Study of the possible association between systemic lupus erythematosus and Epstein-barr virus

Background and systemic lupus erythematosus [SLE] is an autoimmune rheumatic disease with no known cure. In predisposed individuals, the initial stimulus is likely to be one or more of the environmental agents interacting with susceptibility genes. For many years, investigators have suspected that Epstein-Barr virus [EBV] might somehow by involved in the aetiopathogenesis of systemic lupus. Studies have examined this possibility from various angles and have arrived at different conclusions. The present work was carried out to evaluate the role of EBV as an environmental risk factor for lupus in our population and to assess the role of this virus in the clinical course of the disease. the study included 25 lupus patients satisfying the American College of Rheumatology criteria for diagnosis of SLE. Twenty age and sex matched healthy subjects were chosen as controls. All patients were subjected to complete history taking and full clinical assessment. Routine laboratory investigations were carried out as well as study of immunologic parameters including antinuclear antibodies, anti-double stranded DNA and complement components C3 and C4. in all study subjects, serology for EBV viral capsid antigen [VCA] IgG was performed using both enzyme linked immunosorbent assay [ELISA] and indirect immunofluorescence assay [IFA]. EBV DNA was detected in peripheral blood mononuclear cells by polymerase chain reaction using primers specific for EBV nuclear antigen-1 gene. Besides, interleukin-10 [IL-10] levels were determined in sera by ELSA. Results and twenty three lupus patients [92%] were positive for EBV DNA compared to 12 control subjects [60%], the difference being statistically significant [p= 0.14]. Virtually all study subjects had seroconverted against EBV. When antibody titres were expressed as the geometric mean titre [GMT] after logarthmic transformation, patients with SLE had a significantly higher GMT compared to control subjects [mean +/- SD 3.46 +/- 0.34 vs 2.93 +/- 0.25, t = 5.12, p < 0.001]. When the anti-VCA titre of lupus patients was correlated with different clinical and laboratory findings, a significant positive correlation was detected with disease activity as measured by SLE disease activity index [SLEDAI], while a significant inverse correlation existed with each of C3 and C4. IL-10 levels in SLE patient were significantly higher than those in controls [mean +/- SD 61.37 +/- 90.65 vs 9.73 +/- 20.33 pg/ml. p = 0.002]. Moreover, elevated IL-10 levels correlated significantly with SLEDAI and with titre of anti-VCA in lupus patients. This study provide evidence that EBV infection contributes to the aetiology and/or pathogenesis of SLE and that the presence of the virus may influence the clinical course of the disease

Degenerative joint disease: a new cartilage marker

The aim of the present study was to quantity COMP level in serum of patients with newly developed and late OA in attempt to the prognostic value of its serum measurement as a new cartilage marker. The study was carried out on thirty patients with OA diagnosed according to ARA criteria subdivided into 2 groups [IA and IB] representing early and late OA, and twenty healthy normal individuals as controls [II]. group IA, IB and II were subject to clinical evaluation, routine investigations and determination of serum Ca, phosphorus. uric acid, RF, and X-ray of the affected joints. COMP level estimation in serum was done to all patients and controls Serum concentration of COMP ranged from 1.53-2.1 microg/ml, 2.18-2.65 microg/ml, and -2.65 3.02 microg/ml in the control group, group IA and IB respectively. COMP serum levels is significantly increased in GIA and IB than control [p < 0001]. Also, the comparison is significant between IA and IB patients [p < 0.001] For uric acid, Ca, and phosphorus no difference could be demonstrated between IA and IB. Serum level of COMP is significantly higher in late OA, than early cases, yet both groups are higher than control. The determination of serum COMP may be tried as indicative of therapy in OA cases especially when using chondroprotective therapeutic agents

Defective growth hormone secretion and hypogonadism in the new syndrome of congenital hypoparathyroidism, growth failure and dysmorphic features.

A child with extreme growth failure, dysmorphic features, hypoparathyroidism, and abnormal skeletal survey was studied. He was a product of first degree consaguineous marriage who had intrauterine growth retardation and presented at 14 days of age with hypocalcemic tetany with normal cardiovascular system and immune function. Endocrine evaluation after infancy revealed defective growth hormone (GH) secretion in 2 provocation tests and lack of clinical and testosterone response to human chorionic gonadotrophin (HCG) therapy.

Empty sella in short children with and without hypothalamic-pituitary abnormalities.

A study was conducted on growth hormone (GH) response to oral clonidine (0.15 mg/m2), GH and cortisol responses to i.m. glucagon (0.1 mg/kg), and glucose response to an oral load of glucose (1.75 g/kg). Measurements were made on the circulating concentrations of free thyroxine (FT4), thyroid stimulating hormone (TSH) and different growth parameters and CT sellar images in 25 GH deficient children (Peak GH response to clonidine and glucagon < 7 ug/ml), 15 growth retarded children (Ht < 5th percentile for age and gender) with sickle cell disease (SCD) and GH deficiency, 30 randomly selected children with normal variant short stature (NVSS) (HtSDS 2SD below the mean for age and gender with normal GH response to stimulation (> 10 ug/ml) and 20 age-matched normal children were evaluated. Out of the 25 children with GH deficiency, five had multiple pituitary hormonal deficiency (GH < TSH and/or ACTH. deficiencies), and 20 had isolated GH deficiency. Empty sella, either complete or partial, was detected in 9 out the 20 children with isolated GH deficiency (45%), 4 out of the 5 children with multiple pituitary deficiency (80%), all the children with SCD and GH deficiency (100%), 3 out of the 30 children with NVSS (10%) and in none of the normal children. The insulin-like growth factor-I (IGF-I) concentrations were significantly lower in the two groups of children with GH deficiency compared to those with NVSS. The height standard deviation scores (HTSDS) were significantly lower and the annual growth velocity was slower in children with idiopathic GH deficiency and empty sella compared to those with NVSS and those with empty sella associated with SCD. The bone age delay (yr) did not differ among the 3 groups of children with short stature. All children with isolated GH deficiency associated with empty sella had normal body mass indices (BMI), while all the children with SCD and empty sella had BMI below the 5th percentile for the corresponding age and gender. None of the children had glucose intolerance. In conclusion, children with growth retardation and abnormal hypothalamic pituitary functions have high incidence of empty sella. However, empty sella is detected in considerable number (10%) of short children with normal hypothalamic pituitary function.