Clinical Overview > Hormone > PTH

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Tohru Eguchi Department of Internal Medicine, Uwajima City Hospital, 1-1 Gotenmachi, Uwajima, Ehime, 798-8510, Japan

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Shozo Miyauchi Department of Internal Medicine, Uwajima City Hospital, 1-1 Gotenmachi, Uwajima, Ehime, 798-8510, Japan

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Summary

A 43-year-old Japanese woman was admitted to our hospital with weakness. Laboratory findings showed hypokalemia, hypocalcemia and elevation of the serum creatinine phosphokinase levels, but intact parathyroid hormone levels. Further evaluations suggested that she had primary aldosteronism (PA), secondary hyperparathyroidism and bilateral adrenal tumors. She was treated successfully by laparoscopic right adrenalectomy. This case not only serves to the diagnosis of bilateral adrenal tumors in which selective adrenal venous sampling (SAVS) proved to be useful, but also for physicians to be aware of secondary hyperparathyroidism and the risk of secondary osteoporosis caused by PA.

Learning points

  • The classic presenting signs of PA are hypertension and hypokalemia.

  • Hypokalemia can induce rhabdomyolysis.

  • PA causes secondary hyperparathyroidism.

  • Patients with PA have the risk of osteoporosis with secondary hyperparathyroidism.

  • SAVS is useful in bilateral adrenal tumors.

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Angela S Lee Department of Endocrinology, Royal Prince Alfred Hospital, Camperdown, New South Wales, 2050, Australia
Sydney Medical School, Charles Perkins Centre, The University of Sydney, Sydney, New South Wales, 2006, Australia

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Stephen M Twigg Department of Endocrinology, Royal Prince Alfred Hospital, Camperdown, New South Wales, 2050, Australia
Sydney Medical School, Charles Perkins Centre, The University of Sydney, Sydney, New South Wales, 2006, Australia

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Summary

Adrenal insufficiency is a rare cause of hypercalcaemia and should be considered when more common causes such as primary hyperparathyroidism and malignancy are excluded. Opioid therapy as a cause of adrenal insufficiency is a possibly under-recognised endocrinopathy with potentially life-threatening adverse effects. We report on a case of opioid-induced secondary adrenal insufficiency presenting as hypercalcaemia. The patient was a 25-year-old man who developed hypercalcaemia during the recovery stage after a period of critical illness. Systematic investigation of his hypercalcaemia found it to be due to secondary adrenal insufficiency, developing as a consequence of methadone opioid analgesia. Treatment with i.v. saline and subsequent glucocorticoid replacement led to resolution of the hypercalcaemia. The hypoadrenalism resolved when opioids were subsequently weaned and ceased. These two interacting endocrinopathies of opioid-induced adrenal insufficiency and consequent hypercalcaemia highlight the importance of maintaining awareness of the potentially serious adverse clinical outcomes which can occur as a result of opioids, particularly considering that symptoms of hypoadrenalism can overlap with those of concomitant illness. Treatment with hydration and glucocorticoid replacement is effective in promptly resolving the hypercalcaemia due to hypoadrenalism. Hypoadrenalism due to prescribed and recreational opioids may be more common than is currently recognised.

Learning points

  • Opioid therapy can cause clinically significant secondary adrenal insufficiency, and this may be more common than is currently recognised.

  • Adrenal insufficiency is reversible after discontinuation of the opioid therapy.

  • Hypercalcaemia can occur as a consequence of adrenal insufficiency, and may be the presenting feature.

  • Treatment of hypercalcaemia due to adrenal insufficiency involves i.v. saline and glucocorticoid replacement.

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Marisa M Fisher Division of Pediatric Endocrinology, Department of Pediatrics, Riley Hospital for Children, Indiana University School of Medicine, 705 Riley Hospital Drive, Room 5960, Indianapolis, Indiana, 46220, USA

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Susanne M Cabrera Division of Pediatric Endocrinology, Department of Pediatrics, Medical College of Wisconsin, Children's Hospital of Wisconsin, 9000 W. Wisconsin Avenue, PO Box 1997, Milwaukee, Wisconsin, 53201, USA

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Erik A Imel Division of Pediatric Endocrinology, Department of Pediatrics, Riley Hospital for Children, Indiana University School of Medicine, 705 Riley Hospital Drive, Room 5960, Indianapolis, Indiana, 46220, USA
Division of Endocrinology, Department of Medicine, Indiana University School of Medicine, 541 North Clinical Drive, Indianapolis, Indiana, 46202, USA

