Bone/Parathyroid Case 7

A 19-year-old Caucasian male presented for assessment of subacute right knee pain and bilateral hip discomfort with exertion during military recruit training. He reported a history of foot and wrist fractures during childhood and chronic backache. The patient’s family history was notable for two brothers with a constellation of fractures including clavicular, foot, and wrist fractures. Radiographs of the right knee and pelvis demonstrated femoral meta-diaphyseal widening and cortical thickening, respectively. Radiographs of the cervical, thoracic, and lumbar spine showed diffuse vertebral body endplate sclerosis “rugger jersey spine appearance.”  Initial laboratory studies including serum calcium, alkaline phosphatase, albumin, 25-hydroxy vitamin D, parathyroid hormone and complete blood count were all normal. DXA scan showed Z-scores of + 0.5 at femoral neck, + 1.4 total hip, and 0.0 at lumbar spine.

Figure
Erlenmeyer flask deformity X-ray of knee (left), pelvis x-ray with cortical thickening and sclerosis (center), rugger jersey spine x-ray (right).

References:  

Palagano E, Menale C, Sobacchi C, Villa A. Genetics of Osteopetrosis. Curr Osteoporos Rep. 2018;16:13-25. 

Wu CC, Econs MJ, DiMeglio LA, et al. Diagnosis and Management of Osteopetrosis: Consensus Guidelines From the Osteopetrosis Working Group. J Clin Endocrinol Metab. 2017;102(9):3111-3123.  

Moore JB, Hoang TD, Shwayhat AF.  Osteopetrosis. Mil Med. 2017;182(3): e1886-e1888.   

Question 1

What is the diagnosis?

A. Renal osteodystrophy
B. Paget disease of bone
C. Osteopetrosis
D. Fluorosis
Incorrect!
Correct!
Correct Answer
C. Osteopetrosis

Osteopetrosis (C) is an inherited connective tissue disease resulting in abnormally dense bones prone to fracture. Mutations in more than a dozen known genes result in dysfunctional osteoclasts and accumulation of old bone normally resorbed. In severe cases, malfunctioning endochondral bone replaces the marrow space, resulting in inadequate hematopoiesis. Resultant pancytopenia can lead to opportunistic infection and death in childhood. Compensatory hepatosplenomegaly ensues as a result of extramedullary hematopoiesis. Cranial nerve deficits can manifest as blood cell production in concert with ongoing hypertrophy enlarges bony structures of the skull. The continued production of abnormal endochondral bone also results in brittleness predisposing to fracture, which occurs even in patients with less severe forms and normal life expectancy.   

A diagnosis of osteopetrosis is based on a thorough clinical evaluation, detailed medical history, X-ray imaging, and bone mineral density measurements.  Genetic testing can identify the mutation in 90% of cases. In our patient, genetic testing revealed 2 heterozygous PLEKHM1 mutations (exon 4 and exon 7).  PLEKHM1 gene is important to endosomal and lysosomal vesicular function.  Defects within the PLEKHM1 gene result in defective osteoclastic ruffled border formation and consequential inadequate bone resorption. This patient’s lack of hematologic deficiencies and survival into adulthood portend an improved long-term prognosis.  

Renal osteodystrophy (A) refers to specific changes in bone morphology associated with chronic kidney disease and was excluded in our patient who does not have chronic kidney disease. The serum alkaline phosphatase was normal, making paget disease of bone (B) unlikely.  Our patient did not have a history of excess fluoride consumption, thus, fluorosis (D) is unlikely.  

Bone/Parathyroid Case 6

A 56-year-old man with prostate adenocarcinoma, who has undergone a prostatectomy, androgen deprivation therapy, and chemotherapy including prednisone presents for an initial DXA referral. A DXA scan (Fig. A) shows total lumbar BMD of 0.815 g/cm2 and a T-score of –2.5. Individual lumbar T-scores were: L1 = –3.3, L2 = 1.6, L3 = –4.2, and L4 = –3.6. An artifact overlays L2 and the adjacent soft tissue. The patient discloses he had computed tomography (CT) imaging earlier the same day with oral and intravenous (IV) iodine-based contrast. 

 

References:  

Sala A, Webber C, Halton J, et al. Effect of diagnostic radioisotopes and radiographic contrast media on measurements of lumbar spine bone mineral density and body composition by dual-energy x-ray absorptiometry. J Clin Densitom. 2006;9:91-96.  

The International Society for Clinical Densitometry. Official Positions – Adult. 2015 ISCD. Available at: www.iscd.org. Accessed March 1, 2019. 

Morgan SL, Lopez-Ben R, Nunnally N, et al. The effect of common artifacts lateral to the spine on bone mineral density in the lumbar spine. J Clin Densitom. 2008;11:243-249. 

Spiro A, Hoang TD, Shakir MKM. Artifacts Affecting Dual-energy X-ray Absorptiometry Measurements. AACE Clinical Case Rep. Aug 2019;5(4):e263-266.  

Question 1

What is the next best step for further evaluation of this patient? 

