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Hyperparathyroid crisis is a rare manifestation of parathyroid disease. We present the case of a 53-year-old gentleman with a review of the current literature. He presented in acute renal failure with epigastric pain and vomiting. His serum-corrected calcium (CCa2+) was raised at 5.2 mmol/L, in addition to a massively raised parathyroid hormone (PTH) level (3957 ng/L). Ultrasound studies of the neck revealed a 2 cm well-defined mass inferoposterior to right thyroid lobe. CT scans of the neck showed a normal mediastinum and confirmed no associated lymphadenopathy. Having undergone medical resuscitation for 9 days, a neck exploration revealed a cystic mass, which was excised. Histological investigations revealed a 9.25 g, cystic parathyroid adenoma with no features of malignancy. His PTH and CCa2+ returned to normal postoperatively. This suspicious presentation of benign disease, including a marked elevation in PTH, highlights the challenges facing the endocrine surgeon in dealing with parathyroid disease.

Introduction

Hypercalcemia can be associated with vitamin D (1,25(OH)2D3) -mediated granulomatous disorders in addition to primary hyperparathyroidism (PHPT). Although most patients with granulomatous disease-related hypercalcemia are asymptomatic, symptoms and signs of chronic hypercalcemia can occur. There are many reports about co-presentation of a parathyroid adenoma and a granulomatous disorder in the literature. However, granulomatous inflammation within a parathyroid adenoma is very rare.

Case presentation

A 50-year-old Caucasian woman presented with generalized bone pain and muscular weakness. Biochemical findings suggested PHPT. She underwent excision of an enlarged right inferior parathyroid gland. Histopathological analysis revealed features of a parathyroid adenoma with foci of epithelioid non-caseating granulomas. The etiology of the granulomatous infiltration could not be determined. She is still normocalcemic at the ninth month after surgery and is being followed for the possible manifestation of an occult disease.

Conclusion

Granulomatous infiltration of a parathyroid adenoma is a rare condition. Pathological examination of the excised adenoma is the only way to diagnose the underlying occult granulomatous disorder. Clinicians should also consider persistent hypercalcemia to be a possible indicator of concomitant parathyroid adenoma.

Objective

To describe a patient presenting with the rare constellation of synchronous parathyroid carcinoma, parathyroid adenoma, and papillary thyroid carcinoma.

Methods

Review of clinical presentation, diagnostic workup, surgical management, and pathological findings, and review of pertinent literature.

Results

The patient was a 59-year old man who presented with severe clinical manifestations of longstanding primary hyperparathyroidism (HPT), serum calcium of 14.4 mg/dL, and parathyroid hormone level of 2,023 pg/ml. The patient was found to have a 3.4 cm parathyroid carcinoma on the left side and a 3.2 cm papillary thyroid carcinoma on the right side. In addition, a 917 mg parathyroid adenoma was found on the right side.

Conclusion

Synchronous parathyroid and thyroid carcinomas are extremely rare. Our patient is the first documented case with a parathyroid adenoma in addition to synchronous parathyroid and thyroid carcinomas. The presence of concurrent parathyroid carcinoma and adenoma can cause diagnostic confusion and should be considered in patients presenting with severe HPT. Any concomitant thyroid nodules need to be investigated to rule out thyroid carcinoma.

Background

Parathyroid adenoma is the most common cause of primary hyperparathyroidism. Preoperative serum calcium and intact-parathyroid hormone levels are the most useful diagnostic parameters that allow differentiating primary hyperparathyroidism from non-parathyroid-dependent hypercalcemia. Parathyroidectomy is the definitive treatment for primary hyperparathyroidism. Approximately 5% of patients who underwent parathyroidectomy present with persistent or recurrent hyperparathyroidism due to ectopic localization of the adenoma. Functioning oxyphil parathyroid adenoma is an uncommon histological form, seldom causing primary hyperparathyroidism. Parathyroid adenoma with hypercalcemia exhibiting normal parathyroid hormone level is rare. An incidence of 5% to 33% has been documented in the literature; no etiologic explanation has been given. In 1987, parathyroid-hormone-related peptide was isolated as a causative factor of humeral hypercalcemia of malignancy. The presence of parathyroid-hormone-related peptide in parathyroid tissue under normal and pathological conditions has been described in the literature; however, its role in causing hyperparathyroidism has not yet been defined.

Case presentation

We present a case of persistent hypercalcemia with a normal level of intact-parathyroid hormone due to a substernal parathyroid adenoma, treated with radioguided parathyroidectomy. The final histological diagnosis was oxyphil adenoma, positive for parathyroid-hormone-related peptide antigens.