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Summary

Neonatal severe hyperparathyroidism (NSHPT) is a rare disorder caused by inactivating calcium-sensing receptor (CASR) mutations that result in life-threatening hypercalcemia and metabolic bone disease. Until recently, therapy has been surgical parathyroidectomy. Three previous case reports have shown successful medical management of NSHPT with cinacalcet. Here we present the detailed description of two unrelated patients with NSHPT due to heterozygous R185Q CASR mutations. Patient 1 was diagnosed at 11 months of age and had developmental delays, dysphagia, bell-shaped chest, and periosteal bone reactions. Patient 2 was diagnosed at 1 month of age and had failure to thrive, osteopenia, and multiple rib fractures. Cinacalcet was initiated at 13 months of age in patient 1, and at 4 months of age in patient 2. We have successfully normalized their parathyroid hormone and alkaline phosphatase levels. Despite the continuance of mild hypercalcemia (11–12 mg/dl), both patients showed no hypercalcemic symptoms. Importantly, patient 1 had improved neurodevelopment and patient 2 never experienced any developmental delays after starting cinacalcet. Neither experienced fractures after starting cinacalcet. Both have been successfully managed long-term without any significant adverse events. These cases expand the current literature of cinacalcet use in NSHPT to five successful reported cases. We propose that cinacalcet may be considered as an option for treating the severe hypercalcemia and metabolic bone disease found in infants and children with inactivating CASR disorders.

Learning points

  • NSHPT due to mutations in the CASR gene occurs with hypercalcemia and metabolic bone disease, but not always with severe critical illness in infancy.

  • NSHPT should be considered in the differential diagnosis for a newborn with a bell-shaped chest, osteopenia, and periosteal reactions.

  • Neurodevelopmental consequences may occur in children with hypercalcemia and may improve during treatment.

  • Calcimimetics can be used to successfully treat the pathophysiology of NSHPT directly to control serum calcium levels.

Open access
Maria P Yavropoulou Division of Clinical and Molecular Endocrinology, 1st Department of Internal Medicine, AHEPA University Hospital, Aristotle University of Thessaloniki, 1 Stilponos, Kyriakidi Street, Thessaloniki, 54636, Greece

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Nikolina Gerothanasi Division of Clinical and Molecular Endocrinology, 1st Department of Internal Medicine, AHEPA University Hospital, Aristotle University of Thessaloniki, 1 Stilponos, Kyriakidi Street, Thessaloniki, 54636, Greece

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Athanasios Frydas Division of Clinical and Molecular Endocrinology, 1st Department of Internal Medicine, AHEPA University Hospital, Aristotle University of Thessaloniki, 1 Stilponos, Kyriakidi Street, Thessaloniki, 54636, Greece

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Evangelia Triantafyllou Division of Clinical and Molecular Endocrinology, 1st Department of Internal Medicine, AHEPA University Hospital, Aristotle University of Thessaloniki, 1 Stilponos, Kyriakidi Street, Thessaloniki, 54636, Greece

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Chris Poulios Pathology Department, Faculty of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece

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Prodromos Hytiroglou Pathology Department, Faculty of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece

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Panagiotis Apostolou Research Genetic Cancer Centre Ltd (RGCC Ltd), Florina, Greece

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Ioannis Papasotiriou Research Genetic Cancer Centre Ltd (RGCC Ltd), Florina, Greece

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Symeon Tournis Laboratory of Research of Musculoskeletal System ‘Th. Garofalidis’, Medical School, KAT Hospital, University of Athens, Athens, Greece

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Isaak Kesisoglou 3rd Department of Surgery, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece

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John G Yovos Division of Clinical and Molecular Endocrinology, 1st Department of Internal Medicine, AHEPA University Hospital, Aristotle University of Thessaloniki, 1 Stilponos, Kyriakidi Street, Thessaloniki, 54636, Greece

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Summary

Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome caused primarily by benign mesenchymal tumors. These tumors typically follow a benign clinical course and local recurrence occurs in <5% of cases. We investigated a 49-year-old man with a recurrent mesenchymal phosphaturic tumor showing no signs of malignancy. The patient suffered from chronic muscle weakness, myalgia and cramps. His medical record included the diagnosis of oncogenic osteomalacia, for which he was submitted to tumor resection in the left leg three times before. Laboratory examination showed hypophosphatemia, hyperphosphaturia and an elevated serum FGF23 level. A radical surgical approach (amputation) was advised, however, complete biochemical and clinical remission was not reached. Molecular analysis of the tumor cells demonstrated overexpression of growth factor receptors implicated in tumor angiogenesis and metastatic potential (platelet derived growth factor type A (PDGFRA), PDGFRB and vascular endothelial growth factor receptor) together with increased expression of FGF23, x-linked-phosphate-regulating endopeptidase and KLOTHO. TIO is usually associated with benign phosphauturic tumors and, when identified, resection of the tumor leads to complete remission in the majority of cases. The underlying pathophysiology of recurrences in these tumors is not known. This is the first report showing increased expression of growth factor receptors in a locally aggressive but histopathologically benign phosphaturic mesenchymal tumor.

