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APRIL (A Proliferation Inducing Ligand) is a member of the tumor necrosis factor (TNF) family. It is essential for the survival of normal and malignant B lymphocytes. Increased expression of APRIL is noted in most of hematological malignancies and auto immune diseases. We investigated the expression level of APRIL mRNA in 50 de novo acute myeloid leukemia (AML) patients, together with 20 healthy controls using a Real-Time Quantitative Reverse-Transcriptase Polymerase Chain Reaction (RTQ-PCR) with a specific aim of determining its relation to clinical features and laboratory findings at diagnosis and its impact on the response to therapy. APRIL mRNA expression level was significantly higher in AML patients than in controls (p = 0.001). APRIL expression level was significantly higher in patients who didn't achieve CR compared to those who achieved CR (p 0.001). Patients who did not achieve CR also had higher TLC, lower platelets and older age than CR patients. The difference was statistically significant (p 0.001, p = 0.047, p = 0.019) respectively. APRIL levels showed significant positive correlation with TLC (r = 0.743.p 0.001), with age (r = 0.296,p = 0.037) and a negative correlation with platelets count (r = -0.443,p = 0.001) and no correlation with gender, Hb level, BM blast, HSM or LNs enlargement. Our study has shown that APRIL is overexpressed in AML patients, its level might serve as an indicator for disease progression. APRIL might be an indicator for poor prognosis and treatment resistance in AML patient; therefore, APRIL antagonists may represent a novel therapeutic approach for the treatment of AML.

BACKGROUND Outcome of childhood acute lymphoblastic leukemia (ALL) in low- and middle-income countries is lagging in many aspects including diagnosis, risk stratification, access to treatment and supportive care. OBJECTIVE to report the outcome of childhood ALL at Ain Shams University Children's Hospitals with the use of risk-based protocols before the implementation of minimal residual disease technology and to evaluate the use of double delayed intensification (DDI) in standard risk patients. METHODS Two hundred and twenty patients with ALL diagnosed between January 2005 and December 2014 were included in the study. Patients were treated according to a modified CCG 1991 and 1961 for standard and high risk respectively. Patients were stratified into three risk groups: standard risk (SR), high-risk standard arm (HR-SA), and high-risk augmented arm (HR-AA). RESULTS Among the whole cohort, the 10-year event-free survival (EFS) and overall survival (OS) were 78.1% and 84.3% respectively. Patients with Pre-B immunophenotype (IPT) had significantly better outcome than T-cell IPT (EFS 82.0% versus 58.6%, p

FAT1 is a type 1 transmembrane protein belonging to the cadherin superfamily. Many reports showed either overexpression of FAT1 gene or its loss in solid cancers. Limited studies evaluated its importance in leukemogenesis. Real-time quantitative reverse transcriptase polymerase chain reaction (RTQ-PCR) was used to examine the levels of FAT1 mRNA expression in 50 paediatric acute lymphoblastic leukaemia (ALL) and 50 adult cytogenetically normal acute myeloid leukaemia (CN-AML). Each group was compared with 20 age- and gender-matched healthy controls. Peripheral blood (PB) samples were collected at time of diagnosis from all patients and controls. FAT1 mRNA was detected in 66% of the paediatric ALL cases, 50% of the adult CN-AML cases, while not expressed in the PB of the control groups. T cell ALL (T-ALL) cases showed high statistical significant difference in the expression levels of FAT1 when compared to B cell precursor (BCP)-ALL (P = 0.001). Paediatric FAT1high ALL expressors showed poor response to induction therapy than FAT1low ALL (P = 0.001) as well as FAT1pos expressors in adult CN-AML when compared to FAT1neg (P = 0.01). FAT1 plays an important role in leukemogenesis; its expression levels may be used as an independent prognostic indicator in paediatric ALL and may help in distinguishing an important risk group in adult CN-AML.

