Discussion and Conclusions
The rheumatoid nodule is the hallmark of extra-articular manifestation of RA. The lesion is usually asymptomatic and, as indicated in this and in previously described cases, it is associated with seropositive cases (positive RF) and methotrexate treatment.[6,13,14] It has been repeatedly reported that an interruption to methotrexate medication leads to a decrease in the size of the rheumatoid nodules.[15–17] Other features, which characterized our case, were the average levels of antithyroid antibodies, the lack of clinical symptoms, and the presence of typical rheumatoid nodules with central fibrinoid necrosis and palisading histiocytes at the periphery. Such nodules are commonly encountered in synovial joints (destructive polyarthritis) and extra-articular organs including skin and subcutaneous tissues,[5,18] heart,[19] lungs,[6] kidneys,[20] nervous system,[10] and gastrointestinal system.[8]
Common extra-articular manifestations include anemia (61%), thrombocytosis (16%), and pulmonary involvement (10%), while renal amyloidosis, vasculitis, and Felty syndrome occur less frequently (6%, 2%, and 1%, respectively).[20] Skin manifestations are probably the result of small vessel vasculitis. They are often associated with hemorrhages, ulcers, digital gangrene, and pyoderma gangrenosum.[5] Pulmonary manifestations in RA are rather frequent. In fact, autopsy studies reported pleural effusions in 50% of cases, although only a small proportion of them are clinically detected.[21]
Furthermore, the disease is frequently associated with interstitial lung disease.[22] Oral manifestations include dryness and swelling of salivary glands and often Sjögren's syndrome.[8] Gastrointestinal complications in RA have been reported as being mainly drug-induced. Primary involvement of the gastrointestinal tract may also occur in the form of mesenteric vasculitis causing intestinal infarction but is extremely rare.[8] There is also an increased risk of cardiovascular disease,[9,19] with the risk for myocardial infarction in female patients with RA being twice to three times higher than that of women without RA.[9] Anemia is, by far, one of the most common extra-articular manifestations of RA.[23] The cause of anemia in the case of RA is multifactorial: it is mainly caused by medications, gastrointestinal hemorrhage, or bone marrow suppression. Neurological manifestations in the form of peripheral neuropathy are not uncommon in patients with RA.[10] The underlying mechanism is small vessel vasculitis of the vasa vasorum of the nerves leading to ischemic neuropathy and demyelination. Cerebral strokes are common.
Rheumatoid nodules or endocrine manifestations have not been reported in endocrine organs in patients with RA. There has been, of course, an unusual case of active RA with a rheumatoid nodule developing at the thyroid bed after total thyroidectomy for Hashimoto's thyroiditis.[24] Note that the previously resected thyroid parenchyma was free of rheumatoid nodules. It is interesting, however, that while Hashimoto's autoimmune thyroiditis is usually accompanied by the presence of thyroid peroxidase (TPO) and thyroglobulin (TG) antibodies, focal lymphocytic thyroiditis is not; it may, however, represent an early subclinical form of autoimmune thyroiditis.[25] It appears, therefore, that rheumatoid nodules can develop independently of a thyroid background.
RA is a chronic inflammatory disease of an autoimmune nature characterized by articular involvement, often in the presence of RF and rheumatoid nodules. Although considered a joint disease, RA is not infrequently associated with extra-articular involvement. Yet, the reported case is the first described in endocrine gland parenchyma and was free of symptoms. Extra-articular RA is, in general, a severe condition, usually associated with an increased mortality rate. Early recognition and treatment are essential to the patients' welfare.
Abbreviations
anti-TG: Antithyroglobulin; anti-TPO: Thyroid peroxidase antibodies; RA: Rheumatoid arthritis; RF: Rheumatoid factor; T3: Triiodothyronine; T4: Thyroxine; TG: Thyroglobulin; TPO: Thyroid peroxidase; TSH: Thyroidstimulating hormone
Acknowledgements
The authors report no conflict of interest related to this study.
Funding
We declare no funding.
Availability of data and materials
All data and material were available to us except the cytological smear due to processing at a private laboratory, as mentioned in the text.
Ethics approval and consent to participate
Not applicable.
Consent for publication
Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for the review by the Editor-in-Chief of this journal.
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J Med Case Reports. 2019;13(159) © 2019 BioMed Central, Ltd.
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