Learning points

  • TIO is usually associated with benign soft tissue or bone neoplasms of mesenchymal origin.

  • These tumors typically follow a benign clinical course and even in the rare malignant cases local recurrence occurs in <5%.

  • Successful identification and removal of the tumor leads to full recovery in the majority of cases.

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Lara Ulrich General Surgery, Kingston Hospital, London, UK

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Graham Knee Pathology, Kingston Hospital, London, UK

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Colin Todd Radiology, Kingston Hospital, London, UK

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Summary

Haemorrhage of a parathyroid adenoma is a rare clinical presentation. This report describes a previously fit and well 54-year-old woman who presented with acute neck swelling and pain with an overlying ecchymosis. Admission laboratory tests revealed a raised parathyroid hormone and hypercalcaemia. A computed tomography (CT) scan showed widespread anterior cervical haemorrhage and a lesion at the inferior pole of the left thyroid gland. A working diagnosis of spontaneous haemorrhage from a parathyroid adenoma was made. As she was haemodynamically stable, she was treated conservatively with a period of observation in hospital to monitor for signs of neck organ compression. Follow-up imaging with CT, ultrasound and sestamibi confirmed the likely source of haemorrhage as a parathyroid nodule with significant vascularity. The diagnosis was confirmed on histopathological analysis after elective surgical exploration of the neck 6 months after her presentation. This revealed a benign parathyroid adenoma with evidence of acute and chronic bleeding. The patient made a full recovery with immediate normalisation of her biochemistry post-operatively. Despite developing a hoarse voice in the immediate post-operative period, this resolved completely within 1 month. This case report provides further evidence to support a minimal delay for elective surgery after conservative management to reduce the risks associated with recurrent bleeding.

Learning points

  • Haemorrhage of a parathyroid adenoma should be a differential for all cases of acute cervical swelling or ecchymosis with no precipitating factor.

  • The clerking should identify any risk factors for endocrine disease.

  • Blood tests to screen for abnormal parathyroid biochemistry should be performed on admission.

  • Detailed imaging of the neck is essential to identify the source of haemorrhage and risk of compression to vital neck organs.

  • Conservative management is a suitable option for patients who remain haemodynamically stable but all should undergo a period of observation in hospital.

  • Conservatively managed patients should be considered for definitive surgical exploration within a month of presentation to avoid the risks of recurrent bleeding.

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E Castellano
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M Pellegrino
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R Attanasio Endocrinology Service, Galeazzi Institute IRCCS, Milan, Italy

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V Guarnieri Genetics Unit, Casa Sollievo della Sofferenza, IRCCS, San Giovanni Rotondo, Italy

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A Maffè Genetics and Molecular Biology, Santa Croce and Carle, Cuneo, Italy

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G Borretta
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Summary

We report the association of primary hyperparathyroidism (PHPT) and Klinefelter's syndrome (KS) in a 22-year-old male complaining of worsening fatigue. PHPT was asymptomatic at the diagnosis, but the patient had worsening hypercalcemia and osteoporosis, and developed acute renal colic. He then underwent parathyroidectomy with resection of a single adenoma and normalization of calcium and parathyroid hormone levels. Clinical and therapeutic implications of this rare association are discussed.

Learning points

  • The coexistence of KS and PHPT is very uncommon.

  • Patients with mild PHPT often have nonspecific symptoms that may be confused and superimposed with those of hypogonadism.

  • KS patients, especially when young and already osteoporotic at diagnosis, should be screened for other causes of secondary osteoporosis, in particular PHPT.

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Manas Ghosh Sanjiban Hospital, Kolkata, India

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Ambarish Bhattacharya Department of Medicine, Sanjiban Hospital, Kolkata, India

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Kaushik Ghosh Department of Medicine, Malda Medical College, Malda, West Bengal 732101, India

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Atri Chatterjee Department of Neurology, NRS Medical College, Kolkata, India

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Sisir Chakraborty Department of Medicine, College of Medicine and Sagore Dutta Hospital, Kolkata, India

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Sanat Kumar Jatua Department of Medicine, NRS Medical College, Kolkata, India

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Summary

Motor neuron disease (MND) is a progressive devastating neurodegenerative disease, which universally progresses towards death. Hence, every attempt should be made to find out if there are any treatable conditions, which can mimic MND. Herein, we describe a case of hypercalcaemia due to primary hyperparathyroidism confused as MND and subsequently cured with parathyroid surgery.