Conclusion

In clinical practice, this atypical biochemical presentation of primary hyperparathyroidism should be considered in the differential diagnosis of hypercalcemia. The parathyroid-hormone-related peptide should be considered not only in the presence of malignancy.

Primary hyperparathyroidism (PHPT) is not an uncommon endocrine disorder. However, acute primary hyperparathyroidism, or parathyroid crisis (PC), is a rare clinical entity characterized by life-threatening hypercalcemia of a sudden onset in patients with PHPT. We describe a patient with PC who presented with acute worsening of depressive symptoms, nausea and vomiting, and required emergency surgery. Serum calcium, alkaline phosphatase, and parathyroid hormone were elevated and serum phosphorus was low. An emergency hemithyroidectomy was performed because of none medical control of hypercalcemia. A giant intrathyroidal parathyroid adenoma was diagnosed. PHTP can be a life-threatening situation for patients, requiring immediate surgical treatment. A giant intrathyroidal parathyroid adenoma is an uncommon cause of PC.

INTRODUCTION

Parathyroid adenoma associated with a thymoma is a rare clinical entity and few cases have been reported in the literature. This association can be explained by the common embryologic origin of the parathyroid glands and the thymus. These patients may present only with clinical signs and symptoms of primary hyperparathyroidism making it difficult to suspect the coexistence of thymoma.

PRESENTATION OF CASE

A 68-year-old female with medical history of primary hyperparathyroidism underwent surgical excision of a single parathyroid adenoma. Intra-operatively a small mass was detected in the proximity of the parathyroid adenoma and was also removed. Pathologic examination revealed parathyroid adenoma as suspected pre-operatively whereas the small mass excised was identified as a type A thymoma. The postoperative course of the patient was favourable, with normal serum calcium levels and in six months follow-up the patient is symptom-free and with no recurrence.

DISCUSSION

Objective of this study is to report the rare case of a female adult with a parathyroid adenoma and a coexisting thymoma in order to underline the importance of these two pathologies and the ideal treatment that should be followed according to the latest records.

CONCLUSION

Surgical removal of parathyroid adenoma is the treatment of choice for primary hyperparathyroidism, with complete recovery and no postoperative complications. Thymoma may be associated with primary hyperparathyoridism, with or without clinical signs and symptoms of myasthenia gravis and this is a rare clinical entity as very few cases have been described worldwide. To our knowledge this is the first case reported in Greece.

Objective

To report the use of immunohistochemical staining for parafibromin, APC and galectin-3 to evaluate the malignant potential of the resected parathyroid specimen in a patient initially presenting with primary hyperparathyroidism secondary to four-gland hyperplasia who subsequently developed metastatic parathyroid carcinoma.

Methods

We describe a patient with primary hyperparathyroidism who underwent a 3 gland resection of hypercellular parathyroids with post-operative normalization of her serum calcium and parathyroid hormone levels. She returned four years later with recurrent hypercalcemia and underwent partial resection of her remaining hypercellular gland without improvement of her hypercalcemia. Selective venous sampling localized the source as draining into her azygous vein, and she was ultimately diagnosed with metastatic parathyroid carcinoma.

Results

Immunohistochemical staining for parafibromin, APC and galectin-3 suggested the malignant potential of the atypical adenoma removed during the patient’s original operation, which is believed to be the source of her metastatic disease. Access to this information by the treating surgeon may have prompted a more extensive en bloc resection or more vigilant follow-up that could have altered the patient’s clinical course.

Conclusion

Immunohistochemical staining for parafibromin, APC and galectin-3 can be used to help distinguish the source of metastatic disease in parathyroid carcinoma. Selective venous sampling may help localize metastatic parathyroid carcinoma when it is otherwise not apparent.

Introduction

Hypercalcaemic hyperparathyroid crisis is a rare but life-threatening complication of primary hyperparathyroidism. Parathyroid carcinoma is a rare malignancy with an incidence of 0.5% to 4% of all reported cases of primary hyperparathyroidism.

Case presentation

We report the case of a 60-year-old Caucasian man with hypercalcaemic hyperparathyroid crisis associated with parathyroid carcinoma. He presented with a classic hypercalcaemic syndrome and his serum calcium and parathyroid hormone levels were at 4.65 mmol/L and 1743 ng/L, respectively. He initially presented with a two-week history of weakness and lethargy and a one-week history of vomiting, polyuria and polydipsia. An emergency left thyroid lobectomy and left lower parathyroidectomy were performed. There was a prompt decrease in his parathyroid hormone level immediately after surgery. Histology revealed that our patient had a 4-cm parathyroid carcinoma.