Many risk factors may contribute to renal disease in patients with hemophilia A. Aim: We aimed to evaluate functional and structural renal abnormalities among a group of Egyptian children with severe and moderate hemophilia A using technetium-99m diethylene triamine pentaacetic acid (99mTc-DTPA) and technetium-99 m dimercaptusuccinic acid (99mTc-DMSA) scan. We also aimed to determine the relation between these abnormalities and different risk factors and disease severity. Patients and methods: Forty male patients, 16 with severe and 24 with moderate hemophilia A, were enrolled in this study. Their mean age was 10.2 ± 4.3 years (range, 5-17 years). Full history taking, clinical examination, laboratory, and radionuclide investigations including serum creatinine, blood urea nitrogen (BUN), urine analysis, creatinine clearance, 24-hour urinary protein, 99mTc-DTPA scan, and 99mTc-DMSA scan were performed to all enrolled patients. Results: Serum creatinine and BUN were normal in all patients, and corrected creatinine clearance was diminished in 2 patients. However, 99mTc-DTPA results yielded 19 (47.5%) patients with diminished glomerular filtration rate (GFR). Moreover, it showed that 14 (35%) had obstructive uropathy, 15 (37.5%) had obstructive nephropathy, while 11 (27.5%) patients showed normal scan. One patient had atrophy of 1 kidney on 99mTc-DMSA scan. Among our cohort, 5 (12.5%) patients were hypertensive. Microscopic hematuria was detected in 14 (35%) patients while 72.5% had proteinuria. We found an association between hematuria and hypertension with diminished GFR. Conclusion: Despite normal kidney functions (serum creatinine and BUN), we found a high rate of diminished GFR and obstructive uropathy and nephropathy as detected by 99mTc-DTPA scan among children with hemophilia A.

The α hemoglobin stabilizing protein (AHSP) binds α-Hb and prevents its precipitation limiting free α-Hb toxicities. Our aim was to study AHSP expression in β thalassemia syndromes in relation to their clinical severity and to compare it with its level in sickle cell anemia. We compared patients with β-thalassemia (n=37) (β-thalassemia major (BTM) (n=19) and β-thalassemia intermedia (BTI) (n=18)) with 12 patients with sickle cell anemia as regards clinical severity, age at presentation, transfusion dependency, mean pre-transfusion hemoglobin level, use of hydroxyurea and AHSP expression by real time quantitative PCR. Median (and IQR) AHSP expression was significantly higher in patients with sickle cell anemia 2275 (3898) compared to thalassemia 283 (718), P=0.001, with no significant difference between BTM and BTI (P=0.346). It was also significantly higher in non-transfusion dependent patients with β thalassemia (NTDT) compared to transfusion dependent ones (P=0.019), and in patients on hydroxyurea therapy (P0.001). However, there was no significant difference in its level according to clinical severity score (P=0.946) or splenectomy status (P=0.145).AHSP expression was higher in patients with sickle cell anemia versus thalassemia, with no significant difference between BTM and BTI. Expression was higher in patients with NTDT and on hydroxyurea therapy.

Pulmonary fibrosis and cardiotoxicity are a common and dose-limiting side-effect of ionizing radiation used to treat cancers of the thoracic region. This study aims at investigating the role of Bcl-2, Bax protein and caspase-3 in the pathogenesis of tissue damage induced by gamma irradiation (IRR) and the protective potential role of vitamin E (Vit E) and/or L-carnitine (L-car) against γ-irradiation induced oxidative injury. Irradiation was performed as a whole body γ-irradiation (5Gy). Immnuohistochemistry was used to estimate Bcl-2 expression. The level of Bax and caspase 3 activity were determined using enzyme-linked immunosorbent assay. C-reactive protein was determined using immunoturbidimetric assay. Results revealed that γ-irradiation (5Gy) induced apoptosis via the mitochondrial pathway by downregulating Bcl-2 expression, upregulating Bax protein and activating caspase-3. Administration of Vit E (50mg/kg) and/or L-car (300mg/kg) prior to gamma-irradiation decreased apoptosis through changing the expression of Bcl-2, Bax and caspase-3 activity. Exposure to γ-irradiation increased triglyceride, cholesterol, low density lipoprotein-cholesterol (LDL-C), C-reactive protein (CRP) and potassium levels, creatine kinase (CK-MB) and lactate dehydrogenase (LDH) activities and decreased high density lipoprotein-cholesterol (HDL-C) levels. The altered lipid profile, CRP and potassium levels, CK-MB and LDH activities induced by exposure to γ-irradiation were significantly renovated in Vit E and/or L-car pretreated γ-irradiated rats. In conclusion, Vit E and/or L-car might ameliorate γ-irradiation induced apoptosis via modulation of Bcl-2, Bax and caspase-3.

