Abstract
Endocrine diseases are a heterogeneous group of disorders which can affect nearly any body system including the musculoskeletal system. Rheumatic manifestations of endocrine disorders may present as a definite rheumatic disease (such as pseudogout in hyperparathyroidism), as rheumatic symptoms such as arthralgia and myalgia, as positive immune serology, or may mimic rheumatic diseases (e.g., skeletal abnormalities in hypoparathyroidism can mimic ankylosing spondylitis). The rheumatic manifestations may result from a direct effect of the hormones, the occurrence of several autoimmune phenomena in the same person (due to genetic or environmental influences), secondary to endocrine disease complications or effects of advanced glycation end products in the case of diabetes. Rheumatic manifestations of diabetes, thyroid, pituitary, parathyroid, and adrenal disorders will be discussed.
Rheumatic diseases are associated with endocrine disorders which may have an impact on the clinical aspects of those diseases. The impact of endocrine disorders on rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Sjögren's syndrome (SS) is reviewed. Rheumatoid arthritis is the most common coexisting autoimmune disorder in patients with Grave's disease and Hashimoto thyroiditis. RA patients are more likely to have thyroid-related antibodies, and some studies indicate an increased prevalence of thyroid diseases in RA. Hypothyroidism contributes to the increased risk for cardiovascular diseases and metabolic syndrome in RA patients and may be correlated with RA disease activity and response to treatment. In most studies, thyroid diseases (mainly hypothyroidism) are more common in SLE patients. Their impact on disease activity is controversial. Pregnant SLE patients are more prone to develop thyroid diseases and pospartum thyroitidis, and in case they suffer from thyroid disease, they have an increased prevalence of preterm delivery. Polyautoimmunity is reported in a high percentage of SS patients. The most frequent coexisting disease is autoimmune thyroid disease (AITD) which may be partially explained by the higher prevalence of thyroid dysfunction in middle-aged women rather than a true association. The prevalence of SS among patients with autoimmune thyroiditis is increased by two- to tenfold.
Patients with RA have an increased risk of insulin resistance (IR) and diabetes (DM) secondary to genetic, inflammatory components or to comorbidities and treatment. The impact of diabetes on disease activity is yet to be fully elucidated. Some of the therapies for RA have a positive impact on DM. Although poly-autoimmunity is frequently described in SLE, the association with type 1 DM is uncommon. An association between SLE and insulin resistance and DM type II is described. Glucocorticoids might have an impact on development of DM, while hydroxycholoroquine treatment is protective. DM does not appear to be a major contributor to damage accrual in SLE.
Addison's disease is mainly related to endocrine autoimmunities, and the association with connective tissue diseases is rare. Cushing syndrome in the rheumatic diseases is mainly secondary to glucocorticoid treatment.
Prolactinoma is associated with an increased risk for autoimmune diseases. Autoimmune thyroid disease is the most common, while rheumatic diseases are rare. Data concerning prolactin and RA are conflicting. Hyperprolactinemia has been described in 20–30% of patients with SLE, but the exact origin of the increased prolactin in SLE patients is unknown. Prolactin might be an independent factor related to SLE activity and disease damage. Elevated prolactin during pregnancy in SLE patients is associated with lupus activity and poor outcome. Bromocriptine (a dopaminergic drug) reduced SLE flares in non-pregnant patients and prevented flares and improved fetal and maternal outcome during pregnancy.
Clinical bone disease secondary to primary hyperparathyroidism is rare today thanks to early detection. Chondrocalcinosis may appear in hyperparathyroid patients. Hyperparathyroidism is probably not increased in RA and SLE.
The association between hypoparathyroidism and rheumatoid arthritis is rare. Hypoparathyroidism was found to be increased in SLE patients and may be secondary to anti-parathyroid antibodies.
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