Conclusion

In patients with parathyroid carcinoma, the optimal surgical treatment is en bloc resection with ipsilateral thyroid lobectomy and removal of any enlarged or abnormal lymph nodes. Surgery is the only curative treatment. In our patient, prompt surgical intervention proved successful. At six months the patient is well with no evidence of disease recurrence. This case highlights the importance of considering a hyperparathyroid storm in the context of a parathyroid carcinoma. Parathyroid carcinoma is a rare entity and our knowledge is mainly derived from case reports and retrospective studies. This case report increases awareness of this serious and life-threatening complication. This report also illustrates how prompt and appropriate management provides the best outcome for the patient.

A 60-year-old woman presented with abdominal pain and weight loss and was found to have serum calcium of 15.0 mg/dl. Serum parathyroid hormone-related peptide (PTHrP) returned elevated. Imaging suggested bilateral mature cystic teratomas. Her hypercalcemia was treated initially with intravenous saline, as well as intramuscular and subcutaneous calcitonin. She underwent total abdominal hysterectomy with bilateral salpingo-oophorectomy, and final pathology revealed malignant Brenner tumor in association with a mature cystic teratoma. Her postoperative PTHrP returned less than assay, and her total and ionized calcium fell below normal, requiring supplemental calcium and vitamin D. At follow-up one month after discharge, her calcium had normalized. We present the first reported case of hypercalcemia occurring in association with a malignant Brenner tumor. Malignancy-associated hypercalcemia occurs via four principal mechanisms: (1) tumor production of PTHrP; (2) osteolytic bone involvement by primary tumor or metastasis; (3) ectopic activation of vitamin D to 1,25-(OH)2 vitamin D, and (4) ectopic production of parathyroid hormone. PTHrP-mediated hypercalcemia is the most common mechanism and was responsible in this case. In patients with paraneoplastic hypercalcemia who undergo surgical treatment, close monitoring and management of serum calcium is necessary both pre- and postoperatively.

Introduction

In the treatment of secondary hyperparathyroidism of chronic kidney disease, calcimimetics - allosteric modulators of the calcium-sensing receptor - inhibit glandular hyperplasia and significantly reduce circulating parathyroid hormone levels. They have a major impact on the management of secondary hyperparathyroidism.

Case presentation

We present the clinical case of a 41-year-old Caucasian man undergoing chronic hemodialysis, who had a parathyroidectomy to treat severe secondary hyperparathyroidism resistant to cinacalcet treatment. Preoperatively, 24 months after high-dose cinacalcet hydrochloride, we observed a persistently elevated intact parathyroid hormone serum level, and detected clear parathyroid gland hyperplasia regression on ultrasound. We performed a three-gland parathyroidectomy, which was assumed to be total, associated with a hemithyroidectomy. Our patient then entered a hypoparathyroid state. A histopathological examination showed that the removed parathyroid glands were of small size, with a total weight of 1g, associated with a multifocal small papillary thyroid cancer.

Conclusion

In the management of secondary hyperparathyroidism, cinacalcet hydrochloride effectively reduces total parathyroid gland hyperplasia. However, a persisting elevated intact parathyroid hormone serum level may be observed, demonstrating that reduced parathyroid hyperplastic tissue may still be associated with severe secondary hyperparathyroidism. Even if calcimimetics are very effective in secondary hyperparathyroidism treatment, further studies are necessary for a better understanding of their actions.

Background

Parathyroid carcinoma is a rare cause of primary hyperparathyroidism and may be associated with significant disease related morbidity and mortality. Preoperative diagnosis remains a challenge, which may jeopardize appropriate and successful patient treatment.

Case presentation

We report a case of parathyroid carcinoma diagnosed in a 60-year-old woman that presented with a tender nodule located at the left lower thyroid pole and had been present for several years. Ultrasound examination revealed a 2.7 × 1.6 × 2.7 cm mass within the lower left lobe of the thyroid with cystic and solid areas. Lab measurement of the intact PTH level revealed it to be three times the upper limit of normal and the serum calcium level was within normal limits. A left thyroid lobectomy and isthmusectomy was carried out. Histopathological evaluation was diagnostic for a parathyroid carcinoma. At greater than two years of follow-up, the patient has had no evidence of disease recurrence and her serum PTH and calcium levels have remained within normal.