To assess serum sclerostin levels in relation to severity of arthropathy and bone mineral density (BMD) in children with hemophilic arthropathy. This cross-sectional study included 40 male children suffering from Hemophilia A, and 10 matched healthy controls. Assessment of factor VIII deficiency degree, frequency of bleeding, type of treatment, body mass index (BMI), disease severity using the Hemophilia Joint Health Score (HJHS) and lumbar spine (LS) Z score for bone mineral density (BMD) using dual-energy X-ray absorbiometry was done. Serum sclerostin levels were measured for all patients and controls. Significant difference of serum sclerostin levels between the patient and control groups with Mean ± SD (0.09 ± 0.07 ng/ml) and (0.04 ± 0.01 ng/ml) (P value = 0.028) respectively was found. Significant positive correlations between serum sclerostin levels and the patients’ age, and HJHS (P value

Aim : to determine the prevalence of insulin resistance in a group of RA patients and to clarify the association between IR and the various disease parameters and the subclinical vascular pathology in those patients. Subjects and Methods : The present study included 40 patients with RA in addition to 20 healthy age and sex matched controls. The study participants were subjected to careful history taking, thorough clinical examination and laboratory investigations including CRP, RF, ESR and insulin resistance. VAS and Disease activity score were calculated for all patients. Ultrasound assessment of carotid arteries was also performed. Results : The study included 40 RA patients. The patients comprised 31 females (77.5 %) and 9 males (22.5 %) with a mean age of 42.7 ± 8.3 years and BMI of 28.6 ± 3.2 Kg/m 2 . Patients had significantly higher CIMT when compared with controls. Also, it was found that patients had significantly higher HOMA-IR when compared with control. HOMA-IR was significantly correlated with BMI and CIMT. Conclusions : Insulin resistance is prevalent in RA patients and significantly contributes to the development of subclinical atherosclerosis in those patients.

Introduction The majority of the fibromyalgia syndrome (FMS) patients do not exercise regularly and their physical fitness is low. Physical inactivity accelerates bone loss. This suggests that FMS patients are at risk in terms of osteoporosis. The aim of this study was to measure serum C-telopeptide of type I collagen (CTX-1) as a marker of bone resorption in premenopausal women with FMS. Patients and methods A total of 100 premenopausal female patients with FMS diagnosed according to the American College of Rheumatology (ACR) criteria 1990 and 50 healthy women were chosen to serve as the control group. Serum CTX-1 levels were measured using beta-CrossLaps Roche Elecsys. Results The serum CTX-1 level was significantly higher in patients with FMS compared with the control group. The mean serum CTX-1 in FMS patients was 340.2 ± 112.6 pg/ml compared with 283.6 ± 113.1 pg/ml in controls (P = 0.004). The serum CTX-1 level was positively correlated with the visual analogue scale(VAS) of pain (P = 0.028), the VAS of fatigue (P = 0.031), the VAS of global severity (P = 0.016), the VAS of anxiety (P = 0.013), the Health Assessment Questionnaire score (P = 0.022), the Fibromyalgia Impact Questionnaire (P = 0.010), the Beck Depression Inventory (P = 0.007), the tender points count (P = 0.003), the tender points score (P = 0.004), and the Pittsburg Sleep Quality Index (P = 0.021). The mean serum CTX-1 level was also significantly higher in FMS patients with postexertion pain (P = 0.010), confusion (P = 0.025), dizziness (P = 0.012), depression (P = 0.029), mood disturbance (P = 0.018), anxiety (P = 0.030), short memory difficulties (P = 0.017), and sleep disturbance (P = 0.028) than in those without these symptoms. Conclusion We found a significant increase in serum CTX-1 in FMS patients compared with controls, and this was correlated with the disease severity. Increased CTX-1 may lead to the early development of osteoporosis. More comprehensive and detailed studies are needed to determine the exact role of CTX-1 in FMS.

