Final Diagnosis -- Papillary thyroid carcinoma


FINAL DIAGNOSIS:

  1. PAPILLARY THYROID CARCINOMA, DIFFUSELY INVOLVING BOTH THYROID LOBES WITH METASTASIS TO 5 OF 5 LYMPH NODES.
  2. BACKGROUND THYROID WITH SEVERE CHRONIC LYMPHOCYTIC THYROIDITIS IN A FOLLICULAR DESTRUCTIVE PATTERN.

DISCUSSION:

Papillary carcinoma is the most common type of thyroid carcinoma accounting for approximately 70% of total cases of thyroid carcinoma; however, it only accounts for 1% of overall cancers in the US. Most papillary carcinomas are diagnosed between the ages of 20 and 50 years old. It is more common in females than males (4:1). Papillary carcinomas usually presents as solitary thyroid nodules that are generally cold on radioactive iodine scan (1). Approximately 10-15% of patients have metastases to lymph nodes or (more rarely) lung at the time of presentation; however, the prognosis is excellent with a mortality rate of 5% (2). Poor prognostic factors include age above 40 years, high grade, extensive tumor spread, and size of tumor (7).

There are many different variants of papillary thyroid carcinoma. One variant is diffuse sclerosing. The criteria to diagnose diffuse sclerosing variant includes: diffuse involvement of one or both lobes, numerous small papillary fronds in intrathyroidal clefts, extensive squamous metaplasia, abundant psammoma bodies, marked lymphocytic infiltration, and prominent fibrosis (2). Other characteristics of diffuse sclerosing variant include a high incidence in children and young adults. It is more common in women and is typically more aggressive than typical papillary thyroid carcinoma (8). In this particular case, squamous metaplasia was not present; therefore, this tumor actually does not technically meet the criteria for the diffuse sclerosing variant of papillary thyroid carcinoma. A recent paper documented a case of the simultaneous occurrence of diffuse sclerosing variant of papillary thyroid carcinoma and Graves disease (10). Diffuse sclerosis variant can be a difficult diagnosis to make especially when there is inflammation secondary to another process.

Another interesting aspect of this case is the patient's history of lithium use. It is well known that lithium affects the thyroid gland. Studies have shown lithium increases iodine content in the thyroid, as well as inhibits the secretion of T3 and T4 (3). Approximately half of the patients on lithium have goiter. Usually the thyroid is enlarged but not nodular. Furthermore, cigarette smokers have a greater increase in thyroid size than nonsmokers (5). There has been some controversy over whether lithium causes hypothyroidism. A study done by Bocchetta et al. showed that the incidence of hypothyroidism in patients on lithium was not significantly different than the general population (5). Johnston and Eagles, however, found the prevalence of hypothyroidism among patients on lithium to be 10.4% versus 3.2% in the general population (4). Most studies, with the exception of Bocchetta's, have shown that taking lithium does in fact increase one's risk of hypothyroidism. In this case, the patient did have clinical hypothyroidism which prompted the ultrasound and FNA which led to a thyroidectomy.

There is some evidence that lithium itself may cause an autoimmune thyroiditis, which might be part of the reason for clinical hypothyroidism (6). The pattern is usually one of follicle destruction, as was seen in this case. One study showed an increase in antithyroid antibodies in depressed patients treated with lithium as compared with depressed patients treated with other drugs (9). Any patient taking lithium should be followed for possible thyroid changes.

REFERENCES:

  1. DeLellis RA, Lloyd RV, Heitz PU, Eng C, editors. WHO Pathology and the Genetics of Endocrine Organs. 2004.
  2. Rosai J, Carcangiu ML, and DeLellis RA. Atlas of tumor pathology: Tumors of the thyroid gland. AFIP. Third series, fasicle 5, 1992.
  3. Ahmad-Abhari S, Ghaeli P, Fahimi F, Esfahanian F, Farsam H, Dehpour A, Jahanzad I, Hatmi Z, Dashti S. Risk factors of thyroid abnormalities in bipolar patients receiving lithium: a case control study. BMC Psych. 2003, 3:4.
  4. Johnston AM and Eagles JM. Lithium-associated clinical hypothyroidism: prevalence and risk factors. Br J of Psych. 175; 336-339, 1999.
  5. Bocchetta A, Cherchi A, Loviselli A, Mossa P, Velluzzi F, Derai R, Zompo M, Six-year follow-up of thyroid function during lithium treatment. 94(1); 45-48, 1996.
  6. Surks, MI, ed. Lithium and the thyroid. Up-to-date, May 2004.
  7. Rice DH and Batsakis JG. Surgical Pathology of the Head and Neck. 2000.
  8. Barnes L, editor. Surgical Pathology of the Head and Neck. 2nd ed, 2001, vol 3.
  9. Wilson R, McKillop JH, Crocket GT, et al. The effect of lithium therapy on parameters thought to be involved in the development of autoimmune thyroid disease. Clin Endocrin., 34; 357, 1991.
  10. Paner GP, Hunt JL, Ciesla MC, DeJong S, and LiVolsi V. Simultaneous diffuse sclerosis variant of papillary thyroid carcinoma and diffuse toxic hyperplasia (Graves' disease). Endo Path, 15(1): 77-82, 2004.

Contributed by Deborah Marks, MD and Jennifer Hunt, MD




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