scholarly journals Denosumab can be used successfully as a bridge to surgery in patients with severe hypercalcemia due to primary hyperparathyroidism

Author(s):  
Mohammad Shafi Kuchay ◽  
Anu Mathew ◽  
Parjeet Kaur ◽  
Sunil Kumar Mishra
2021 ◽  
Author(s):  
Laura Teodoriu ◽  
Maximilian Hogea ◽  
Viorel Scripcariu ◽  
Bianca Ioan ◽  
Letitia Leustean ◽  
...  

2010 ◽  
Vol 2 (3) ◽  
pp. 131-133
Author(s):  
Geoffrey B Thompson ◽  
Benzon M Dy ◽  
Bianca Vazquez ◽  
Peter J Tebben ◽  
Seema Kumar

ABSTRACT Introduction Severe hypercalcemia due to primary hyperparathyroidism (PHPT) is rare in the setting of MEN 2A. Materials and methods Two patients with MEN 2A and severe hypercalcemia were identified recently. Their clinical presentation, evaluation, surgical management and outcomes are reviewed. Results Two patients with MEN 2A were identified with severe hypercalcemia secondary to a parathyroid adenoma. Calcium levels were elevated to 12.7 mg/dL and 15.1 mg/dL, respectively (normal range = 8.9-10.1 mg/dL). In each case, a single parathyroid adenoma was identified and surgically excised with normalization of parathyroid and calcium levels postoperatively. Clinical manifestations at the time of diagnosis included constipation, polyuria, hypercalciuria, and decreased bone mineral density. Conclusion Severe elevation of serum calcium is a rare presentation of PHPT in MEN2A. The differential diagnosis should include parathyroid adenoma, hyperplasia and parathyroid carcinoma. Early surgical management is essential in the treatment of hyperparathyroidism with severe hypercalcemia to prevent further complications.


Author(s):  
Carine Ghassan Richa ◽  
Khadija Jamal Saad ◽  
Ali Khaled Chaaban ◽  
Mohamad Souheil El Rawas

Summary The objective of the study is to report a case of acute pancreatitis secondary to hypercalcemia induced by primary hyperparathyroidism in a pregnant woman at the end of the first trimester. The case included a 32-year-old woman who was diagnosed with acute pancreatitis and severe hypercalcemia refractory to many regimens of medical therapy in the first trimester of pregnancy. She was successfully treated with parathyroidectomy in the early second trimester with complete resolution of hypercalcemia and pancreatitis. Neonatal course was unremarkable. To our best knowledge, this is a rare case when primary hyperparathyroidism and its complications are diagnosed in the first trimester of pregnancy. In conclusion, primary hyperparathyroidism is a rare life-threatening condition to the fetus and mother especially when associated with complications such as pancreatitis. Early therapeutic intervention is important to reduce the morbidity and mortality. Parathyroidectomy performed in the second trimester can be the only solution. Learning points: Learning how to make diagnosis of primary hyperparathyroidism in a woman during the first trimester of pregnancy. Understanding the complications of hypercalcemia and be aware of the high mortality and sequelae in both fetus and mother. Providing the adequate treatment in such complicated cases with coordinated care between endocrinologists and obstetricians to ensure optimal outcomes.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A266-A267
Author(s):  
Timur Gusov ◽  
John Chen Liu ◽  
Sowjanya Naha ◽  
F N U Marium ◽  
Joseph Theressa Nehu Parimi ◽  
...  

Abstract Primary hyperparathyroidism (PHPT) is defined as excessive secretion of parathyroid hormone (PTH) originating from the parathyroid gland. The most common cause is a single parathyroid adenoma which is typically solid. Cystic parathyroid adenomas (CPA) are the cause of about 1–2% of cases of primary hyperparathyroidism. It is known that cystic parathyroid adenomas are a result of degeneration of an existing parathyroid adenoma. SestaMIBI is an imaging study based on uptake of radioactive technetium99 and used to localize parathyroid adenomas. We describe an unusual case of severe hypercalcemia secondary to 99mTc sestaMIBI negative atypical parathyroid cystic adenoma. A 56-year-old male presented to our facility with nausea and vomiting. His past medical history included hypertension and hepatitis C with no history of fractures or kidney disease. Physical examination was normal. Upon admission the patient was afebrile with blood pressure of 170/120 mmHg and heart rate of 62 bpm. Chemistry showed Calcium of 14.5 mg/dL (8.6–10.2mg/dL), phosphorus 2.2 (2.7–4.5) mh/dL, magnesium 1.8 (1.7–2.6)mg/dL, intact PTH of 375 (15–65) pg/mL, PTH-related peptide <2.0 pmol/L(<2 pmol/L), 25-OH vitamin D of 19 ng/ml (30–80), Creatinine 1.22 (0.7–1.2)mg/dL, alkaline phosphatase 95 (40–129) units/L. He was started on aggressive hydration, calcitonin 4 units/kg, 4 mg of IV Zolendroninc acid. Neck sonogram revealed a large, complex, predominantly anechoic lesion with solid vascular components and thick internal septations in the inferior and medial aspect of the right thyroid lobe measuring 3 x 2 x 5.5 cm. Findings were confirmed with CT of the neck. Since Sestamibi scan (planar and SPECT/CT) did not show uptake in parathyroid glands, the cyst was thought to be of thyroid origin. Fine needle aspiration was not able to detect cellular material, but PTH was >100 pg/ml on the FNA sample. Otolaryngology service was consulted for parathyroidectomy. During the surgical treatment, the right upper parathyroid gland was removed with no changes in serum PTH. Next, the cystic lesion was removed with normalization of serum PTH (from 218 pg/ml to 35.2 pg/ml respectively). Intraoperative frozen section analysis was read as a cystic parathyroid adenoma. The final pathology report revealed cystic parathyroid tissue favoring parathyroid adenoma with focal atypia. Hypercalcemia resolved. Conclusions: Atypical cystic parathyroid adenomas are a rare cause of PHPT. 90% of parathyroid cysts are nonfunctional. Above mention is a case of a patient presenting with hypercalcemic crisis secondary to cystic parathyroid adenoma, which posed a diagnostic challenge as both neck ultrasound and 99mTc sestaMIBI scan were inconclusive. These findings should trigger suspicion for functional parathyroid lesions. Cystic components should be evaluated for PTH levels and if significantly elevated should be treated as a parathyroid adenoma.