A. muricata L., commonly known as graviola, is a plant widely distributed throughout the world rich in phytochemicals and minerals. The objective of this study was to investigate the influence of A.muricata on oxidative stress in the liver, kidney and pancreas along with variations in glucose, insulin, lipid profile, liver and kidney functions in diabetic (DM) and γ-irradiated rats (IRR). Diabetes was induced by a single intraperitoneal injection of streptozotocin (65 mg/Kg body weight). Irradiation was performed as whole body γ-irradiation (5 Gy) administered in a single acute dose. A.muricata leaves aqueous extract (100 mg/Kg body weight) was administered via gavages during 2 weeks to diabetic rats or during 2 weeks before γ-irradiation. Diabetic rats received A. muricata during 2 weeks before irradiation. Animals were sacrificed 24 hours post irradiation and/or A. muricata trearment. A. muricata treatment has significantly attenuated hyperglycemia, hypoinsulinemia and dyslipidemia, and reduced the increase of serum alanine and aspartate amino transferase activities and serum urea and creatinine levels. The amelioration in metabolic variations was associated to significant improvement of oxidative stress in tissues notified by a higher superoxide dismutase (SOD) activity and glutathione (GSH) content and a lower malondialdehyde (MDA) content. It could be suggested that the synergistic relationship between the different elements found in the leaf of A.muricata could be beneficial in ameliorating liver and kidney function and correcting metabolic variations associated with oxidative stress in the liver, kidney and pancreas.

Background: Liver fibrosis is one of the major complications from upper right quadrant radiotherapy. MicroRNA-17-5p (miR-17-5p) is hypothesized to act as a regulator of hepatic stellate cell (HSCs) activation by activation of the canonical Wnt–β-catenin pathway. Diosmin (Dios), a citrus bioflavonoid, is known to possess potent antioxidant, anti-inflammatory, and anti-apoptotic properties. Purpose: To explore the molecular mechanisms that underlie radiation-induced liver fibrosis, and to evaluate the possible influence of Dios on the miR-17-5p–Wnt–β-catenin signaling axis during fibrogenesis provoked by irradiation (IRR) in rats. Also, the effect of Dios on hepatic peroxisome proliferator activated receptor-γ (PPAR-γ) expression as a regulator for HSC activation was considered. Methods: We administered 100 mg·(kg body mass)–1·day–1(per oral) of Dios were administered to IRR-exposed rats (overall dose of 12 Gy on 6 fractions of 2 Gy each) for 6 successive weeks. Results: Data analysis revealed that Dios treatment mitigated oxidative stress, enhanced antioxidant defenses, alleviated hepatic inflammatory responses, abrogated pro-fibrogenic cytokines, and stimulated PPAR-γ expression. Dios treatment repressed the miR-17-5p activated Wnt–β-catenin signaling induced by IRR. Moreover, Dios treatment restored the normal hepatic architecture and reversed pathological alterations induced by IRR. Conclusion: We hypothesize that the stimulation of PPAR-γ expression and interference with miR-17-5p activated Wnt–β-catenin signaling mediates the antifibrotic properties of Dios.

P-glycoprotein (P-gp), a membrane transporter encoded by multidrug resistance 1 (MDR1) gene, influences pharmacokinetics of anticancer drugs and contributes to multidrug resistance phenotype in acute lymphoblastic leukemia (ALL). The MDR1 (C3435T) gene polymorphism is associated with the altered expression and function of P-gp. In this study, we investigated the influence of inherited MDR1 (C3435T) gene polymorphism on the susceptibility to ALL in Egypt in 60 ALL patients (30 childhood and 30 adulthood), together with 60 healthy controls using a polymerase chain reaction–restriction fragment length polymorphism assay. The mutant homozygous T/T genotype was significantly associated with the occurrence of ALL (p = 0.02; odds ratio, 8.000 (95 % confidence interval (CI), 1.425–44.920) in childhood ALL and (p = 0.04; odds ratio, 5.455 (95 % CI, 0.937–31.746) in adulthood ALL patients. The heterozygous C/T genotype was near statistical significance in both childhood and adulthood ALL patients in comparison to controls (p = 0.06). The C/C genotype was associated with worse response to treatment than the mutant type (T/T and C/T; p = 0.009, 0.04) in childhood and adulthood ALL, respectively. These results suggest that the MDR1 T/T genotype might influence risk of development of ALL and the C/C genotype might be linked to a poor prognosis of ALL.

