IntroductionVitiligo is a common acquired pigmentary skin disorder. Vitamin D is responsible for skin pigmentation, increases tyrosinase activity and melanogenesis, and exhibits immunoregulatory functions. Low levels of vitamin D are associated with many autoimmune diseases, including systemic lupus, diabetes mellitus, rheumatoid arthritis, multiple sclerosis and alopecia areata. Few reports have evaluated serum vitamin D levels in vitiligo patients, and their results are conflicting.AimTo evaluate serum vitamin D levels of vitiligo patients and compare the results with controls.Material and methodsIn total, 50 vitiligo patients and 47 controls were enrolled in the study. Vitamin D levels were measured from blood samples. Group comparisons were performed using appropriate statistical methods.ResultsThe patients had lower serum vitamin D levels than the controls, but this difference was not significant (p = 0.570).ConclusionsIt remains unknown whether vitamin D deficiency causes vitiligo. Larger controlled studies are required to prove whether low circulating vitamin D is a causative factor in vitiligo.

Hyperprolactinemia is the most common abnormality of the hypothalamic-pituitary axis. The aim of this study was to investigate the clinical and radiological features of patients with macroprolactinemia. The study population consisted of patients with elevated serum prolactin (PRL) concentrations who presented to our Endocrinology outpatient clinic. Detection of macroprolactin (macroPRL) was performed using the polyethylene glycol precipitation method. Patients in which macroPRL made up more than 60% of total PRL levels were stratified into the macroPRL group, while the remaining patients were placed in the monomeric prolactin (monoPRL) group. A total of 337 patients were enrolled with a mean age of 33.8 ± 10.8 (16-66) years and a male/female ratio of 29/308. Eighty-eight of the patients (26.1%) had an elevated macroPRL level. The mean age in the monoPRL group was higher than in the macroPRL group (35.0 ± 10.1 vs. 30.7 ± 9.8, P = 0.016). The mean PRL levels (ng/ml) in the macroPRL and monoPRL groups were similar (168.0 ± 347.0 vs. 238.8 ± 584.9, P = 0.239). Frequency of amenorrhea, infertility, irregular menses, gynecomastia, and erectile dysfunction were also similar in both groups. More patients in the macroPRL group were asymptomatic compared to the monoPRL group (30.2 vs. 12.0%, P = 0.006). Compared to the macroPRL group, the monoPRL group had a higher frequency of galactorrhea (39.2 vs. 57.1%, P = 0.04) and abnormal magnetic resonance imaging findings (65.3 vs. 81.1%, P = 0.02). Elevated macroPRL levels should be considered a pathological biochemical variant of hyperprolactinemia that may present with any of the conventional symptoms and radiological findings generally associated with elevated PRL levels.

Intra-individual biological variation contributes to the variation in serial results and should therefore be included in the criteria for serum tumour marker assessment.

Endothelial cell-specific molecule-1 (endocan) is an immunoinflammatory marker linked to endothelial activation and dysfunction. We investigated the relationship between obstructive coronary artery disease (CAD), microvascular angina (MVA), and plasma levels of endocan. We included 53 healthy individuals as controls, 40 MVA patients, and 120 patients with obstructive CAD. The severity of CAD was assessed by the Gensini and SYNergy between percutaneous coronary intervention with TAXUS and Cardiac Surgery (SYNTAX) scores. Endocan levels were 382.7 (313.8-470.2) pg/mL in patients with obstructive CAD; 324.3 (277.1-460.7) pg/mL in MVA group, and 268.0 (226.4-336.5) pg/mL (P < .001) in controls. Endocan levels in obstructive CAD and MVA groups were similar but both were significantly higher than for the control group (P < .001 and P = .002, respectively). In subgroup analysis, similar to the hypertensive subgroup results, endocan was still an independent predictor of presence of obstructive CAD in normotensives (odds ratio = 1.005, 95% confidence interval = 1.001-1.010, P = .024). There was also an independent positive correlation between endocan levels and SYNTAX score both in the hypertensives (β = 0.414, t = 3.21, P = .002) and in the normotensives (β = .301, t = 2.23, P = .031). In conclusion, endocan could be a common predictor of the endothelium-dependent inflammatory processes, rather than related with specific risk factors.

Elevated SUA level on admission independently predicts impaired myocardial flow and poor prognosis in STEMI patients undergoing primary PCI.

BACKGROUND AND OBJECTIVESBecause subclinical thyroid dysfunction may be a risk factor for cardiovascular disease, we evaluated the atherosclerosis tendency in subclinical hypothyroid (SCH) patients.PATIENTS AND METHODSFifty-three subclinical hypothyroid patients (serum thyrotropin [TSH] concentrations >4.12 mU/L) were compared with a control group of 50 euthyroid subjects whose age, sex and body mass indices were similar to the patient group. We tested whether serum TSH concentrations were correlated with plasma total homocysteine concentration (tHcy), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC) and triglycerides (TG).RESULTSThere was a significant statistical difference between the patient and control groups for normal free T4 (1.02±0.17 vs. 0.86±0.13, P<.001), TSH (1.64±1.02 vs. 6.62±2.61, P<.001), TC (185±39 vs. 206±42, P=.01), TG (103±54 vs. 132±85, P=.04), LDL-C (114±33 vs. 127±36, P=.04), and TC/HDL-C (3.81±106 vs. 4.19±1.02, P=.04), respectively. No statistically significant difference was found between the two groups for HDL-C, VLDL-C, LDL-C/HDL-C, and tHcy. Serum TSH was significantly correlated with plasma tHcy (r=0.55; P=.001), TC (r=0.52; P=.001), LDL-C (r=0.49; P=.001), TC/HDL-C (r=0.38; P=.002) and LDL-C/HDL-C (r=0.36; P=.004) across all participants.CONCLUSIONOur study suggests that the atherogenicity of SCH is not mediated by hyperhomocysteinemia. Associated hyperlipidemia may explain the observed increased risk of coronary artery disease in patients with SCH.

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Hearing loss has commonly been reported in association with thyroid disorders and during treatment with propylthiouracil. The relationship between hyperthyroidism and the auditory system has not been previously investigated. The aim of this cross-sectional, case-control study was to investigate hearing loss in patients with Graves' disease (GD). The study population consisted of patients with newly diagnosed GD and healthy controls. Pure tone audiometry at frequencies of 250, 500, 1000, 2000, 4000 and 8000 Hz, along with immittance measures including tympanometry and acoustic reflex tests, were performed in all participants. Twenty-two GD patients and 22 healthy controls consented to inclusion in the study. The differences between groups with regards to age and gender distribution were statistically insignificant (P = 0.567 and P = 0.757, respectively). The hearing thresholds of right and left ears were also similar in both groups (P > 0.05). When single-ear evaluations were taken into account (total of 44 ears for both groups), hearing thresholds in the GD group were significantly higher than healthy controls at all frequencies (P < 0.05). Following testing at the designated frequencies, the only significant effect of thyrotoxicosis was observed with frequencies of 4000 and 8000 Hz. The odds ratio for having hearing loss at a frequency of 8000 HZ associated with GD was 14.97 (95% confidence interval 4.03-55.64). In patients with GD, right and left pure tone audiometric findings at a frequency of 8000 Hz correlated positively with FT3, FT4 and negatively with TSH. Our results are highly suggestive of a decrease in hearing ability in patients with GD, particularly at high frequencies. Further studies are needed to help elucidate the mechanisms behind hearing loss which develops in association with GD.