Ultrasonographic evaluation of lower limb enthesis in patients with early spondyloarthropathies

The enthesopathy of seronegative spondyloarthropathies [SpA] is the hallmark of these diseases, the ultrasound examination of these entheses confirms the frequency of their involvement. To detect entheseal abnormalities with ultrasound [US] in the lower limb of patients with early Spondyloarthropathy [SpA] and to evaluate US as a valuable tool in detecting early enthesis. A total of 45 patients with early disease duration of 11.7 +/- 8.5 months, including 10 patients with psoriatic arthritis [PsA], 10 patients with ankylosing spondylitis [AS], 10 patients with reactive arthritis [ReA], eight patients with ulcerative colitis [UC] and seven patients with Crohn's disease and 20 healthy controls of matched age and sex underwent ultraso-nographic evaluation of Achilles, quadriceps, patellar entheses and plantar aponeurosis. Ultrasonographic findings were scored according to the Glasgow Ultrasound Enthesitis Scoring System [GUESS]. On US examination a total of 290/450 [64.4%] of the entheseal sites were abnormal. Mean GUESS score was significantly higher in patients with SpA as compared with controls[p < 0.001], with a higher mean value in patients with PsA, ReA and AS. The mean thickness of all tendons examined was significantly higher in SpA patients than in controls [p < 0.0001] as well as the mean number of enthesophytes and bursitis in all sites examined [p = 0.002, p = 0.003], with a higher prevalence amongst patients with PsA and ReA. The GUESS score was correlated to duration of the disease and the anti-tumour necrosis factor alpha medications. Enthesis involvement occurs early in spondyloarthritis, the enthesis US score appears to be reliable and useful for improving the diagnostic accuracy of early SpA, further studies are needed as US is an evolving technique

Comparative study of kidney affection in SLE patients with and without antiphospholipid syndrome

To evaluate the incidence, clinical associations and outcome of APS nephropathy in SLE patients with 2[ry] APS. We studied 64 female SLE patients with nephritis; 32 of them had 2[ry] APS [group 1] and the rest without 2[ry] APS [group 2]. Demographic, clinical and serological data were prospectively evaluated. Systemic lupus erythematosus disease activity index [SLEDAI] and Systemic Lupus International Collaboration Clinics/ACR damage index [SLICC] were assessed. Renal duplex, renal [99m]Tc-dimercaptosuccinic] scan [DMSA scan] and renal magnetic resonance angiography [MRA] were all used to detect renal vascular affection. There were statistically significant differences between the two examined groups regarding damage index [p = 0.000], hypertension [p = 0.02], thrombocytopenia [p = 0.000], LDL [p = 0.008], C3 [p = 0.01] and TMA [p = 0.04]. In group 1: MR angiography detected 7 patients with RAS: 5 patients with renal artery thrombosis that showed a significant association with TMA and proteinuria [p = 0.002, p = 0.004: p < 0.001, p = 0.02, respectively]. Patients with RAS had DBP, s.creatinine and TGs [p = 0.004, p = 0.005 and p = 0.0003, respectively]. Renal DMSA detected 6 patients with cortical scar which showed a significant association with TMA, proteinuria, livedoreticularis and arthritis [p = 0.001, p = 0.01, p = 0.04 and p = 0.03, respectively] those patients had DBP and RI [p = 0.000 and p = 0.006, respectively]. aPL testing should become a routine investigation in patients evaluated for RAS or renal infarctions especially with hypertension and unexplainable deteriorating renal function. To confirm our results we propose that larger scale, multicentre studies with longer evaluation periods

25-Hydroxy vitamin D levels and its relation to disease activity and cardiovascular risk factors in women with systemic lupus erythematosus

