA levels after acute myocardial infarction (AMI) have been reported. In this study we evaluated variations in PSA levels post-AMI. Twenty-six male patients who had PSA levels within reference limits were included in the study. The diagnosis of AMI was confirmed by clinical findings, ECG (electrocardiogram) and cardiac marker studies. Serum total PSA (tPSA) and free PSA (fPSA) levels were measured at days 0 (day of admission), 1, 2 and 3 after AMI. PSA/albumin ratio was also calculated in order to evaluate the effect of dilution. A statistical analysis of the results of all patients revealed significant decrease in tPSA levels and tPSA/Albumin ratio at day 2 when compared to days 0 and 3, which showed a similar pattern. Changes of fPSA and fPSA/ Albumin ratio according to days were not found significant. In only four patients we found increased levels of tPSA and increased fPSA levels in three of them. These patients displayed severe problems such as renal failure, cardiac failure, ventricular aneurysm and cerebral ischemia due to cardiac arrest. The lower tPSA levels on day 2 suggest that tPSA can be eliminated rapidly from the circulation on days 1 and 2, probably through the formation of complexes of tPSA with acute phase proteins.

We present an interesting case of a 65-year-old man with a pilomatrix carcinoma arising on the previously irradiated face due to the malignant neoplasm of the parotid gland. This is the first report of a pilomatrix carcinoma that has developed on a region that has undergone radiotherapy for another malignancy.

One of the most important endothelium-derived vasoactive mediators is nitric oxide (NO). Endothelial dysfunction by the loss of NO is a critical event during ischemia. Asymmetric dimethylarginine (ADMA) is a competitive inhibitor of NO synthase (NOS) that inhibits vascular endothelial NO production in concentrations found in pathophysiological conditions. The goal of this study was to monitorize overexpression of ADMA in an experimental ischemia-reperfusion flap model. This study was performed using 20 rats. The baseline ADMA levels were measured preoperatively. In Group I (n = 10, control) abdominal flaps were harvested and replaced in situ without creating ischemia. The plasma ADMA levels were measured at 1, 12, and 24 hours postoperatively. In Group II (n = 10, study) abdominal flaps were harvested, and clamping the vascular pedicle created a subsequent 8-hour period of warm ischemia. Clamps were removed and provided tissue reperfusion. The ADMA levels were taken after 1 hour of reperfusion, and at 12th and 24th hours. The mean preoperative ADMA levels in group I and group II were calculated to be 0.37 ± 0.06 (µmol/L) and 0.40 ± 0.06 (µmol/L), respectively. The differences between the preoperative ADMA levels were not statistically significant (p > 0.05). The mean postoperative ADMA levels in group I (control) were calculated to be 0.39 ± 0.09 (µmol/L) at the first hour, 0.42 ± 0.07 (µmol/L) at the 12th hour, and 0.40 ± 0.08 (µmol/L) at the 24th hour. Respectively, the mean postoperative ADMA levels in group II were calculated to be 0.68 ± 0.14 (µmol/L) after 1 hour of reperfusion, 0.62 ± 0.09 (µmol/L) at the 12th hour, and 0.60 ± 0.12 (µmol/L) at the 24th hour. All postoperative ADMA levels were significantly higher in Group II (p < 0.05). These experimental results suggest that systemic production of ADMA is greater in animals having ischemia reperfusion injury of the skin flaps. The strategy of decreasing levels of ADMA may be beneficial to prevent ischemia-reperfusion injury of flaps or composite transplants; thus, ADMA might be an important candidate of therapeutic target in flap or transplantation surgeries.