Nickel sensitization is a growing problem and the most common cause of allergic contact dermatitis. The aim of this study was to investigate whether nickel chloride can induce autoimmunity and cutaneous sclerosis in immunosensitive rats. Nickel chloride, in a dose of 4.5 mg in 0.2 ml NS, was administered by the oral and subcutaneous routes to 20 Brown Norway rats. Autoantibodies (ANA, anti-RNP, anti-SCL70 and anti-centromere) were measured and compared in pre- and post-challenge serum samples. Histological studies were also performed in skin biopsies obtained from six positively responding rats and compared with an equal number of control rats at the 14th week post-challenge. Serum ANA was high in a significant number of rats in both the oral (P < 0.005) and subcutaneously nickel-treated groups (P = 0.02), while the anti-SCL70 was high in a significant number of rats in only the orally nickel-treated group (P = 0.04). Histologically, subcutaneous and oral nickel-treated groups showed sclerodermic features of the skin (P = 0.22, P = 0.5), respectively. It may be concluded that nickel chloride can induce scleroderma-related autoantibodies and cutaneous sclerosis. More prolonged duration of exposure is probably associated with greater risk. This is the first study showing the potential risk of nickel in triggering the development of cutaneous sclerosis in susceptible hosts.
Objective:To uncover the pulmonary manifestations of Systemic Lupus Erythematosus (SLE) patients alone and to compare findings with antiphospholipid syndrome (APS) associated with SLE.Methods:This cross sectional comparative study was carried out at King Khalid University Hospital (KKUH)/King Saud University (KSU), a tertiary care hospital, Riyadh, Kingdom of Saudi Arabia. From June 2012 to March 2014, 96 diagnosed SLE patients with respiratory symptoms were included in the study and divided into two groups. Group one included SLE without antiphospholipid syndrome (APS) and group two SLE with APS. We compared Demographic features, clinical manifestations and findings of chest X-Ray, Arterial Blood Gases, Pulmonary function tests, six minute walk test, ventilation perfusion scan, echocardiography and chest high resolution computed tomography.Results: Demographic and clinical characteristics of two groups were similar. Previous history of deep venous thrombosis (3% vs 27.6%, p=0.001), pulmonary embolism (3% vs34.5%, p<0.0001) and abortions (7.5% vs 27.6%, p=0.019) were significantly more in group two. Levels of Anticardiolipin antibody (0% vs 100%, p<0.0001) and lupus anticoagulant (1.5% vs 79.3%, p<0.0001) were also significantly higher in group two. Hypoxemia measured by pulse oximetry (43.3% vs 65.5% p=0.045, pulmonary Arterial Hypertension (15.5% vs 39.3% p=0.014)), and pulmonary embolism (3.4% vs 21.4% p=0.013) and ventilation perfusion mismatch on V/Q scan (1.5% vs 24.1% p=0.001) were more frequent in group two.Conclusion:Hypoxemia, pulmonary embolism and pulmonary arterial hypertension were significantly high in SLE patients with APS, requiring long term anticoagulation and treatment and close follow-up.
Systemic lupus erythematosus (SLE), is a multifactorial, complex etiological disorder, characterized by inflammation and involvement of multiple organ systems including lungs. Objective: 1-To evaluate whether high resolution computed tomography (HRCT) helps in the diagnosis of pulmonary manifestations of SLE. 2-To study the pattern and extent of lung involvement using HRCT. Design: A Prospective cross -sectional clinical study. Period: Four years, July 2012 to June 2016. Setting: King Khalid University Hospital (KKUH) King Saud University (KSU), Rheumatology division Department of Medicine. Methods: This study included 113 patients attending outpatients or admitted as inpatients having respiratory symptoms and diagnosed as SLE according to American College of Rheumatology (ACR) classification criteria. Chest X-ray, pulmonary function tests, and HRCT chest were done. Investigations to detect other organ involvement were done. Pregnant females and patients having other connective tissue or occupational diseases were excluded. Results: Of the total 113 patients 102 were female and 11 males. Age of patients was 37.1 ±13.0 years. The HRCT abnormalities were pleural effusion, pleural thickening, atelectasis, ground glass opacities including nonspecific interstitial pneumonitis (NSIP) and usual interstitial pneumonitis (UIP), pulmonary arterial hypertension, pulmonary embolism and hilar lymphadenopathy. Conclusion: Various pulmonary manifestations are present in a significant number of symptomatic SLE patients and a variety of HRCT patterns can be seen to diagnose and treat them.
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