Morphological criteria for sporadic multiple parathyroid gland disease

Background. There are no specific morphological signs for sporadic multiglandular disease (MGD) in primary hyperparathyroidism (PHPT).

The aim of the study. To study the structure of the morphological substrate of primary, secondary and tertiary hyperparathyroidism and to assess the effectiveness of morphological criteria in the diagnosis of sporadic multiglandular disease in primary hyperparathyroidism.

Methods. The study included 69  patients; 18  patients with PHPT and sporadic multiglandular disease (n_preparation  =  31) formed the main group, 51  patients (n_preparations  =  104) – the comparison group. The comparison group was divided into 3 subgroups: 1) patients with PHPT and solitary parathyroid gland (PTG) lesions – 26 patients (n_preparations = 26); 2) patients with secondary hyperparathyroidism (SHPT) – 15 patients (n_preparations = 48); 3) patients with tertiary hyperparathyroidism (TGPT) – 10 patients (n_preparations = 30).

Results. The morphological structure of the comparison groups is homogeneous: group  1 is represented by parathyroid adenoma (26  (100  %)), groups  2 and  3 – by hyperplasia (48 (100 %) and 30 (100 %), respectively). Most of the PTG specimens of the main group are represented by hyperplasia (25 (80 %)), and in 1/5 cases – by adenomas (6 (19.4 %)). Sporadic multiglandular disease in PHPT was characterized by a predominant frequency of detecting the absence of a capsule and a rim of unchanged tissue, as well as the presence of adipocytes (p_χ2 < 0.01). Components of the  PTG morphological structure make it possible to identify changes specific to  the  sporadic multiglandular disease in PHPT, with a diagnostic efficiency of 76.5–90.3 %.

Conclusion. Sporadic multiglandular disease in any clinical variant of hyperparathyroidism is characterized by a high prevalence of hyperplasia – 80 % in PHPT and 100  % in SHPT and  TGPT. The following morphological criteria for sporadic multiglandular disease in PHPT have been established: the presence of adipocytes in the PTG parenchyma (diagnostic efficiency (DE) – 90 %)); absence of a capsule (DE = 78 %) and a rim of unchanged gland tissue (DE = 76 %).

1. Mokrysheva NG, Eremkina AK, Mirnaya SS, Krupinova JA, Voronkova IA, Kim IV, et al. The clinical practice guidelines for primary hyperparathyroidism, short version. Problems of Endocrinology. 2021; 67(4): 94-124. (In Russ.). doi: 10.14341/probl12801

2. Bilezikian JP, Bandeira L, Khan A, Cusano NE. Hyperparathyroidism. Lancet. 2018; 391(10116): 168-178. doi: 10.1016/S0140-6736(17)31430-7

3. Barczyński M, Bränström R, Dionigi G, Mihai R. Sporadic multiple parathyroid gland disease – A consensus report of the European Society of Endocrine Surgeons (ESES). Langenbeck’s Arch Surg. 2015; 400: 887-905. doi: 10.1007/s00423-015-1348-1

4. Golokhvastov NN. Criteria for morphological diagnosis of adenoma and hyperplasia of the parathyroid glands in primary hyperparathyroidism. Saint Petersburg; 1995. (In Russ.).

5. Kazantseva IA, Kalinin AP, Bogatyrev OP. Principles of clinical and morphological examination of the parathyroid glands in hyperparathyroidism. Informational letter. Moscow; 1997: 3-15. (In Russ.).

6. Hemmer S. Cytogenetic and molecular genetic alterations in thyroid and parathyroid tumors. Helsinki; 2002.

7. Shakeel S, Mubarak M. Proliferative lesions of parathyroid glands: An update for practicing pathologists. J Coll Physicians and Surg Pak. 2016; 26(1): 51-59.

8. Chen KT. Fat stain in hyperparathyroidism. Am J Surg Pathol. 1982; 6(2): 191-192.

9. Corrado KR, Andrade SC, Bellizzi J, D’Souza-Li L, Arnold A. Polyclonality of parathyroid tumors in neonatal severe hyperparathyroidism. J Bone Miner Res. 2015; 30(10): 1797-1802. doi: 10.1002/jbmr.2516

10. Stojadinovic A, Hoos A, Nissan A, Dudas ME, Cordon-Cardo C, Shaha AR, et al. Parathyroid neoplasms: Clinical, histopathological, and tissue microarray-based molecular analysis. Hum Pathol. 2003;34(1):54-64. doi: 10.1053/hupa.2003.55

11. Palmieri S, Eller-Vainicher C, Cairoli E, Morelli V, Zhukouskaya VV, Verga U, et al. Hypercalciuria may persist after successful parathyroid surgery and it is associated with parathyroid hyperplasia. JClin Endocrinol Metab. 2015;100(7):2734-2742. doi: 10.1210/jc.2014-4548

12. Tominaga Y, Tanaka Y, Sato K, Nagasaka T, Takagi H. Histopathology, pathophysiology, and indications for surgical treatment of renal hyperparathyroidism. Semin Surg Oncol. 1997; 13(2): 78-86. doi: 10.1002/(sici)1098-2388(199703/04)13:2<78::aid-ssu3>3.0.co;2-z

13. Bersenev GA, Aldaranov GYu, Roy TA, Lebedeva DV. Comparative characteristics of the morphological manifestations of primary and secondary hyperparathyroidism. Sbornik tezisov XV Mezhdunarodnoy (XXIV Vserossiyskoy) Pirogovskoy nauchnoy meditsinskoy konferentsii studentov i molodykh uchenykh. Moscow; 2020: 140. (In Russ.)

14. Ilyicheva EA, Bersenev GA, Zharkaya AV, Bulgatov DA, Makhutov VN. Multiglandular parathyroid disease: The results of surgical treatment. Acta biomedica scientifica. 2020; 5(4): 90-97. (In Russ.). doi: 10.29413/ABS.2020-5.4.13