To evaluate the associations of serum 25 hydroxy [OH] vitamin D [25[OH]D] levels with cardiovascular risk factors as well as disease activity in women with SLE. Fifty women with SLE as well as 30 controls were included in our study. Data collected included, demographics, SLE activity and damage assessments, cardiovascular risk factors, medications and laboratory assessment of inflammatory markers and 25[OH]D levels. Stepwise logistic regression analysis were used to estimate the association of 25[OH]D levels with cardiovascular risk factors. A significant lower 25[OH]D levels was found in SLE patients compared to controls [P < 0.001]. A positive correlation was found between 25[OH]D and diastolic blood pressure, fasting blood sugar, cholesterol, triglycerides, LDL, BMI, as well as proteinuria and C3 levels. Furthermore, a significant positive correlation was found between 25[OH]D and the RT carotid artery stenosis and RT carotid artery plaque and the intima media thickness of both left and right carotid arteries. Lower 25[OH]D levels were also significantly associated with higher SLE disease activity and damage scores and steroid cumulative dose. Stepwise logistic regression analysis showed that higher BMI, diastolic blood pressure, cholesterol, triglycerides, LDL and diabetes mellitus act as predictors of lower 25[OH]D levels. Our study found an association between lower 25[OH]D levels and increased cardiovascular disease [CVD] risk factors, as well as increased SLE disease activity and damage indices. Future studies are needed to determine relation of 25[OH]D and cardiovascular risk factors in patients with lupus

C-reactive protein and asymptomatic pericardial effusion in patients with systemic lupus erythematosus

Cardiovascular disease has recently been acknowledged as a primary cause of morbidity and mortality in SLE. There are conflicting reports about CRP values in different spectrum of disease activity in SLE. Though CRP values are higher in active disease compared to inactive disease, its value may or may not correlate with disease activity. Elevated basal CRP has been associated with increased cardiovascular risk, while CRP dysregulation may be a feature of SLE. The aim of the present study was to assess the CRP level in SLE patients asymptomatic for any cardiac involvement especially pericardial effusion and find its relation with clinical and laboratory findings as well as the disease activity and damage indices. Correlation with antiphospholipid antibodies was also considered a point of interest. Thirty female SLE patients were recruited from the Rheumatology department and out patient clinic, Cairo University Hospitals. Patients were asymptomatic for any cardiac involvement. Full history taking, thorough examination, laboratory and relevant radiological investigations were performed for all the patients. Echocardiography was performed to detect pericardial effusion [PE]. Quantitative CRP level was assessed as well as the autoantibodies including anti cardiolipin antibodies [IgG and IgM], anti Ro [SSA] and Anti La [SSB] were detected by ELISA. Disease activity and damage were assessed for all the patients using the SLEDAI and SLICC/ ACR DI. Fifteen age matched female healthy subjects were considered as a control group for the corresponding patients. The mean age of patients was 28.53 +/- 6.77 years, age at disease onset was 24.51 +/- 7.05 years and disease duration was 4.02 +/- 2.57 years. There were 7 patients [23.33%] with pericardial effusion as detected by echocardiography. There was no significant difference in the mean age and disease duration between those with and those with out PE, although there was a tendency to blood pressure elevation in those with PE. Three SLE patients had secondary antiphospholipid syndrome [SAPS]. None of the patients had myocardial infarctions. The mean CRP level in SLE patients with PE was significantly higher than in those with out [33.71 +/- 33.22 and 13.57 +/- 11.51 mg/L, respectively, p 0.017]. Pericardial effusion and serositis may be responsible for the marked elevation of the CRP level in this subset of SLE patients. Those without PE, although active, only had modest CRP elevation. A muted CRP response is seen in the majority of patients with active SLE; levels achieved are generally low. SLE subset with pericardial serositis show marked CRP response, perhaps reflecting the likelihood that SLE is not a single disease entity

Proinflammatory high density lipoproteins and oxidized low density lipoproteins in systemic lupus erythematosus and rheumatoid arthritis patients