Conclusion

Parathyroid carcinoma is a rare endocrine tumor which must be considered in the differential diagnosis of a nodular thyroid mass. En bloc resection remains the treatment of choice for this malignancy. Disease prognosis is influenced by the extent of the initial resection, the presence of metastases, and adequate long-term follow-up.

Aim. Despite an incidence of parathyroid “incidentalomas” of 0.2%–4.5%, only approximately 135 cases have been reported in the literature. We present eight patients in whom an incidental abnormal parathyroid gland was found during routine thyroid surgery. We have reviewed the literature and postulate whether these glands could represent further evidence of a preclinical stage of primary hyperparathyroidism. Methods. A retrospective analysis of all 236 thyroid operations performed by a single surgeon was performed to identify patients in whom abnormal parathyroid tissue was removed at surgery. Results. 8/236 patients (3.39%) had a single macroscopically abnormal parathyroid gland removed and sent for analysis. Seven patients were found to have histological evidence of a parathyroid adenoma or hyperplasia. None of the patients had abnormal serum calcium detected preoperatively. Postoperatively, four patients had normal calcium, three had temporary hypocalcaemia and one refused followup. No patients had recurrent laryngeal nerve impairment. Conclusions. Despite the risk of removing a histologically normal gland, we believe that when parathyroid “incidentalomas” are found during surgery they should be excised and sent for histological analysis. We have found this to be a safe procedure with minimal morbidity to the patient. As the natural history of primary hyperparathyroidism is better understood, these glands found in normocalcaemic patients may in fact represent the early or preclinical phase of the disease. By removing them at the original operation, the patient is saved redo neck surgery with its high complication rate as or when clinically apparent primary hyperparthryoidism develops in the future.

We present a case of a parathyroid adenoma on the ipsilateral side of thyroid hemiagenesis—which, to our knowledge, is the third reported case of this entity. A 41-year-old man with nephrolithiasis was found to have elevated calcium and intact parathyroid hormone levels. Both ultrasound and technetium sestamibi scintigraphy with single photon emission computed tomography confirmed left thyroid hemiagenesis and an adenoma in the left inferior thyroid bed. The patient underwent left neck exploration, which confirmed left thyroid hemiagenesis and a left inferior parathyroid adenoma. The left inferior parathyroid gland was resected. The patient was discharged home the same day of surgery and has remained normocalcemic for 14 months without evidence of hyperparathyroidism.

A 63-year-old woman has had multiple repeated fractures. A diagnosis of primary hyperparathyroidism (PHPT) was made after she was found to be hypercalcaemic with an elevated level of intact parathyroid hormone (iPTH). Radiographs revealed classic and severe bone findings in PHPT, features which were common in the past but are thought to be rare at this modern age. She also had nephrolithiasis and osteoporosis. An enlarged parathyroid gland was seen on ultrasound and CT scan, and hyperfunction was demonstrated by scintigraphy. Parathyroidectomy was performed. Histopathologic analysis revealed a parathyroid adenoma. She developed the hungry-bone syndrome 7 days postoperatively, which resolved with with administration of calcium and calcitriol.

Introduction

To describe the use of combined preoperative imaging and intraoperative parathyroid hormone as a novel approach in the surgical management of a patient with tertiary hyperparathyroidism associated with X-linked hypophosphatemic rickets.

Case presentation

We present the first documented description of combined preoperative imaging and intraoperative parathyroid hormone as well as a review of the literature surrounding the surgical management of tertiary hyperparathyroidism in the setting of X-linked hypophosphatemic rickets.

A 23 year-old female with X-linked hypophosphatemic rickets and renal impairment presented with symptomatic hypercalcemia and tertiary hyperparathyroidism. She had failed medical management and presented for surgical evaluation. Technitium-99 m Sestamibi SPECT imaging and parathyroid ultrasound were used to localize the enlarged parathyroid glands preoperatively. Intraoperative findings correlated well with pre-operative imaging. She underwent successful subtotal parathyroidectomy for four-gland hyperplasia, using intraoperative parathyroid hormone guidance. Despite severe post-operative bone hunger, her serum calcium normalized and she experienced resolution of her preoperative symptoms.

