Metastatic Pulmonary Calcification in Primary Hyperparathyroidism

Cohen, Alan M.; Maxon, Harry R.; Goldsmith, Ralph S.; Schneider, Harold J.; Wiot, Jerome F.; Loudon, Robert G.; Altemeier, William A.

doi:10.1001/archinte.1977.03630160080016

Cited by 25 publications

(17 citation statements)

References 8 publications

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“…Although MPC generally progresses gradually, it may also develop relatively quickly within a short period of time, from several weeks to months [4, 15]. In the present case the MPC developed very rapidly, in only five days, which has been rarely reported before.…”

Section: Discussionsupporting

confidence: 49%

Rapid development of metastatic pulmonary calcifications in primary hyperparathyroidism: a case report and literature review

et al. 2017

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BackgroundMetastatic pulmonary calcification (MPC) is rarely reported in primary hyperparathyroidism, especially MPC develops quickly. We report such a case here with a literature review.Case presentationA 41-year-old woman presented with cough and dyspnea. Data from clinical, radiological, pathological, technetium (99mTc)-methylene diphosphonate (MDP) bone scintillation imaging, and 99mTc-methoxy isobutyl isonitrile (MIBI) thyroid imaging were studied. 99mTc-MIBI thyroid imaging indicated hyperparathyroidism. Chest computed tomography (CT) scans showed rapidly progressive bilateral pulmonary multiple high-density shadows with mass consolidation and exudation in only five days. 99mTc-MDP bone scintillation imaging indicated bilateral pulmonary calcifications. CT-guided lung biopsy showed multifocal irregularities of calcium deposition and calcified bodies in the pulmonary interstitium. The patient showed gradually clinical and radiological improvement after surgical removal of the parathyroid adenoma.ConclusionRapidly progressive MPC tends to be misdiagnosed as many primary pulmonary diseases. 99mTc-MDP bone scintillation imaging and pulmonary biopsy could be performed to differentiate metastatic pulmonary calcification from other diseases. Surgical resection of the parathyroid gland is helpful for treatment of MPC in patients with primary hyperparathyroidism and is regularly recommended.

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Section: Discussionsupporting

confidence: 49%

Rapid development of metastatic pulmonary calcifications in primary hyperparathyroidism: a case report and literature review

et al. 2017

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“…Bone scan ( 99m Tc‐MDP) is sensitive, specific, and less expensive, in the detection of pulmonary calcification. It manifests as increase uptake of the radioisotope …”

Section: Discussionmentioning

confidence: 98%

“…It manifests as increase uptake of the radioisotope. 11 Most patients with MPC remain asymptomatic. There have been reports of MPC resultant respiratory failure, as seen in case 1.…”

Section: Discussionmentioning

confidence: 99%

Metastatic pulmonary calcification: Experience from a single center in Singapore

Teh

Yii

et al. 2018

Hemodialysis International

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Metastatic pulmonary calcification (MPC) was seen in 79% of patients with end-stage renal disease (ESRD) during autopsy. However, it is not commonly diagnosed in vivo. Its pathogenesis is not fully understood. We report a retrospective series of 5 cases of MPC from a single center in Singapore. MPC were diagnosed using radiological or histological features. Mean onset of MPC from diagnosis of ESRD was 22.6 ± 3.1 years. One patient remains asymptomatic. Four patients died, one was related to MPC. All patients had calcifications at the lung apices on radiological studies. Three patients with MPC were diagnosed based on radiological features while 2 had histological features. Four patients underwent parathyroidectomy without radiological changes before parathyroidectomy. Median intact parathyroid hormone of this series was 5.6 pmol/L (IQR 1.3-139.4), alkaline phosphatase 74 U/L (IQR 62-461), calcium 2.10 mmol/L (IQR 1.85-2.40), and phosphate 1.30 mmol/L (IQR 0.87-1.63). The observed low iPTH suggests that MPC might occur in low iPTH. Our case series showed MPC might occur in low iPTH after parathyroidectomy, in contrast to existing literature that suggests MPC is diagnosed in patients with elevated iPTH. Parathyroidectomy does not prevent MPC.

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“…Metastatic calcification can be divided into malignant and nonmalignant causes. 1,14,15 Third, intermittent alkalosis favors the precipitation of calcium salts, but also increases the activity of alkaline phosphatase, which catalyzes the release of phosphates. 1,8 Most of the other benign causes are related to calcium balance.…”

Section: Discussionmentioning

confidence: 99%

“…Second, hyperparathyroidism has been experimentally shown to contribute to pulmonary calcification both in the presence and absence of uremia. 1,14,15 Third, intermittent alkalosis favors the precipitation of calcium salts, but also increases the activity of alkaline phosphatase, which catalyzes the release of phosphates. Finally, a diminished glomerular filtration rate causes hyperphosphatemia, which in turn elevates the calcium-phosphorus product, favoring crystallization.…”

Section: Discussionmentioning

confidence: 99%

Metastatic pulmonary calcification in a dialysis patient: Case report and a review

Eggert

Albright

2006

Hemodialysis International

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A 19-year-old male presented with chest pain and dyspnea. He was anephric following nephrectomy for focal segmental glomerulosclerosis, had a subsequent failed transplant, and had been dialysis dependent for 3 years. Workup revealed hyperparathyroidism and an abnormal chest X-ray and computed tomography scan, significant for massive extra-skeletal pulmonary calcification. A markedly abnormal Technitium99 methylene diphosphonate (Tc99m-MDP) bone scan confirmed the clinical suspicion of metastatic pulmonary calcification. Metastatic pulmonary calcification (MPC) is common, occurring in 60% to 80% of dialysis patients on autopsy and bone scan series. It may lead to impaired oxygenation and restrictive lung disease. Typically, the calcium crystal is whitlockite rather than hydroxyapatite, which occurs in vascular calcification. Four major predisposing factors may contribute to MPC in dialysis patients. First, chronic acidosis leaches calcium from bone. Second, intermittent alkalosis favors deposition of calcium salts. Third, hyperparathyroidism tends to cause bone resorption and intracellular hypercalcemia. Finally, low glomerular filtration rate can cause hyperphosphatemia and an elevated calcium-phosphorus product. There may be other factors. Some authors suggest that the incidence of MPC in recent years may be lower due to improved dialysis techniques. The diagnosis is confirmed by biopsy, but can be suspected by typical findings on a Tc99m-MDP bone scan. Therapy is limited to ensuring adequate dialysis, correcting calcium-phosphorus product, and hyperparathyroidism; discontinuing vitamin D analogues may help. Conflicting reports show that transplantation may either improve or worsen the situation. MPC should be considered in dialysis patients who have characteristic abnormal chest radiography and/or pulmonary symptoms.

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Metastatic Pulmonary Calcification in Primary Hyperparathyroidism

Cited by 25 publications

References 8 publications

Rapid development of metastatic pulmonary calcifications in primary hyperparathyroidism: a case report and literature review

Rapid development of metastatic pulmonary calcifications in primary hyperparathyroidism: a case report and literature review

Metastatic pulmonary calcification: Experience from a single center in Singapore

Metastatic pulmonary calcification in a dialysis patient: Case report and a review

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