Learning points

  • Any patient with neurological disorder should have a screening of all the common electrolytes including calcium as electrolyte imbalance can present with paralysis (e.g. hypokalaemia) to amyotrophic lateral sclerosis (e.g. hypercalcaemia).

  • No patient should be stamped as having MND without having a proper work-up of all its differentials as there might be a treatable condition masquerading as MND.

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Sachiko-Tsukamoto Kawashima Department of Endocrinology and Metabolism, National Hospital Organization Kyoto Medical Center, Kyoto, Japan
Department of Diabetes, Endocrinology and Metabolism Tango Central Hospital, Kyoto, Japan

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Takeshi Usui Clinical Research Institute

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Yohei Ueda Department of Endocrinology and Metabolism, National Hospital Organization Kyoto Medical Center, Kyoto, Japan

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Maiko-Kakita Kobayashi Department of Endocrinology and Metabolism, National Hospital Organization Kyoto Medical Center, Kyoto, Japan

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Mika Tsuiki Department of Endocrinology and Metabolism, National Hospital Organization Kyoto Medical Center, Kyoto, Japan

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Kanako Tanase-Nakao Department of Endocrinology and Metabolism, National Hospital Organization Kyoto Medical Center, Kyoto, Japan

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Kazutaka Nanba Department of Endocrinology and Metabolism, National Hospital Organization Kyoto Medical Center, Kyoto, Japan

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Tetsuya Tagami Department of Endocrinology and Metabolism, National Hospital Organization Kyoto Medical Center, Kyoto, Japan

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Mitsuhide Naruse Clinical Research Institute

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Yoshiki Watanabe Department of Head and Neck Surgery, National Hospital Organization Kyoto Medical Center, 1-1 Mukaihata-cho, Fukakusa, Fushimi-ku, Kyoto 612-8555, Japan

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Ryo Asato Department of Head and Neck Surgery, National Hospital Organization Kyoto Medical Center, 1-1 Mukaihata-cho, Fukakusa, Fushimi-ku, Kyoto 612-8555, Japan

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Sumiko Kato Osaka Saiseikai Ibaraki Hospital, Osaka, Japan

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Akira Shimatsu Clinical Research Institute

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Summary

Parathyroid cystic adenomas are often misdiagnosed as thyroid cysts and routine preoperative diagnostic tools, such as ultrasonography (US) or 99m technetium-sestamibi (99mTc-MIBI) scans, cannot clearly distinguish between these entities. We present a 67-year-old hypercalcemic woman with a cervical cystic lesion who had negative sestamibi scan results. Her laboratory data indicated primary hyperparathyroidism (serum calcium concentration 14.0 mg/dl, phosphate concentration 2.3 mg/dl, and intact parathyroid hormone (PTH) concentration 239 pg/ml). The cervical US and computed tomography scans revealed a large and vertically long cystic mass (12×11×54 mm). A mass was located from the upper end of the left thyroid lobe to the submandibular region and was not clearly distinguishable from the thyroid. For preoperative definitive diagnosis, we carried out a parathyroid fine-needle aspiration (FNA) and PTH assay (PTH–FNA) of liquid aspirated from the cyst. The intact PTH–FNA concentration was 1.28×106 pg/ml, and the patient was diagnosed with primary hyperparathyroidism due to a cystic mass. She underwent a left upper parathyroidectomy and her serum calcium and intact PTH concentration immediately decreased to normal levels. This report describes the usefulness of PTH–FNA for localizing and differentiating an atypical functional parathyroid lesion from nonfunctional tissue in primary hyperparathyroidism.

Learning points

  • Cystic parathyroid lesions, even in the case of elevated PTH levels, can produce negative results in 99mTc-MIBI scans.

  • Preoperative diagnosis of parathyroid cysts detectable on US is possible by parathyroid FNA and PTH assay (PTH–FNA) of liquid aspirated from the cyst, if malignancy is not suspected.

  • PTH–FNA could be helpful in the differential diagnosis of an equivocal cervical tumor.