2019 ◽  
Vol 62 (4) ◽  
pp. 156-160 ◽  
Author(s):  
Luca Foppiani ◽  
Gianluca Bottoni ◽  
Arnoldo Piccardo

A nonagenarian hypertensive man with chronic kidney disease (CKD) was admitted to the emergency department for gastrointestinal symptoms and worsening symptoms of depression. Severe hypercalcemia (15.3 mg/dL) was found and he was hospitalized. Fluids, loop diuretics and glucocorticoids were administered intravenously, which partially reduced calcium levels over a few days and improved his clinical condition. PTH levels proved increased (306 pg/mL) and 25-OHD levels were reduced; primary hyperparathyroidism (PHPT) was diagnosed. Neck ultrasonography (USG) did not show parathyroid enlargement, nor did 99mTechnetium-sestamibi (SESTAMIBI) scintigraphy reveal hyperfunctioning parathyroid glands. By contrast, 18F-choline PET/CT evidenced a nodule located close to the oesophagus, behind the right thyroid lobe, which proved compatible with a hyperfunctioning parathyroid gland. Since the patient declined surgery, and zoledronate was unfit owing to areas of rarefaction of the jaw, the calcimimetic cinacalcet was started; the dosage was progressively titrated up to 120 mg/day with normalisation of calcium levels over time. PTH levels, however, proved erratic and showed an upward trend over the first year of therapy; however its levels partially decreased following increase of vitamin D levels by replacement therapy. Cinacalcet is a useful and safe drug, which can normalise calcium levels and improve the clinical condition, even in very old patients with severe PHPT who decline or are unfit for surgery.


Author(s):  
A. Kemal Topaloglu ◽  
Bilgin Yuksel ◽  
Recep Tuncer ◽  
Neslihan O. Mungan ◽  
Guler Ozer

AbstractA 2 month-old male infant presented with severe hypercalcemia due to parathyroid hyperplasia. A total parathyroidectomy and partial heterotopic autotransplantation were carried out. Hypercalcemia recurred two months later. Normocalcemia was re-established after removing one half of the implanted tissue. Despite two separate surgical explorations and several imaging studies, including


2019 ◽  
Vol 7 ◽  
pp. 232470961882380 ◽  
Author(s):  
Ron T. Varghese ◽  
Khaled Khasawneh ◽  
Raman K. Desikan ◽  
Anandaraj Subramaniam ◽  
Todd Weaver ◽  
...  

Objective. To report a case of severe hypercalcemia, exacerbated by vitamin A supplementation and hydrochlorothiazide, in a patient with primary hyperparathyroidism. Methods. Clinical and laboratory findings are presented along with response to therapy. Results. A 68-year-old white female presented to the emergency department complaining of nausea, vomiting, and altered mental status. Laboratory findings revealed calcium 15.8 mg/dL (8.4-10.2), albumin 4.1 g/dL (3.8-4.8), and parathyroid hormone 62 pg/mL (14-64). Serum calcium improved after intravenous hydration with normal saline. Prior to this hospitalization, over-the-counter medications were significant for calcium (600 mg daily), vitamin A (11 000 IU daily), and vitamin D (800 IU daily).The patient’s prescription medications were significant for hydrochlorothiazide (12.5 mg daily). Twenty-four-hour urine calcium was subsequently found to be 146 mg (35-250). Myeloma, lymphoma, and sarcoidosis were ruled out as the etiology for hypercalcemia. The diagnosis of primary hyperparathyroidism was confirmed. She was treated surgically for primary hyperparathyroidism. The right and left superior parathyroid showed hypercellular parathyroid on pathology. The patient was normocalcemic after surgery. Conclusion. Previous reports suggest that very high doses of vitamin A is required to cause hypercalcemia. This case suggests that in a setting of primary hyperparathyroidism and hydrochlorothiazide therapy, vitamin A may contribute to the development of severe hypercalcemia in patients who are on calcium and vitamin D supplements. Given their biologic effects, public awareness needs to be created regarding the injudicious use of vitamins.


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