Plasma cell granuloma of the thyroid: A case report and review of the literature

Archives of Pathology & Laboratory Medicine,  May 2002  by Martinez, Fernando,  Filipowicz, Ewa,  Hudnall, S David

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* Plasma cell granuloma of the thyroid is an uncommon lesion; only 6 cases have been reported in the English literature to date. All reported cases occurred in women, mostly after the age of 50 years. We report a case of plasma cell granuloma of the thyroid in a 46-year-old woman with a 20-year history of euthyroid goiter and a positive family history of goiter in 3 close relatives. The lesion was composed of sheets of plasma cells involving the entire parenchyma that histologically resembled plasmacytoma. Plasmacytoma was excluded by demonstration of polyclonal kappa/lambda light chain immunostaining and by lack of evidence of clonal bands by polymerase chain reaction for immunoglobulin heavy-chain gene rearrangement. Similarly, the predominant histologic pattern in all previously reported cases is that of marked plasma cell infiltration. A family history of thyroid disease (goiter, thyroiditis) was associated with diffuse involvement of the thyroid. Prognosis after surgery is excellent, and to our knowledge no cases of malignant transformation or recurrence have been described.

(Arch Pathol Lab Med. 2002;126:595-598)

Plasma cell granuloma (PCG) of the thyroid is an uncommon lesion; a search of the English literature identified only 6 previously reported cases. Although considered by some authorities as a form of inflammatory myofibroblastic tumor (IMT; also referred to as inflammatory pseudotumor), the histologic features of PCG of the thyroid differ so significantly from those of IMT that classification as a distinct entity appears justified. Inflammatory myofibroblastic tumor encompasses a heterogeneous group of benign tumors characterized by various degrees of myofibroblastic proliferation and chronic inflammation.1 Plasma cell granuloma of the thyroid, on the other hand, is characterized by diffuse infiltration of the thyroid parenchyma by a benign plasmacytic infiltrate without myofibroblastic infiltration. We report the detailed pathologic and immunophenotypic features of a case of PCG of the thyroid in a 46-year-old woman with a long history of euthyroid goiter and a strong family history of goiter, and we present a comprehensive review of the literature.

REPORT OF A CASE

A 46-year-old black woman with history of goiter since the age of age 25 years presented to an outpatient clinic with a large painless neck mass. Her only concern was cosmetic, and she had no other symptomatology. Her mother and 2 brothers were affected by goiters that required subtotal thyroidectomy. Specific pathologic diagnoses were unavailable for review. Physical examination revealed a nontender enlarged thyroid gland. The patient's thyroid-stimulating hormone levels were normal. The entire gland was surgically removed, and her postsurgical course was uneventful.

The specimen weighed 241 g and measured 11.0 x 10.0 x 5.5 cm. The cut surface was fleshy and nodular with 3- to 15-mm oval nodules separated by fibrous bundles (Figure, a). No capsule was present. Numerous plasma cells with occasional Russell bodies surrounded thyroid follicles with HUrthle cell changes (Figure, b). Inconspicuous fibrous bands with only rare smooth muscle actin-positive, ALK-1-negative myofibroblasts divided the infiltrate into small nodules. Some thyroid follicles contained CD68-positive multinucleated giant cells within the colloid (Figure, c). Scattered lymphocytes and macrophages were present throughout the infiltrate, and a few small reactive lymphoid follicles were present. The plasma cells were CD20 negative (Figure, d) and had a cytoplasmic kappa/lambda ratio of 4:1 (Figure, e and fi. The mitotic rate was low; less than 5% of the plasma cells were Ki67 positive (Figure, g). Most of the small lymphoid cells were CD3-positive T cells (Figure, h). Polymerase chain reaction analysis for immunoglobulin heavy-chain gene rearrangement revealed no distinct clonal bands, thus confirming the reactive polyclonal nature of the infiltrate.

COMMENT

The clinicopathologic features of all 7 reported cases of PCG of the thyroid are presented in the Table. All cases occurred in adult women and showed no apparent racial predilection.2 All cases were characterized by a marked polyclonal plasma cell infiltration of the thyroid parenchyma. In 4 cases thyroid involvement was focal,2-5 while in 3 cases (including the present case) the entire gland was involved.6,7 Authors described the diffuse lesions as unencapsulated, firm, gray-white nodular lesions, whereas the focal lesions were circumscribed but unencapsulated nodules. Right and left lobes of the thyroid were affected equally. The lesions evolved over variable periods of time, ranging from "recent onset" to 20 years (present case). In 2 cases the lesion arose within goiters, and in 1 case from Hashimoto thyroiditis.7 Thyroid function tests were reported in 5 cases; 3 cases were hypothyroid, while 2 cases (including our case) were euthyroid (Table). Although tracheat deviation and paratracheal adhesions have occurred, in no case was there extension of the infiltrate to extrathyroid sites. Concomitant marrow plasmacytosis was described in only 1 case.6 However, this patient was reported as alive and well 10 years postthyroidectomy, with no apparent development of plasma cell dyscrasia. Hurthle cell change of thyroid parenchyma has been reported only in glands with generalized involvement (present case and others6,7). In only 2 cases (ours and 1 other 6) was a positive family history of thyroid disease described. In both of these cases, the process was generalized rather than localized.