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Causes of Lupus

Author: Shelley Ensz. Scleroderma is highly variable. See Types of Scleroderma. Read Disclaimer
Overview
Coronin-1A Gene
Environmental Exposures
Genetics
Hormones
Medication
Microbes
Viruses and Bacteria

Overview

Possible causes of lupus include genetics, environmental exposures such as insecticides and smoking, hormones, medications, and infections. (Also see Autoimmune Diseases and Overview of Lupus)

Homocysteine (HHcy) serum levels are increased and correlate with disease severity in patients with lupus erythematosus (LE). Hcy levels were higher in patients with different forms of cutaneous LE and correlated with disease activity, therefore HHcy could be related to LE pathogenesis and might be a triggering factor in predisposed individuals. PubMed, Clin Exp Rheumatol, 01/08/2016.

Pathogenesis and prevention of rheumatic disease: focus on preclinical rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). This review focuses on the preclinical stages of RA and SLE, as our current understanding of these diseases can be used to present an overall model of the development of autoimmune rheumatic diseases that might ultimately be used to develop screening programmes and preventive strategies. PubMed, Nat Rev Rheumatol, 2014 Feb 11. (Also see Rheumatoid Arthritis Causes)

Coronin-1A Gene

New Genetic Mutation That Halts The Development Of Lupus Discovered. The lupus-suppressing action is the result of what is known as a nonsense mutation of the Coronin-1A gene (Coro1a) required for the development of the disease. ScienceDaily.

Environmental Exposures

Environmental exposures and the development of systemic lupus erythematosus. Identifying the environmental risk factors related to risk of SLE is essential as it will lead to increased understanding of pathogenesis of this complex disease and will also make risk factor modification possible for those at increased risk. PubMed, Curr Opin Rheumatol, 2016 Sep;28(5):497-505.

Genetics

Evaluation of polymorphic variants in apoptotic genes and their role in susceptibility and clinical progression to systemic lupus erythematosus. Our data support a role for apoptosis in SLE susceptibility. PubMed, Lupus, 11/30/2016.

Genome-wide association studies in Sjögren's syndrome (SS): What do the genes tell us about disease pathogenesis? Genetic findings are discussed with particular attention paid to the genes identified, the strength of associations, and how the SS-associated genes compare to what has been discovered previously in systemic lupus erythematosus (SLE). PubMed, Autoimmun Rev, 2014 Jul;13(7):756-761. (Also see Sjogren's Syndrome)

Hormones

Hormonal Modulation of Dendritic Cells (DC) Differentiation, Maturation and Function: Implications for the Initiation and Progress of Systemic Autoimmunity. In this review, we discuss recent data relative to the role of different hormones (estrogen, prolactin, progesterone and glucocorticoids) in DC function during systemic autoimmune pathogenesis. PubMed, Arch Immunol Ther Exp (Warsz), 09/01/2016.

Medications

Oral contraceptives are a possible cause of lupus.

Contraception in patients with systemic lupus erythematosus and antiphospholipid syndrome. Contraceptive choice in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) is challenging but important. Long-acting forms of contraception such as the progesterone intrauterine device (IUD) or subdermal implant are preferable for most patients. Sage Journals, Lupus, October 2014 vol. 23 no. 12 1242-1245.

Microbes and Diet

Systemic Lupus Erythematosus (SLE): Another Autoimmune Disorder Influenced by Microbes and Diet? In this review, the aim is to compile the available evidence on the contributions of diet and gut microbes to SLE occurrence and pathogenesis. PubMed, Front Immunol, 2015 Nov 30;6:608.

Viruses and Bacteria

Correlation between systemic lupus erythematosus (SLE) and cytomegalovirus infection (CMV) detected by different methods. This data confirmed that the human CMV infection was related to the development of SLE. PubMed, Clin Rheumatol, 2015 Apr;34(4):691-8.

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