Background: Systemic lupus erythematosus (SLE) is the most heterogeneous chronic autoimmune disease; it is characterized by the presence of auto reactive B and T cells, responsible for the aberrant production of a broad and heterogeneous group of autoantibodies. Recent studies using various detection methods have demonstrated the elevations of circulating DNA in SLE patients.Aim of the study: The current study aimed to measure cell-free DNA (cf-DNA) in SLE patients as a potential tool to predict disease activity and treatment follow up.Subjects and methods: 52 of SLE patients with age ranging from 10 to 48 years were randomly selected and 25 healthy subjects with age and gender matched with the patients were included as a control group. Thorough clinical examination stressing on the central nervous system, vascular, renal, rash, musculoskeletal, mucocutaneous manifestations, and fever was done for patients. The following investigations were done: Complete blood count (CBC), kidney function tests, Creactive protein (CRP), routine autoantibodies for autoimmune diseases, complements (C3 & C4), anti-nucleosome antibodies and cf-DNA by real time PCR (RT-PCR).Results: The levels of anti-double stranded DNA (anti-dsDNA), anti-nucleosome Ab, and cf-DNA were significantly increased in SLE patients compared to controls. The cf-DNA level was correlated to markers of disease severity namely CRP and anti-nucleosome. A significant reduction in levels of cf-DNA, anti-nucleosome Ab and anti-dsDNA was noticed after therapy. Production and hosting by Elsevier B.V. on behalf of Ain Shams University. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Please cite this article in press as: Hendy OM et al., Circulating cell free DNA as a predictor of systemic lupus erythematosus severity and monitoring of therapy, Egypt J Med Hum Genet (2015), http://dx. Conclusion:Our findings support that the measurement of cf-DNA appears to be a useful marker in addition to laboratory tests used in SLE diagnosis. High correlation with markers of disease severity suggesting its role in disease pathogenesis and decreasing its level after therapy makes it to be a marker of treatment follow-up.Ó 2015 Production and hosting by Elsevier B.V. on behalf of Ain Shams University. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Objectives. The aim of this study was to investigate the occurrence of myocardial injury in critically ill children through assessment of cardiac troponin T levels and whether levels are associated with disease severity and myocardial dysfunction measured by echocardiography. Methods. Over a 6-month period, this case control study included 50 patients admitted to Pediatric Intensive Care Unit of Zagazig University Children's Hospital. Twenty-five healthy children were included as a control group. Demographic and clinical data including the pediatric index of mortality II score were recorded. Echocardiographic examination was done and level of cardiac troponin T was measured using Elecsys Troponin T STAT Immunoassay. Results. Cardiac troponin T levels were significantly higher in critically ill in comparison to healthy children (median 22 (18–28) pg/mL versus 10 (10-10) pg/mL, P < 0.05). Cardiac troponin T levels correlated positively with duration of ventilation as well as with disease severity and correlated negatively with left ventricular fractional shortening. Moreover, cardiac troponin T levels were significantly higher in nonsurvivors when compared to survivors (median 34.5 (27.5–41.5) pg/mL versus 20 (18–24) pg/mL, P < 0.05). Conclusion. In critically ill children, cardiac troponin T levels were elevated and were associated with duration of ventilation and disease severity.
Background: There is a large variation in the magnitude of the response to asthma medications. Pharmacogenetics is responsible for a significant part of this variation. We aimed at studying the effect of the Glucocoricoid receptors NR3C1 BCLI single nucleotide polymorphism (SNP) on the susceptibility to bronchial asthma in children and to evaluate its effect on the response to inhaled corticosteroids (ICS). Method: Seventy five asthmatic children and a control group of 66 non asthmatic children were included in the study. The level of asthma symptom control and pulmonary function tests were measured initially and 3 months after treatment with inhaled corticosteroids. The genotypes were studied using PCR-RFLP method. Results: No statistically significant difference was found between asthmatic group and the control group as regard the studied genotype. Among asthmatic children, The CC genotype was statistically associated with controlled asthma symptoms 3 months after treatment and the GG genotype was associated with poor asthma symptom control. Also, FEV1% after 3 months of treatment was statistically lower in children with the GG genotype as compared to children with the CG and CC genotypes. Conclusion: glucocorticoid receptor NR3C1 SNP was not associated with asthma susceptibility in the studied group. However, the presence of the GG genotype was associated with decreased response to ICSs among asthmatic children as regards asthma symptom control and FEV1% response.
Sodium valproate is an effective antiepileptic drug used as monotherapy or adjuvant/alternative with other antiepileptic drugs. Haematological toxicity of this drug, though rare, is now an established fact and comprises mainly of neutropenia, thrombocytopenia and aplastic anemia. Very few cases of Pure Red Cell Aplasia (PRCA) following valproate therapy were reported in last 35 years but none presented as acute emergency. We report a case of a 7-year-old child suffering from absence seizure who developed features of acute heart failure due to anemia after 2 months of sodium valproate monotherapy. No underlying haematological or cardiological cause was found. Bone marrow study showed evidence of PRCA. After discontinuation of the drug patient improved gradually and never relapsed again. This case highlights the importance of haematological evaluation both clinically and by laboratory investigation during follow up visits after starting sodium valproate therapy.
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