This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Pavlovic, D. Articles by Brzac, H. T. Search for Related Content PubMed PubMed Citation Articles by Pavlovic, D. Articles by Brzac, H. T.

Unusual Changes in Parathyroid Glands in Patients with Chronic Renal Failure¹

Drako Pavlovi

Sveti Duh General Hospital Zagreb, Croatia

Hrvojka Tomi Brzac

Clinical Hospital Rebro, University of Zagreb Zagreb, Croatia

We were interested to read the recent paper of Nylen et al. (1). We would like to present four patients with severe secondary hyperparathyroidism and with unusual changes in the parathyroid glands (PTG).

In the first patient all four PTG were enlarged, the lower left one being greater than the other three.(2) The volume of that gland was 3.92 cm³, and initially fine-needle aspiration biopsy (FNAB) showed parathyroid cell hyperplasia. Four months after FNAB was performed, the patient felt sudden pain in the left side of her neck. She observed a red patch on the skin surface, about 2 cm in diameter. She had elevated body temperature (37.5 C) and elevated erythrocyte sedimentation rate (41 mm/hr). Parathormone (c-terminal) was 1600 pmol/L (normal range 15–40 pmol/L). Thyroid hormone, TSH, and T3 tests were within the normal limits, and no thyroid antibodies were detected. Thyroid echography (real time, 7.5 MHz) showed regular patterns in both lobes. All four PTG were visualized, the lower left one being larger than 4 months before (volume was 9.1 cm³). FNAB showed moderate parathyroid cell proliferation with multiple granulocytes, histiocytes, and clusters of fibroblasts, suggesting an inflammatory process. Lymphatic cells were observed. After 3–4 days the pain in the neck ceased spontaneously, body temperature returned to normal, but no changes in parathormone level were detected. Six months later, the volume of the lower left PTG was 0.66 cm³ and FNAB showed clusters of parathyroid cells reacting positively to argyrophilic granules, some phagocytes, and no fibroblasts or inflammatory cells.

We believe that acute inflammation of the largest PTG of unknowen etiology occurred in this patient. A possible viral etiology of the inflammation, similar to subacute thyroiditis, remains an open question. On the other hand, the inflammatory reaction could hardly have occurred consequentially to the FNAB performed 4 months earlier.

The next three patients (3) came to us with similar clinical symptoms, i.e. symptoms like subacute thyroiditis. They all had neck pain and swelling, two had fever, and one hoarseness. Thyroid tests were normal, and we excluded subacute thyroiditis. Parathormone level was 1280 pmol/L, 1000 pmol/L, and 1120 pmol/L, respectively. On echographic examination all patients had enlargements: one of PTG, two with inhomogenously patterns, and one with cystic changes. The volume was 8.5 cm³, 9.1 cm³, and 32.5 cm³,respectivly. The glands were more than twice as big as 3–4 months earlier. FNAB were performed. Normal parathyroid cells, degenerate damaged cells, foreign body giant cells, histiocytes, and degenerate changes in nuclei were found with fibroblasts in one patient. All symptoms decreased after a few days. Four to eight months later significant reduction of PTG volume was noticed, 0.6 cm³, 0.5 cm³, and 4.8 cm³ respectively. Later, one patient was operated upon, and hemorrhagic changes and fibrosis were found in the PTG.

In our opinion hemorrhage was the main cause of sudden PTG enlargement in patients with subsequent fibrosis and spontaneous sclerosis of the gland. Clinical and cytological findings with signs of inflammation suggest that other factors could be responsible for acute changes in PTG. Remission of the hyperparathyroidism in our patients did not occur following enlargement of the other PTG.

Secondary hyperparathyroidism is one of the most common complications in patients with chronic renal failure. The mechanism leading to secondary hyperparathyroidism is not completely understood. It is known that factors involved in the pathogenesis of secondary hyperparathyroidism are phosphorus retention, decreased levels of calcitriol, relatively low levels of calcium, abnormal parathyroid gland function, and skeletal resistance to parathormone action. (4, 5). The control of normal parathyroid cell growth, division, and death is not completely understood, but the increase in PTG size, caused by diffuse parathyroid hyperplasia in chronic renal failure is well known.(6) The degree of hyperplasia is different among PTG in the same patient.(6, 7) In long-standing dialysis patients, nodular parathyroid growth occurs within diffuse hyperplastic tissue. PTG with nodular patterns of growth are larger (6). All of our patients had very large PTG, i.e. volume was more than 3 cm³, and is it possible that glands with nodular patterns are more susceptible to spontaneous necrosis and hemorrhage. At present, however, this view is speculation.

Based on our experience (2, 3) and on the results of Nylen and colleagues (1), we believe that our knowledge of parathyroid pathology is insufficient at this time. New diagnostic methods, particularly ultrasound and FNAB (7, 8), may teach us more about the pathologic changes in parathyroid glands in primary, secondary, and tertiary hyperparathyroidism.

Footnotes

¹ Address correspondence to: Dr. Drako Pavlovi, Sveti Duh General Hospital, 10000 Zagreb, Sveti Duh 64, Croatia.

Received July 31, 1996.

References

1. Nylen E, Shah A, Hall J. 1996 Spontaneous remission of primary hyperparathyroidism from parathyroid apoplexy. J Clin Endocrinol Metab. 81:1326–1328.[CrossRef][Medline]
2. Tomi Brzac H, Pavlovi D, repinko I. 1991 Spontaneous inflammation-induced remission of parathyroid tumour in secondary hyperparathyroidism. Nephrol Dial Transplant. 6:134–138.
3. Tomi Brzac H, Pavlovi D, Bence-igman Z, Halbauer M, repinko I. Unexpected echographic changes of parathyroid tumour in secondary hyperparathyroidism. The 7th Congress of the European Federation of Societies for Ultrasound in Medicine and Biology, Jerusalem, 1960, p 261 (Abstract).
4. Slatopolsky E, Delmez JA. 1994 Pathogenesis of secondary hyperparathyroidism. Am J Kidney Dis. 23:229–236.
5. Cunningham J. 1996 Parathyroid pathophysiology in uremia. Nephrol Dial Transplant. 11(Suppl 3):106–120.
6. Drueke TB. 1995 The pathogenesis of parathyroid gland hyperplasia in chronic renal failure. Kidney Int. 48:259–272.[Medline]
7. Tomi Brzac H, Pavlovi D, Halbauer M, Pasini J. 1989 Parathyroid sonography in secondary hyperparathyroidism: correlation with clinical findings. Nephrol Dial Transplant. 4:45–50.[Abstract/Free Full Text]
8. Halbauer M, repinko I. Tomi Brzac H, imonovi I. 1991 Fine needle aspiration cytology in the preoperative diagnosis of ultrasonically enlarged parathyroid glands. Acta Cytol. 35:728–735.[Medline]

This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Pavlovic, D. Articles by Brzac, H. T. Search for Related Content PubMed PubMed Citation Articles by Pavlovic, D. Articles by Brzac, H. T.