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K Nadarasa Department of Endocrinology, St Bartholomew's Hospital, London, UK

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M Bailey Department of Endocrinology, St Bartholomew's Hospital, London, UK

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H Chahal Imperial Centre for Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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O Raja Department of Endocrinology, St Bartholomew's Hospital, London, UK

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R Bhat Department of Neonatology, King's College Hospital, London, UK

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C Gayle Department of Diabetes, King's College Hospital, London, UK

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A B Grossman Department of Endocrinology, St Bartholomew's Hospital, London, UK

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M R Druce Department of Endocrinology, St Bartholomew's Hospital, London, UK

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Summary

We present the case of a patient with metastatic parathyroid carcinoma whose hypercalcaemia was medically managed through two pregnancies. The diagnosis was made when the patient presented with chronic knee pain and radiological findings consistent with a brown tumour, at the age of 30. Her corrected calcium and parathyroid hormone (PTH) levels were significantly elevated. Following localisation studies, a right parathyroidectomy was performed with histology revealing parathyroid carcinoma, adherent to thyroid tissue. Aged 33, following biochemical recurrence of disease, the patient underwent a second operation. A subsequent CT and FDG–PET revealed bibasal pulmonary metastases. Aged 35, the patient was referred to our unit for treatment of persistent hypercalcaemia. The focus of treatment at this time was debulking metastatic disease using radiofrequency ablation. Despite advice to the contrary, the patient conceived twice while taking cinacalcet. Even though there are limited available data regarding the use of cinacalcet in pregnancy, both pregnancies continued to term with the delivery of healthy infants, using intensive medical management for persistent hypercalcaemia.

Learning points

  • Parathyroid carcinoma is a rare cause of primary hyperparathyroidism.

  • Hypercalcaemia during pregnancy can result in significant complications for both the mother and the foetus.

  • The use of high-dose cinacalcet in pregnancy has been shown, in this case, to aid in the management of resistant hypercalcaemia without teratogenicity.

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Deep Dutta Departments of Endocrinology and Metabolism

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Chitra Selvan Departments of Endocrinology and Metabolism

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Manoj Kumar Departments of Endocrinology and Metabolism

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Saumik Datta Departments of Endocrinology and Metabolism

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Ram Narayan Das Pathology, IPGMER and SSKM Hospital, Room-9A, 4th Floor Ronald Ross Building, 244 AJC Bose Road, Calcutta 700020, India

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Sujoy Ghosh Departments of Endocrinology and Metabolism

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Satinath Mukhopadhyay Departments of Endocrinology and Metabolism

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Subhankar Chowdhury Departments of Endocrinology and Metabolism

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Summary

Parathyroid cysts are rare (0.8–3.41% of all parathyroid lesions) and usually arise secondary to cystic degeneration of parathyroid adenomas. Intrathyroidal parathyroid cysts are extremely rare with only three cases reported till date. We present a 24-year-old female with clinical and biochemical features of primary hyperparathyroidism (PHPT; Ca2 +: 12.1 mg/dl; intact parathyroid hormone (iPTH): 1283 pg/ml) and poor radiotracer uptake with minimal residual uptake in the left thyroid lobe at 2 and 4 h on Tc99m sestamibi imaging. Neck ultrasonography (USG) revealed 0.6×1 cm parathyroid posterior left lobe of thyroid along with 22×18 mm simple thyroid cyst. USG-guided fine-needle aspiration (FNA) and needle tip iPTH estimation (FNA-iPTH) from parathyroid lesion was inconclusive (114 pg/ml), necessitating FNA of thyroid cyst, which revealed high iPTH (3480 pg/ml) from the aspirate. The patient underwent a left hemithyroidectomy. A >50% drop in serum iPTH 20 min after left hemithyroidectomy (29.4 pg/ml) along with histopathology suggestive of intrathyroidal cystic parathyroid adenoma (cystic lesion lined by chief cell variant parathyroid cells without any nuclear atypia, capsular or vascular invasion surrounded by normal thyroid follicles) confirmed that the parathyroid cyst was responsible for PHPT. This report highlights the importance of FNA-iPTH in localizing and differentiating a functional parathyroid lesion from nonfunctional tissue in PHPT.

Learning points

  • Fine-needle aspiration from suspected parathyroid lesion and needle tip iPTH (FNA-iPTH) estimation from the saline washing has an important role in localizing primary hyperparathyroidism (PHPT).

  • FNA-iPTH estimation may help in differentiating functional from nonfunctional parathyroid lesion responsible for PHPT.

  • iPTH estimation from aspirate of an intrathyroid cyst is helpful in differentiating intrathyroidal parathyroid cyst from thyroid cyst.

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