ObjectiveChemerin was reported to regulate adipogenesis, metabolism, and immunity. But, its relation to cancer remains controversial. In breast cancer, chemerin expression has only been studied in serum, however, its expression in tissue, to our knowledge, has not been studied. The aim of this study was to investigate chemerin expression in breast cancer tissue in comparison to the adjacent normal tissue, and to assess its relationship to disease prognosis.MethodsWe examined chemerin expression in tissue with immunohistochemistry and analyzed the association of chemerin expression with the patients’ clinical and pathological characteristics to determine its role as a predictor of the disease and its relation to disease prognosis.ResultsWe detected a significantly higher expression of chemerin in the malignant vs the non-cancerous tissue specimens in 30/53, (56%) patients, (P=0.001). Moreover, its expression was significantly higher in the metastatic lymph nodes in comparison to the tumor tissues, (P=0.01). Chemerin expression was significantly correlated with weight (r=0.256, P=0.04), body mass index (r=0.233, P=0.03), tumor size (r=0.235, P=0.03), lymph node metastasis (r=0.265, P=0.045), distant metastasis (r=0.267, P=0.02), and tumor grading, (r=0.421, P=0.004), while it was inversely significantly correlated with estrogen receptor and progesterone receptor expression in malignant breast tissues (P=0.038, r=−0.437, and P=0.047, r=–0.316), respectively. The area under the receiver operating characteristic curve for chemerin as a predictor of breast cancer was 0.82, (P<0.001, sensitivity 89%, and specificity 69%). The Kaplan–Meier survival curves revealed that patients with higher chemerin expression had worse overall survival in comparison to those with a lower chemerin expression, (P=0.001).ConclusionOur results revealed higher chemerin expression in malignant vs adjacent normal breast tissue and lend support to a presumable role of chemerin tissue expression as an independent predictor of poor prognosis in breast cancer patients.

Background: Although recent meta-analyses indicates a consistent significant inverse relation of serum 25 (OH) D and the prevalence of gestational diabetes mellitus (GDM), the mechanism is unclear and conflicting opinions continue to be reported. Objectives: The objectives are: 1) comparison of vitamin D status in diabetic and non-diabetic pregnant women; 2) trying to determine the level of vitamin D associated with GDM, and its sensitivity and specificity; 3) determination of the relation of hypovitaminosis D with insulin resistance. Subjects and Methods: One hundred consecutive pregnant women (<28 weeks gestational period) from the attendants of the out-patient clinic at our hospital were diagnosed for GDM by glucose tolerance test (GTT) (75 g 2 h). Among them, 40 patients met the inclusion criteria for this study (group I). As a comparative group, another 40 pregnant ladies were included, 20 of them (group II) had pre-gestational type II DM, and the other 20 (group III) had normal glucose tolerance (NGT) as a control. For all the participants, we estimated fasting blood glucose, fasting serum insulin, homeostasis model assessment of (HOMA-IR and HOMA-B), quantitative insulin sensitivity check index (QUICKI), and serum 25-OH vit D. The ROC curve analysis was used to determine the optimal threshold value of vit D in relation to DM. Results: Compared to the control group, the diabetic patients showed a statistically significant increase in the levels of fasting glucose, 1-hour postprandial glucose, 2-hour post prandial glucose, fasting insulin, and HOMA-IR, (P=0.000 for all). None of the diabetic patients showed optimal vit D level. Vit D insuficiency (10 -29 ng/ml) was found in 32.5% of patients in group I, 55% in group II, and 50% in group III. Vit D deficiency (<10 ng/ml) was found in 67.5% of patients in group I, 45% in group II, and 0% in group III. Significant negative correlation was found for vit D with fasting insulin and FBS. The AUC for 25 OH vit D was 97%, CI was 95% and p-value was 0.0001. The sensitivity, specificity, and positive and negative predictive values of 25 OH vit D in GDM versus control persons were 97%, 90%, 95.1%, 94.7% respectively at a cut-off level <22 ng/ml. Conclusions: Although it might seem premature to draw a sharp relation between hypovi- taminosis D and GDM, this study showed the importance of vit D in GDM, the need for supplementation below 22 ng/ml, and the role of hypovitaminosis D in increasing insulin resistance. Further randomized studies with vit D supplementation are recommended.

Background: Recent evidence for the effects of vitamin D and recognition of the high prevalence of its deficiency has increased the interest in it. Vitamin D-sub nutrition may contribute to the risk of a wide range of disorders. Methods: The females in the child-bearing period attending the endocrinology and orthopedic out-patient clinics complaining of pain and/or tenderness at the groin were evaluated. Patients with chronic metabolic or skeletal illness, primary hyperparathyroidism, and patients receiving drugs that interfere with bone mineral metabolisms were excluded. One hundred accepted and consented to participation in the study. All the participants were subjected to full history taking, clinical evaluation, laboratory investigations including serum Ca, Ph, PTH, ALP, TSH, F T4, F T3, Cortisol level, and 25(OH)D level. Plain X-ray was done for the regions of bony tenderness. The subjects were divided into 2 groups based on the presence or absence of pseudo-fractures (looser zones). They were treated and followed up till normalization of the laboratory parameters and healing of the looser zones. Results: The mean age for patients was 30.45 ± 5.8, their mean 25(OH) vitamin D level was 14.7 ± 5.9 ng/ml, the mean PTH was 195.7 ± 162.6, and looser zones were evident in the X-rays of 34 patients 184sun exposure, low dairy products consumption, and lack of vitamin D supplementation. Successful medical treatment may be helpful to satisfy the patient, avoid true fracture and further major surgical treatments.

Objective: To investigate the possible role of signal transducer and activator of transcription 5 (STAT5) in the pathogenesis of liver fibrosis in Egyptian patients with chronic hepatitis C (CHC) virus infection and its relation to hepatic stellate cells (HSC). Subjects and Methods: Sixty-five patients (46 males and 19 females) were divided into 4 groups based on the severity of fibrosis as detected by Fibroscan as follows: F1, n = 15; F2, n = 21; F3, n = 13; and F4, n = 16. Twenty age- and gender-matched healthy persons volunteered as controls. The serum levels of STAT5, TGF-β1, α-smooth muscle actin (α-SMA), fasting blood sugar, and fasting insulin, as well as homeostasis model assessment of insulin resistance (HOMA-IR), were determined and compared for all groups. The usefulness of the studied serum biomarkers for predicting liver fibrosis was evaluated using a receiver operating characteristic curve. Results: Serum levels of STAT5 were significantly lower in patients compared to controls (9.69 ± 5.62 vs. 14.73 ± 6.52, p ≤ 0.001); on the contrary, TGF-β1, α-SMA, and HOMA-IR were significantly higher in patients compared to controls (mean: 1,796.04 vs. 1,636.94; 14.94 vs. 8.1; and 7.91 vs. 4.18; p ≤ 0.01 and 0.001, respectively). TGF-β1 and α-SMA showed a progressive increase with advancing severity of hepatic fibrosis (mean TGF-β1: 2,058.4 in F1-F2 and 1,583.8 in F3-F4, p ≤ 0.04; mean α-SMA: 13.59 in F1-F2 and 16.62 in F3-F4, p ≤ 0.05). STAT5 had a significant negative correlation with TGF-β1 (p ≤ 0.001), while no correlation was detected with α-SMA (p ≤ 0.8). Conclusions: STAT5 may play a significant role in hepatic fibrogenesis through the induction of TGF-β1 but not through the activation of hepatic stellate cells.

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