Conclusion

X-linked hypophosphatemic rickets is an uncommon disorder of phosphate metabolism resulting in bone deformity. Patients are predisposed to the development of secondary hyperparathyroidism due to chronic vitamin D supplementation which may progress to tertiary hyperparathyroidism with autonomous parathyroid function. Preoperative evaluation with Technitium-99 m Sestamibi SPECT and ultrasound imaging, as well as the use of intraoperative parathyroid hormone are effective in guiding surgical resection. Subtotal parathyroidectomy with cryopreservation is indicated to produce operative cure and limit the risk of recurrence. Although these patients are susceptible to severe postoperative bone hunger, appropriate supplementation with intravenous and oral calcium can minimize hypocalcemic symptoms.

The case is described of a woman who died with a functioning parathyroid carcinoma 19 years after removal of two parathyroid tumours, considered at the time to be benign. Following operation hyperparathyroidism subsided, with a short period of hypocalcaemia, and severe osteitis fibrosa cystica healed. Five years before death progressive renal failure developed with normal and later raised serum calcium levels. At necropsy a parathyroid carcinoma infiltrated the thyroid at the site of the previous operation and there was a solitary hepatic metastasis. A remaining parathyroid gland was nodularly hyperplastic and the bones showed evidence of active osteitis fibrosa. The relationship between parathyroid hyperplasia and neoplasia is discussed. Acceptable cases of parathyroid carcinoma are rare, but carcinoma is an important cause of recurrent hyperparathyroidism even months or years after removal of an `adenoma'.

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Background

Thyroid hemiagenesis is a rare anomaly, more commonly seen on the left side (ratio 4:1) and in females (ratio 3:1). The first to describe this anomaly was Handfield Jones in 1852.

Case presentation

We present a 66 year old female patient with right thyroid hemiagenesis, parathyroid adenoma on the side of hemiagenesis and parathyroid hyperplasia on the contralateral side. The patient had neck pain and was diagnosed as Hashimto thyroiditis with hyperparathyroidism. Parathyroid hormone, thyroglobulin antibodies (Tg-Ab) and thyroid peroxidase antibodies (TPO-Ab) were elevated. Neck ultrasound and technetium 99mTc-methoxyisobutyl isonitrile (MIBI) scintigraphy confirmed the right thyroid hemiagenesis, but not adenoma of parathyroid glands. Intraoperatively, right thyroid hemiagenesis was confirmed and left loboistmectomy was performed with removal of left inferior hyperplastic parathyroid gland. Postoperative PTH (parathyroid hormone) levels were within normal range. Five months after the operation PTH level was elevated again with calcium values at the upper limit. MIBI scintigraphy was performed again which showed increased accumulation of MIBI in the projection of the right parathyroid gland. Surgical reexploration of the neck and excision of the right upper parathyroid adenoma was performed which was located behind cricoid laryngeal cartilage. After surgery a normalization of calcium and PTH occured.

Conclusion

From available literature we have not found the case that described parathyroid adenoma on the side of thyroid hemiagenesis,with parathyroid hyperplasia on the contralateral side.

A 71 yo woman with primary hyperparathyroidism awaiting surgery because of significant hypercalcemia and hypercalciuria presented to the local emergency department with the chief complaints of discomfort in her neck, sore throat, and difficulty swallowing. She was found to be hypocalcemic with a calcium level of 8.1 mg/dL. She was seen by her endocrinologist three days later at which time serum calcium, iPTH, and serum phosphate levels were all within normal limits. Based on history and a series of ultrasounds the patient was diagnosed with spontaneous infarction of her parathyroid adenoma, which resulted in resolution of her primary hyperparathyroidism.

A patient admitted for acute abdomen was incidentally found with elevated serum calcium level. In surgery, under conservative treatment of the hypercalcemia, a perforated duodenal ulcer was found and simple closure was performed. Postoperatively, calcium level continued to rise, parathyroid hormone was elevated and ultrasonographic examination showed a lesion in the right anterior neck, while serum gastrin level was normal, thus documenting the diagnosis of primary hyperparathyroidism. Conservative treatment had no effect on calcium level and the patient was subjected to emergency neck exploration, where a large parathyroid adenoma was removed. After surgery, calcium and PTH levels were normalized and the patient was discharged on the 5th postoperative day. Peptic ulcer and its complications are usual manifestations of primary hyperparathyroidism, with or without increased gastrin level. On the other hand, cases of a perforation of peptic ulcer as the first clinical manifestation of primary hyperparathyroidism are extremely rare.

