The exact<unk>  of sarcoidosis is not known. The current working hypothesis is, in genetically susceptible individuals, sarcoidosis is<unk> d through alteration to the immune response after exposure to an environmental, occupational, or infectious agent. Some<unk> s may be<unk> d by treatment with tumor necrosis factor (TNF) inhibitors like etanercept. Genetics The heritability of sarcoidosis varies according to ethnicity. About 20% of African Americans with sarcoidosis have a family member with the condition, whereas the same figure for European Americans is about 5%. Additionally, in African Americans, who seem to experience more severe and chronic disease, siblings and parents of sarcoidosis<unk> s have about a 2.5-fold increased risk for developing the disease. In Swedish individuals heritability was found to be 39%. In this group, if a first-degree family member was affected, a person has a four-fold greater risk of being affected. Investigations of genetic susceptibility yielded many candidate genes, but only few were confirmed by further investigations and no reliable genetic markers are known. Currently, the most interesting candidate gene is BTNL2; several HLA-DR risk alleles are also being investigated. In persistent sarcoidosis, the HLA haplotype HLA-B7-DR15 is either cooperating in disease or another gene between these two loci is associated. In nonpersistent disease, a strong genetic association exists with HLA DR3-DQ2. Cardiac sarcoid has been connected to tumor necrosis factor alpha (TNFA) variants. Infectious agents Several infectious agents appear to be significantly associated with sarcoidosis, but none of the known associations is specific enough to suggest a direct<unk> tive role. The major implicated infectious agents include: mycobacteria, fungi, borrelia, and rickettsia. A meta-analysis investigating the role of mycobacteria in sarcoidosis found it was present in 26.4% of<unk> s, but they also detected a possible publication bias, so the results need further confirmation. Mycobacterium tuberculosis catalase-peroxidase has been identified as a possible antigen catalyst of sarcoidosis. The disease has also been reported by transmission via organ transplants. A large epidemiological study found little evidence that infectious diseases spanning years before sarcoidosis diagnosis could confer measurable risks for sarcoidosis diagnosis in the future. Autoimmune Association of autoimmune disorders has been frequently observed. The exact mechanism of this relation is not known, but some evidence supports the hypothesis that this is a consequence of Th1 lymphokine prevalence. Tests of delayed cutaneous hypersensitivity have been used to measure progression.
medical cause of Hypercalcaemia
medical cause of Hyperphosphatemia
medical cause of Hyperkalemia
complications of Hypercalcaemia
medical cause of Hypophosphatemia
medical cause of Hyperthermia
medical diagnosis of Hyperparathyroidism
medical cause of Chronic kidney disease