Lung cancer is the second most common malignancy in the USA, and it is the leading cause of cancer-related deaths among men and women. Regulatory T cells (Tregs) in peripheral blood play crucial roles in suppressing antitumor immune responses in cancer patients. A defect in the immune response may contribute to tumor growth. This study was conducted to test the hypothesis that regulatory T cell lymphocytes might contribute to immune dysfunction in non-small cell lung carcinoma (NSCLC) patients, with a specific aim of determining its role in the development and progression of NSCLC. CD4+ CD25+ Treg cell enumeration by flow cytometry was performed for 30 NSCLC patients both preoperatively and postoperatively, together with 20 controls. Higher percentages of CD4+ CD25+ Treg cells were found in NSCLC patients both pre- (11.24 ± 5.34) and postoperatively (8.75 ± 4.66) in comparison to the control group (2.16 ± 0.97); this difference was statistically significant (p

Introduction : Several polymorphisms have been implicated and associated with osteoarthritis (OA), including vitamin D receptor (VDR). VDR is present in many tissues, including chondrocytes. Vitamin D has been found to increase synthesis of proteoglycan in vitro , suggesting that it may affect the cartilage metabolism. Objective: to investigate the frequency of the VDR gene polymorphism in Egyptian patients with knee OA, and compared them with controls. Subjects and Methods : 200 patients with primary knee OA according to the American College of Rheumatology criteria and 200 matched controls who had no OA. Clinical impact of OA were assessed using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) questionnaire. VDR gene polymorphism Bsm I, Apa I, FokI and Taq I restriction fragment length polymorphisms (RFLPs) were determined by the polymerase chain reaction (PCR). Results : The frequency of ApaI genotype and alleles did not differ significantly between the knee OA patients and the controls. However, three genotypes where significantly higher in knee OA patients than in controls: the bb genotype of BsmI, TT genotype of TaqI and FF genotype of FokI. Knee OA patients with osteophytes had significantly more frequent bb genotype of BsmI, TT genotype of TaqI and FF genotype of FokI. BsmI, TaqI and FokI genotypes or alleles did not show any association with the presence of joint space narrowing (JSN). Knee OA patients who had bb genotype of BsmI, TT genotype of TaqI and FF genotype of FokI are associated with significantly higher WOMAC scores. Conclusion : The current study suggests that VDR gene polymorphism may be associated knee OA in the studied group of Egyptian patients. Association was mostly with severe clinical manifestation and osteophyte formation but not with JSN.

Immune thrombocytopenic purpura (ITP) is an autoimmune syndrome involving platelets destruction and suppression of platelet production that may predispose to bleeding. Protein tyrosine phosphatase non-receptor 22 gene (PTPN22) is an important negative regulator of signal transduction through the T-cell receptors (TCR). A single nucleotide polymorphism (SNP) 1858C > T within this gene was reported to be associated with increased risk of autoimmune diseases. The aim of the work was to study the frequency of the 1858C > T single nucleotide polymorphism in the PTPN22 gene in Egyptian ITP patients. After full clinical and laboratory examination of our subjects, the expression of the PTPN22 (1858C > T) gene polymorphism was analyzed in 60 ITP patients—40 childhood ITP (26 acute and 14 chronic) and 20 adulthood ITP (eight acute and 12 chronic)—and 100 healthy controls using a polymerase chain reaction-restriction fragment length polymorphism assay [PCR-RFLP]. The PTPN22 1858C > T SNP was significantly overrepresented in ITP patients than controls. It was detected in 11 childhood ITP (27.5%) and five adulthood ITP (25.0%) compared to 8.0% in controls (p = 0.002, p = 0.02) when comparing childhood ITP and adulthood ITP to controls, respectively. The T allele was significantly higher in ITP patients than controls. It was 20% for childhood ITP, 15% in adulthood ITP and 4% in controls (p = 0.002, p = 0.05) when comparing childhood ITP and adulthood ITP to controls, respectively. From this study we concluded that the PTPN22 1858C > T polymorphism is more prevalent in ITP patients; thus, it may be considered as a genetic risk factor in development of ITP in Egyptian patients.

