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[2] While the cause of rheumatoid arthritis is not clear, it is believed to involve a combination of genetic and environmental factors. [1] The underlying mechanism involves the body's immune system attacking the joints. [1] This results in inflammation and thickening of the joint capsule. [1] It also affects the underlying bone and cartilage. [1]
High levels of rheumatoid factor (in general, above 20 IU/mL, 1:40, or over the 95th percentile; there is some variation among labs) occur in rheumatoid arthritis (present in 80%) and Sjögren's syndrome (present in 50-70% of primary forms of disease). [11] The higher the level of RF the greater the probability of destructive articular disease.
GATA2 deficiency is a grouping of several disorders caused by common defect, namely, familial or sporadic inactivating mutations in one of the two parental GATA2 genes. Being the gene haploinsufficient, mutations that cause a reduction in the cellular levels of the gene's product, GATA2, are autosomal dominant.
Hypoprothrombinemia can be the result of a genetic defect, may be acquired as the result of another disease process, or may be an adverse effect of medication.For example, 5-10% of patients with systemic lupus erythematosus exhibit acquired hypoprothrombinemia due to the presence of autoantibodies which bind to prothrombin and remove it from the bloodstream (lupus anticoagulant ...
GATA2 or GATA-binding factor 2 is a transcription factor, i.e. a nuclear protein which regulates the expression of genes. [5] It regulates many genes that are critical for the embryonic development , self-renewal , maintenance, and functionality of blood-forming , lymphatic system-forming , and other tissue-forming stem cells .
These autosomal dominant mutations cause a reduction in the cellular levels of the gene's product, GATA2. The GATA2 protein is a transcription factor critical for the embryonic development, maintenance, and functionality of blood-forming, lymph-forming, and other tissue-forming stem cells. In consequence of these mutations, cellular levels of ...
LECT2 and its gene, LECT2, are currently areas of active research that seek to implicate them as contributors to, markers for the presence of, and/or prognostic indicators for the severity of not only amyloidosis but also osteoarthritis, rheumatoid arthritis, and other types of inflammation-related disorders; the metabolic syndrome and diabetes ...
The protein product of this gene, adenosine deaminase 2 (ADA2), is an extracellular enzyme that breaks down adenosine and may also serve as a growth factor. Pathogenic mutations decrease this enzymatic activity in patient blood, leading to disease manifestations. However, mutational status and residual enzyme activity levels do not explicitly ...