The case history of a 40-year-old woman with a fatal haemorrhage from a duodenal ulcer, jejunitis, renal lithiasis, hypertrophy of the adrenal glands, multiple adenomas of the pancreas, and three adenomas of both the parathyroid and pituitary glands is reported. Though there was histological evidence, in the bones, of hyperparathyroidism, the serum levels of calcium, phosphorus, and phosphatase and the urinary excretion of calcium were normal.

The significance of low calcium and high phosphorus excretion in the urine as an indication of parathyroid disorder is discussed.

“Multiple endocrine adenoma syndrome” is suggested as the appropriate designation for the clinical disorders in which adenomas of one or more endocrine glands are associated with disorders of the alimentary tract when patients present with recurrent peptic ulceration, pancreatic dysfunction, or watery diarrhoea.

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We report a case of parathyroid hormone-related protein-mediated hypercalcemic crisis in a 36-year-old pregnant woman, who was admitted to women hospital with recurrent vomiting and epigastric pain. She was diagnosed with uterine fibroid since the first month of her pregnancy, but the pregnancy had been uneventful. Serum calcium was 4.8 mmol/l, while parathyroid hormone was low. Hypercalcemia was attributed to humoral hypercalcemia associated with uterine fibroid as other causes of hypercalcemia were excluded.

No clinical or laboratory data allow a preoperative diagnosis of parathyroid carcinoma and only occasionally does a definitive finding differentiate an adenoma from a carcinoma. We present a case of primary hyperparathyroidism presenting with severe elevation of parathyroid hormone and serum calcium as well as complications. We go on to discuss the case in the light of a literature review. The severity of the elevation of the parathyroid hormone, other biochemical alterations, the presence of skeletal and renal complications and of a neck mass should alert the clinician to a possible parathyroid carcinoma. Radical surgery is the only effective therapy for parathyroid carcinoma, and should always be performed if a preoperative suspicion is entertained.

Two cases of vitamin D deficient osteomalacia with secondary hyperparathyroidism are presented. In both cases treatment with vitamin D replacement therapy resulted in elevated calcium levels and a failure of parathormone levels to normalise, indicating autonomous parathyroid activity. Subsequent surgery in one case resulted in removal of a parathyroid adenoma. The importance of osteomalacia and its complications are discussed.

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Objective:

To present a case of hypercalcemia associated with thyrotoxicosis in a patient with vitamin D deficiency and review biochemical changes during the course of treatment.

Methods:

We report a case, describe the changes in serum calcium, phosphorus, parathyroid hormone in Graves’ disease and concomitant Vitamin D deficiency. We compare our findings to those reported in literature.

Results:

Our patient had hypercalcemia secondary to thyrotoxicosis alone, which was confirmed by low parathyroid hormone level and resolution of hypercalcemia with treatment of thyrotoxicosis. The case was complicated by a concomitant vitamin D deficiency. Serum calcium elevation in patients with thyrotoxicosis occurs secondary to hyperthyroidism alone or due to concurrent hyperparathyroidism. Hypercalcemia from thyrotoxicosis is usually asymptomatic and is related to bone resorption. Vitamin D deficiency can be seen in patients with thyrotoxicosis because of accelerated metabolism, poor intestinal absorption and increased demand during bone restoration phase. Coexistence of hypercalcemia and Vitamin D deficiency in patients with thyrotoxicosis is rare, but possible, and 25-hydroxyvitamin D levels should be checked. The definite treatment for hypercalcemia in thyrotoxicosis is correction of thyroid function.

Conclusion:

Hypercalcemia in thyrotoxicosis should be distinguished from concomitant hyperparathyroidism and confirmed by resolution of hypercalcemia with control of thyrotoxicosis. Patients with hypercalcemia and thyrotoxicosis may also have vitamin D deficiency and 25-OH Vitamin D levels should be checked.

A patient with many symptoms and signs of primary hyperparathyroidism had hypocalcaemia when first seen. Bone section histology showed osteomalacia and osteitis fibrosa, and the hyperparathyroidism at this stage was considered to be secondary to osteomalacia with postgastrectomy steatorrhoea. On treatment with vitamin D (with disappearance of her bone pains and weakness) she developed hypercalcaemia. She regained her health after removal of a 6-g. parathyroid adenoma. Normal histology was shown in another parathyroid gland.

We believe that the initial hypocalcaemia was due to vitamin-D deficiency, which produced ineffective hyperparathyroidism until it was corrected. A review of the few reports of patients with autonomous hyperparathyroidism with steatorrhoea and osteomalacia does not support the argument that these patients had “tertiary” disease. It suggests that most of them, like our patient, had primary hyperparathyroidism.