In the recent years, the role of melatonin (MLT) in the pathogenesis of inflammatory arthritis has been investigated, and the serum levels of MLT have been evaluated, but clinical study concerning MLT and ankylosing spondylitis (AS) is little reported in literature. We aimed to investigate the serum levels of MLT and their relation with the disease activity parameters of patients with AS. Forty AS patients and 40 healthy controls (matched for age and sex with the patients) participated in this study. Demographic and clinical data were collected and assessed. Disease activity of AS patients was assessed clinically according to the Bath AS Disease Activity Index (BASDAI), while AS functional impairment was assessed using the Bath AS Functional Index (BASFI). Serum samples were collected from all subjects to evaluate serum MLT, ESR, and CRP. Serum MLT levels were significantly increased in AS patients as compared to healthy controls (95% CI: 4.63, 8.77, P < 0.001). ESR and CRP are significantly higher in the AS patients compared with the controls (P < 0.001). AS patients with active disease had significantly higher ESR (P = 0.0151), CRP (P = 0.0124), and BASFI (P = 0.0016). Also, the MLT serum level in AS patients with BASDAI ≥40 was 39.7 ± 6.2 pg/ml compared with 35.2 ± 3.5 pg/ml in AS patients with BASDAI

Aim To clarify the value of dobutamine stress tissue Doppler in the evaluation of LV functional improvement after elective PCI. Methods The study included 60 patients with hibernating viable myocardium proved by DSE referred for an evaluation of myocardial viability prior to revascularization. Hemodynamic and echocardiographic variables (LVEF, WMSI and TDI Sm) were assessed at rest and during stress. 1 month after PCI follow up echocardiography and TDI were done. Patients were divided into 2 groups: (Group I): 18 patients (30%) with no global functional recovery and (Group II): 42 patients (70%) with global functional recovery. Results SBP, DPB, HR, EF, WMSI and (Sm) increased significantly at stress P = 0.001. After 1 month patients were divided into 2 groups according to functional recovery. There were no statistically significant differences between two groups neither as regards age, sex, risk factors ( P > 0.05) nor as regards SBP, DBP, HR, rate/pressure product, EF and WMSI during stress but Sm increased during stress and after1 month follow up in Group II ( P = 0.001). Univariate regression showed that (Sm) is the only predictor for global functional recovery. ROC curve statistical analysis shows that (Sm) is more sensitive and accurate than (WMSI) in the detection of viable myocardium which predicts improvement after revascularization (sensitivity 100%, 50% and accuracy 93.3%, 83.3% respectively). Conclusion Stress TDI provides a feasible and quantitative technique that improves reproducibility of DSE. Sm during stress showed better accuracy than WMSI for the prediction of functional recovery following revascularization and was simple, sensitive and accurate for the detection of subtle myocardial systolic velocity changes.

Vitamin D is critical for calcium, phosphate homeostasis and for mineralization of the skeleton, especially during periods of rapid growth. Vitamin D Deficiency leads to rickets (in children) and osteomalacia (in adults). Expression and activation of the vitamin D receptor (VDR) are necessary for the effects of vitamin D, in which several single nucleotide polymorphisms have been identified especially (FokI, BsmI). In this study serum 25 (OH) vitamin D3 levels were estimated by Enzyme Linked Immunosorbent Assay [ELISA], VDR (FokI, BsmI) gene polymorphisms were analyzed by polymerase chain reaction-restriction fragment length polymorphism assay [PCR–RFLP].Serum levels of calcium, phosphorus, alkaline phosphatase and ferritin were determined in 50 Pediatrics beta thalassemia major patients and 60 controls. Patients had significantly lower serum calcium (p 30 ng/ml). Patients harboring mutant (Ff,ff) and wild (BB) genotypes were associated with lower serum calcium (p = 0.08, 0.02) respectively, lower vitamin D3 levels (p 0.05). In conclusion, these results suggest that the VDR (FokI, BsmI) gene polymorphisms influence vitamin D status, (Ff,ff), BB genotypes had lower vitamin D levels, so they might influence risk of development of bone diseases in beta thalassemia major.