Premature atherosclerosis is a major comorbid condition in SLE patients. Oxidation of LDL is an important factor in atherogenesis. Normal high-density lipoproteins [HDL] protects LDL from oxidation, serving an anti-inflammatory role. HDL, however are chameleon like lipoproteins, with the capacity to be proinflammatory during acute phase responses. The present study was undertaken to assess the functional capacity of HDL, and levels of ox-LDL in SLE and RA patients in relation to control subjects and its association with disease activity and different disease manifestations specially those related to atherosclerosis. The study was conducted on 31 female SLE patients, 15 female RApatients, and 25 healthy age matched female controls. The mean age of SLE patients was 29.82 +/- 5.585 years and mean age of RApatients was 37.4 +/- 8.66years. All the patients were subjected to full history taking, general examination, locomotor system examination, and laboratory investigations including complete blood count, ESR, urinalysis, liver function tests, serum creatinine, serum total cholesterol, high density lipoprotein [HDL], low density lipoprotein LDL, and serum triglycerides. Serum rheumatoid factor [RF] was done for all RApatients, and antinuclear antibodies [ANA] and anti n-DNA antibodies for all SLE patients. Traditional risk factors for atherosclerosis were evaluated. Proinflammatory HDL was measured by cell free assay and ox-LDL level was measured by ELISA. Serum levels of oxLDL were significantly higher in SLE and RA patients [mean +/- SD 189.02 +/- 81.04 mg/dl and 92.2 +/- 47.37 mg/dl respectively] versus 39.648 +/- 7.97 mg/dl in controls with p =0.0001 between SLE and controls, and P =0.0001 between RA and controls]. The levels of oxLDL were statistically significantly higher, in SLE patients with CAD compared with patients without CAD [P=0.045], in addition, patients with lupus nephritis had statistically significant higher levels of oxLDL [P=0.004]. SLE and RA patients had more proinflammatory HDL [mean +/- SD score 1.01 +/- 0.2 FU and 0.97 +/- 0.29 FU respectively] versus 0.68 +/- 0.3 FU in controls [SLE versus controls, P=0.002 and RA versus controls P=0.004]. Thirty two% of SLE patients had high proinflammatory HDL, while 46.7% of RA patients had proinflammatory HDL.SLE patients with CAD, CVS,and hypertention had significantly higher proinflammatory HDL scores than patients without [p= 0.003, 0.012, and 0.014 respectively].Levels of proinflammatory HDL correlated significantly with the mean ESR in both SLE [r=0.545, P=0.002] and RA [r=0.577, P=0.035]. Levels of oxLDL correlated significantly with levels of proinflammatory HDL in SLE [r= 0.507, P=0.004] and RA patients [r=0.885, P=0.0001]. HDL are more proinflammatory in a significant proportion of SLE and RA patients and are associated with elevated levels of oxLDL

Anterior pituitary hormones in systemic lupus erythematosus patients

To evaluate the function of anterior pituitary gland in SLE patients and its association with different disease manifestations and disease activity index. The study was conducted on 20 female SLE patients, and 12 healthy age matched female controls. The mean age of SLE patients was 28.95 +/- 5.216 years. All the patients were subjected to full history taking, general examination, locomotor system examination, and laboratory investigations including complete blood count, ESR, urine analysis, liver function tests, serum creatinine, ANA and anti n-DNA antibodies. Disease activity was assessed on the day of endocrinological investigations using SLEDAI. Basal serum levels of anterior pituitary hormones: adrenocorticotropic hormone [ACTH], prolactin [PRL], follicle stimulating hormone [FSH], luiteinizing hormone [LH], growth hormone [GH], and thyroid stimulating hormone [TSH] were measured in all individuals by ELISA. SLE patients had statistically significant higher basal levels of FSH [mean 11.245 +/- 2.76 SD P=0.0001], LH [mean 2.358 +/- 3.6 SD P=0.001] and PRL [mean 19.34 +/- 7.79SD P=0.033].PRL serum levels was significantly positively correlated with disease activity measured by SLEDAI [r=0.683, P=0.001] as well as ESR [r=0.571, P=0.009]. Patients with lupus nephritis had higher levels of PRL [mean 22.9 +/- 7.089 SD compared to patients without nephritis, with P=0.02.The patients had lower levels of ACTH compared to control subjects but the difference was not statistically significant [P=0.07]. Higher than normal levels of prolactin in SLE patients appear to constitute immunostimulatory hormone environments in this disease. The presence of pituitary hormones abnormalities suggest that predisposing or even modulatory relationships exist between lupus disease and LH, FSH and PRL