Abstract
Sjogren’s Syndrome is an autoimmune dysfunction of the exocrine glands that causes dryness of the eyes, mouth, skin. One of its worst complications is MALT lymphoma, which is caused by deregulation of B-cell proliferation. In this case report a female patient with primary Sjogren’s Syndrome presents a parotid swelling, concluded by biopsy that was a lymphoma. After resection, she was treated with rituximab. The immunotherapy caused the remission of the lymphoma and the symptoms of the primary disease. The use of immunotherapy might be an alternative to the traditional immunosuppressants used for Sjogren’s Syndromea.
Highlights
Sjogren’s Syndrome (SS) is a dysfunction of the exocrine glands in response to lymphocytic infiltration and deposition of immune complexes, which leads to a chronic condition and a progressive glandular destruction
The objective of this paper is to report a case of a patient who presented parotid lymphoma secondary to Sjogren’s Syndrome and was treated with rituxumab after a partial parotidectomy
Sjogren’s Syndrome is an autoimmune systemic disease characterized by lymphocyte infiltration into secretory glands causing dryness of the eyes, mouth, larynx, pharynx and vagina
Summary
Sjogren’s Syndrome (SS) is a dysfunction of the exocrine glands in response to lymphocytic infiltration and deposition of immune complexes, which leads to a chronic condition and a progressive glandular destruction. It is up to 40 times more likely to develop lymphoma in a patient with Sjogren’s Syndrome than in the general population [1]. The objective of this paper is to report a case of a patient who presented parotid lymphoma secondary to Sjogren’s Syndrome and was treated with rituxumab after a partial parotidectomy. 49 years old, diagnosed with primary Sjogren’s Syndrome (being the diagnostic clinical criteria xerostomia, dry eye, parotid hypertrophy and in the biopsy of parotid gland) in 2017, treated with azathioprine and prednisone for control [2]. Larger salivary gland parenchyma and architecture was extensively damaged by the presence of dense lymphoid proliferation, predominantly of small cells, in which multiple foci of lymphoepithelial lesions (epimioepithelial islands) are observed [3]. A marked atrophy of the acinar epithelium with lymphoid proliferation was observed permeating nerve threads and extending to the peri-glandular adipose tissue
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