Aim Recently, a large body of studies has focused on the leptin levels in psychiatric disorders. This study aimed to measure serum leptin levels in fibromyalgia syndrome (FMS) due to a significantly higher prevalence of psychiatric disorder and to determine the relationship between leptin and FMS. Methods The present study was a cross-sectional descriptive study. Fifty FMS female patients and 50 healthy females serving as a control group were included. Serum samples tested for serum leptin levels were determined by a specific enzyme-linked immunosorbent assay (ELISA). Results Serum leptin levels were significantly lower in FMS patients compared to the control group. The mean serum leptin in patients with FMS was 7.1 ± 6.8 ng/mL compared to 9.4 ± 4.5 ng/mL in the controls (mean difference, −2.48, 95% CI: −4.78, −0.18, P = 0.035). Serum leptin level is inversely correlated with visual analogue scale (VAS) of pain (P = 0.016), VAS of fatigue (P = 0.002), VAS of global severity (P = 0.011), VAS of anxiety (P = 0.027), global self-rating index (P = 0.020), Health Assessment Questionnaire score (P = 0.016), fibromyalgia impact questionnaire (FIQ) (P = 0.025), Beck Depression Inventory (P = 0.002), tender points (TPs) count (P = 0.041), TPs score (P = 0.015), and Pittsburg Sleep Quality Index (P = 0.006). Mean serum leptin levels were also significantly lower in FMS patients with post-exertion pain (P = 0.010), depression (P = 0.029), mood disturbance (P = 0.018), anxiety (P = 0.030), short memory difficulties (P = 0.017), sleep disturbance (P = 0.028), restless leg syndrome (P = 0.016), temperomandibular joint syndrome affection (P = 0.043), palpitation (P = 0.022), and irritable bowel syndrome (P = 0.028) than those without. Conclusion We found a significant decrease in serum leptin in FMS patients compared to controls and this decrease correlated with disease severity.

Reports suggest leptin, which was initially described as a hormone that regulates food intake and energy balance, has an intimate relationship, and interacts with the immune system. Leptin consumption in the synovial cavity in patients with rheumatoid arthritis (RA) reported to have protective effect against erosion. To determine the difference in serum leptin and synovial/serum leptin ratio between RA and control and to assess whether these parameters correlate with systemic inflammation in RA. Also, the hypothesis that synovial/serum leptin ratio could be linked to joint erosion in RA was evaluated. The study subjects consisted of 40 consecutive patients with RA, 30 patients of them had knee effusion, and 30 controls. Ten of these controls had acute knee injury and their synovial fluid was obtained for comparison of synovial/serum leptin ratio with patients with RA. The mean serum leptin in patients with RA was significantly higher than controls. Also, the synovial leptin and synovial/serum leptin ratio in the RA patients with effusion was significantly higher than in the 10 control subjects with traumatic effusion. Serum leptin in the 30 RA patients with effusion was higher than the matched synovial leptin. In RA patients with effusion, synovial/serum leptin ratio was also significantly higher in RA patients with erosion than RA patients without erosion. Serum leptin level and synovial/serum leptin ratio are significantly correlated with the RA duration, DAS28, ESR, CRP, TNF-α, and IL-6. Finally, in regression analysis, only the synovial/serum leptin ratio was positively associated with erosion in patients with RA. In RA, there is a significant increase in circulating leptin levels and synovial/serum leptin ratio compared to non-RA controls. Serum leptin and synovial/serum leptin ratio are significantly in erosive RA than non-erosive RA. Both parameters are correlated with disease duration and parameters of RA activity. In regression analysis, only the synovial/serum leptin ratio was positively associated with erosion in patients with RA. These results indicate that local consumption of leptin in the joint cavity has a protective role against the destructive course of RA.