A Case of Primary Hyperparathyroidism With Spontaneous Remission Following Infarction of the Adenoma With Development of Hypocalcemic Tetany

Johnston, C. Conrad; Schnute, Richard B.

doi:10.1210/jcem-21-2-196

Cited by 31 publications

(11 citation statements)

References 3 publications

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“…This may be due to delayed presentation, but agrees with some case reports of patients with normal or low calcium concentration at the time of presentation 12 8 11 Of those cases in whom PTH concentration had been measured at the time of presentation, most showed a decrease in PTH soon after the episode of necrosis 29 However, our patient had a persistently raised PTH level at presentation and subsequently showed a further rise to 49.4 pmol/l.…”

Section: Discussionsupporting

confidence: 89%

“…So far, only around 10 cases have been reported in the literature. Its presentation can be quite variable, including pressure symptoms due to haemorrhage,3-6 neck pain,7-9 hypercalcaemia due to acute release of stored PTH,10 hypocalcaemia due to autoparathyroidectomy,1 2 8 11 or normalisation of plasma calcium 912 13 The biochemical changes can be drastic if there is significant necrosis, and death has been reported due to severe hypercalcaemia 10.…”

Section: Discussionmentioning

confidence: 99%

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Spontaneous necrosis of parathyroid adenoma: biochemical and imaging follow-up for two years

Chan

Chow

King

et al. 2000

Postgraduate Medical Journal

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SummaryWe report a patient with a biochemically and radiologically confirmed parathyroid adenoma, which underwent spontaneous resolution by necrosis. The patient was followed-up over the subsequent two years during which time the tumour and hypercalcaemia recurred. Sequential radiological and biochemical changes at the time of diagnosis, spontaneous necrosis and recurrence are documented fully. Keywords: hyperparathyroidism; hypocalcaemia; apoplexy Primary hyperparathyroidism is one of the commonest endocrine disorders. However, spontaneous resolution by necrosis of a parathyroid adenoma is rare. Although there have been approximately 10 reported cases since the condition was first described in 1946, 1 in most cases the infarcted gland was removed soon after diagnosis. Therefore, the natural history, biochemical and hormonal changes following spontaneous infarction are not well known. We report a patient who had spontaneous infarction of her parathyroid adenoma, while awaiting surgery, with detailed documentation of the above-mentioned features. Case reportA 78-year-old woman was referred to our clinic for further management of Type 2 diabetes. She gave a history of renal stone, with right nephrectomy, 8 years before. She was put on oral hypoglycaemic therapy. She was found incidentally to have hypercalcaemia with a calcium concentration of 3.43 mmol/l (normal range 2.20-2.62 mmol/l) together with a reduced phosphate concentration of 0.55 mmol/l (0.82-1.40 mmol/l). Alkaline phosphatase was normal at 85 IU/l (45-145 IU/l). There was renal impairment with a plasma creatinine concentration of 160 µmol/l (44-107 µmol/l), but she had stable glycaemic control as indicated by a HbA 1c concentration of 7.4%. Physical examination revealed mild peripheral neuropathy and the nephrectomy scar, but no obvious neck mass. Further investigations confirmed primary hyperparathyroidism. Her parathyroid hormone (PTH) was 44 pmol/l (1.16-5.67 pmol/l, intact PTH assay; coefficient of variation 7%) with concomitant plasma calcium of 3.40 mmol/l and ionized calcium of 1.61 mmol/l (1.13-1.32 mmol/l).Ultrasound of the abdomen confirmed the previous right nephrectomy but showed no other abnormality. Her hypercalcaemia improved to approximately 2.8 mmol/l with adequate hydration, a low calcium diet and oral phosphate solution. She was referred for parathyroidectomy and was on the waiting list for surgery. During subsequent follow-up, her alkaline phosphatase gradually increased to 1465 IU/l, indicating development of parathyroid bone disease. Her glycaemic control was stable on oral hypoglycaemic therapy and there was no further deterioration of diabetic complications.She was put on the waiting list for surgery, which was very long in our hospital. Two years later, she underwent pre-operative imaging to localise the parathyroid adenoma. Computed tomography (CT) showed a 2.5 × 1.5 cm welldefined parathyroid adenoma posterior to the upper pole of the left lobe of the thyroid. The adenoma was of homogenous soft tissue attenuation and revea...

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Spontaneous necrosis of parathyroid adenoma: biochemical and imaging follow-up for two years

Chan

Chow

King

et al. 2000

Postgraduate Medical Journal

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“…Spontaneous remission in primary HPT is uncommon and is attributed to necrosis of a parathyroid adenoma [1,2]. Such a mechanism may be responsible for the fea tures observed here although parathyroid glands are usu ally hyperplastic in renal failure.…”

Section: Discussionmentioning

confidence: 79%

“…Improvement in bone disease may be obtained either with calcium and vitamin D supplements or surgery in the case of autonomous HPT. Spontaneous remission has, however, been reported in primary HPT associated with adenoma [1,2] or parathyroid carcinoma [3], but it has apparently not yet been described in the case of para thyroid gland hyperplasia induced by chronic renal failure. Since this manuscript was submitted, a similar case has been reported [8].…”

Section: Introductionmentioning

confidence: 99%

Spontaneous Remission of Severe Hyperparathyroidism in Chronic Renal Failure

Charhon¹,

Sellem²,

Meunier³

et al. 1983

Nephron

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The sudden onset of hypocalcemia occurring in a patient undergoing hemodialysis led to the diagnosis of spontaneous remission of severe hyperparathyroidism. This was confirmed by a marked reduction in immunoreactive parathyroid hormone level. The hypocalcemia was controlled by 1,25-dihydroxycholecalciferol. A dramatic improvement of hyperparathyroid bone disease, as assessed by radiographic and histomorphometric examination, was observed.

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“…Necrosis of a large parathyroid gland (a wellrecognized, though unusual, event in primary hyperpara thyroidism due to a single parathyroid adenoma) [2,3], was correctly supposed to be the most likely explanation for the sudden hypocalcemia in the patient described, even though all parathyroid glands are usually hyperplastic in chronic renal failure. Unfortunately, Charhon et al [1] were unable to give a pathologic confirmation of their suggestion; the authors [4] of a second recent report of a very similar case could not do so either.…”

Section: Spontaneous Remission Of Severe Hyperparathyroidism In Chronmentioning

confidence: 95%

Spontaneous Remission of Severe Hyperparathyroidism in Chronic Renal Failure

Colussi¹,

Surian²,

Ferrari³

et al. 1983

Nephron

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A Case of Primary Hyperparathyroidism With Spontaneous Remission Following Infarction of the Adenoma With Development of Hypocalcemic Tetany

Cited by 31 publications

References 3 publications

Spontaneous necrosis of parathyroid adenoma: biochemical and imaging follow-up for two years

Spontaneous necrosis of parathyroid adenoma: biochemical and imaging follow-up for two years

Spontaneous Remission of Severe Hyperparathyroidism in Chronic Renal Failure

Spontaneous Remission of Severe Hyperparathyroidism in Chronic Renal Failure

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