Parathyroid adenoma apoplexy as a temporary solution of primary hyperparathyroidism: a case report

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Journal of Medical Case Reports

BioMed Central

Open Access

Case report

Parathyroid adenoma apoplexy as a temporary solution of primary hyperparathyroidism: a case report Francisco A Pereira, Daniel F Brandão, Jorge Elias Jr and Francisco JA Paula* Address: Department of Internal Medicine, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil Email: Francisco A Pereira - [email protected]; Daniel F Brandão - [email protected]; Jorge Elias - [email protected]; Francisco JA Paula* - [email protected] * Corresponding author

Published: 17 November 2007 Journal of Medical Case Reports 2007, 1:139


Received: 14 February 2007 Accepted: 17 November 2007

This article is available from: © 2007 Pereira et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract Introduction: The natural history of patients with spontaneous parathyroid necrosis is unknown. In this case report we describe the clinical course, laboratory, radiographic, bone densitometry tests, parathyroid ultrasonography and scintigraphy examinations of a patient performed over a period of eight years after she first presented with a sudden episode of spontaneous resolution of primary hyperparathyroidism (PHPT). Case presentation: A 24-year-old woman with a clinical history and laboratory and radiographic tests compatible with PHPT suffered a sudden episode of cervical pain and presented with clinical evidence of hypocalcemia. Biopsy of a cervical nodule revealed necrotic material compatible with ischemia of the parathyroid. The follow-up of the patient presented four distinct phases: the first, which lasted two years, was compatible with a period of bone hunger during which it was necessary to introduce calcitriol and calcium carbonate. During this period, the patient showed bone mass gain. The second phase was characterized by normalization of calcium and parathyroid hormone levels and its end was difficult to define. During the third phase there was a recurrence of hypercalcemia associated with elevated parathyroid hormone (PTH) levels and loss of bone mass. The last phase corresponded to the interval after parathyroidectomy, which was characterized by normalization of serum levels of calcium and PTH, as well as bone mass gain. Conclusion: This case report indicates that spontaneous resolution of PHPT by adenoma necrosis is potentially temporary. Thus, in cases in which a conservative approach is chosen, clinical and laboratory follow-up is indispensable. Bone mass measurement is a useful tool in the follow-up of these cases. However, this option exposes the patient to a potential roller-coaster ride of bone mass gain and loss, whose long term consequences are still unknown.

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Journal of Medical Case Reports 2007, 1:139

Introduction Although the natural history of primary hyperparathyroidism (PHPT) is incompletely understood, in many cases the calcium level remains stable when monitored on a regular basis [1,2]. In parallel, over the last two decades the number of reported cases that do not follow this pattern has increased [3]. The first case of cyclic PHPT was recently reported [4] and sporadic cases of spontaneous resolution due to apoplexy of parathyroid adenomas have been reported more frequently [3,5,6]. In the latter situation most patients were submitted to early surgery or were followed for as long as 30 months but this did not include bone mass evaluation. In this case study we report the details of a patient who presented with spontaneous remission of PHPT and was followed for eight years after the apoplexy episode, at which time she presented with recurrence of hypercalcemia. In this case, in addition to obtaining clinical and laboratory documentation, the authors prospectively evaluated the patient's bone densitometry.

Case presentation In 1998, a 24-year-old white female attended the endocrinology outpatient clinic of the Medical Center of the School of Medicine of Ribeirão Preto, USP, with complaints of bone pain and muscle weakness of ten years duration. She reported pain intensification in the upper and lower limbs for the past two years. In addition, over the past year she had started to develop nocturia, asthenia, and weight loss of about 8 kg. She also had had episodes of renal colic. She reported that long bone radiography had shown evidence of bone lesions. According to the patient, a bone biopsy had revealed the presence of a benign tumor. When seen at our outpatient clinic, the patient was found to be in good general condition, without any detectable cervical nodule. The patient had

already had the following tests: calcium = 11.9 mg/dl, phosphorus (Pi) = 1.8 mg/dl, and alkaline phosphatase (ALP) = 1642 U/L. The initial by in our service confirmed the previous biochemical profile: calcium = 11.9 mg/dl (8.5–10.5 mg/dl), phosphorus = 1.7 mg/dl (2.5–4.5 mg/ dl), ALP = 2352 U/L (40–160 U/L), creatinine = 0.5 mg/dl (0.7–1.1 mg/dl) chloride = 106 mEq/L (98–106 mEq/L), ionized calcium Ca++ = 1.57 mmol/L (1.14–1.29 mmol/ L), and chloride/Pi ratio = 62.3 (
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