A. Initiate medical treatment for osteoporosis
B. Interpret the DXA scan as it is
C. Review and compare with the previous DXA
D. Advise patient to come back for a repeat DXA in 7-10 days
Incorrect!
Correct!
Correct Answer
D. Advise patient to come back for a repeat DXA in 7-10 days

The artifact is consistent with the presence of oral contrast in the colon.  CT imaging performed one hour before the DXA scan, showed oral contrast at the hepatic flexure. The repeat scan done 10 days later, no longer showed the artifact (Fig. B). Iodine-based contrast enhances radiodensity by limiting the ability of X-rays to pass through tissue. It has been previously demonstrated that DXA performed immediately after administration of IV and oral iodine-based contrast causes increased measurement of bone mineral content; however, DXA repeated 7 days later produces results that are not significantly changed from baseline. In our patient, the contrast increased the BMD at L2, to such an extent that it nearly altered the DXA diagnosis from osteoporosis to osteopenia (option D). 

It is important to recognize the artifact on the DXA scan in order to make an accurate diagnosis.  Inaccurate diagnosis of DXA will affect the medical treatment and monitoring. A correct diagnosis of DXA (excluding artifacts) must be made first before initiating medical treatment for osteoporosis (option A). 
 
Interpretation of the DXA as it is with the presence of artifacts will result in an inaccurate diagnosis and wrong medical treatment decisions (option B). 
 

When interpreting DXA scans, physicians need to review and compare the current DXA with previous DXAs for interval changes.  However, this is the first DXA for this patient; thus, it is not applicable (option C). 

Bone/Parathyroid Case 5

A 55-year-old male patient presents to your clinic for evaluation of back pain which started 2 weeks ago. Treatment with OTC non-steroidal anti-inflammatory agent has not provided relief. Patient has history of lymphoma which was treated with chemotherapy in the past and is cancer free now. A plain film of lumbar spine shows a compression fracture of L4 vertebra with significant height loss. A clinical diagnosis of osteoporosis is made while pending further diagnostic testing with DXA scan. 

Examination shows sparse body and facial hair, mild gynecomastia and small testicles on both sides. Gonadal labs show a fasting, morning total testosterone of 145 ng/dL with LH of 35, low 25 OH vitamin D at 18 g/ml. along with mild normocytic anemia. Other biochemical laboratory tests are normal. 

Question 1

What is not associated with high fracture risk in this patient?

A. Low T score
B. Low TBS score
C. Low estrogen level
D. High estrogen level because of presence of gynecomastia
E. Low 25-hydroxy vitamin D level
Incorrect!
Correct!
Correct Answer
D. High estrogen level because of presence of gynecomastia

Hypogonadal men usually have lower estrogen levels and not high level which adds to fracture risk due to bone loss. Gynecomastia is associated with change in the ratio of estrogen/testosterone in favor of estrogen and not due to absolute increase in estrogen.  

Androgens promote the proliferation and differentiation of osteoblasts, as well as inhibit osteoclast activity resulting in decreased bone density. Androgens mediate recruitment and signaling of both osteoblasts and osteoclasts, promoting the former and inhibiting the latter. Androgens also get converted to estrogen by aromatase enzyme which is found in bone along with other tissues. Estrogen is the final mediator of bone turnover in both genders. It inhibits bone resorption, principally by directs effects on osteoclasts, although effects of estrogen on osteoblast proliferation and activation also play a role. A decrease in estrogen level in hypogonadal men such as this patient, due to reduced levels of substrate testosterone, contribute to bone loss and fracture risk. Even though there is a relative reduction of estrogen in hypogonadal men, the ratio of estrogen to testosterone is altered and is high which results in gynecomastia. In primary hypogonadism, high FSH also potentiates aromatase activity. Besides, low estrogen promoting bone loss, fracture risk is also higher in hypogonadal men due to sarcopenia fall risk and reduced exercise ability.  

Bone/Parathyroid Case 4

A 70-year-old man is referred for the evaluation of low back pain and paresthesia in both pelvic limbs. His past medical history reveals COPD diagnosis at age 50, treated with budesonide/formoterol 160/4.5mcg inhaled twice daily for the past 2 years. Family history is relevant for osteoporosis and hip fracture in his mother and lung cancer in his father. In anthropometry the patient has a low BMI of 18kg/m2 and complaints of height loss of more than 4cm. 

The workup comes back with the following results: normal serum calcium, normal phosphate, normal alkaline phosphatase, normal liver function. Complete blood count is normal. Serum 25-OH-Vitamin D is 25ng/ml (62nmol/L), normal 24-hour urine calcium, creatinine and sodium. Total testosterone of 350ng/dL. Dual energy X-ray Absorptiometry (DXA) reveals a low BMD, with a T-score of -2.7 in L1-L4 and a T-score of -2.1 in the femoral neck, VFA technique was performed during DXA and it shows multiple vertebral fractures. 

Question 1

According to the available evidence which of the following treatments is indicated to treat osteoporosis in this patient, particularly due to the fact that it reduces vertebral fracture incidence in men?  

A. Vitamin D supplementation with calcitriol 0.25mg daily.
B. Zoledronic acid 5mg IV every 12 months.
C. Risedronate 35mg weekly PO.
D. Denosumab 60mg SC every 6 months.
E. Testosterone supplementation with testosterone undecanoate 1000mg every 12 weeks.
Incorrect!
Correct!
Correct Answer
B. Zoledronic acid 5mg IV every 12 months.

This male patient has age related osteoporosis, although he has exposure to corticosteroids the type, dose and duration of it is not sufficient to consider his diagnosis as glucocorticoid induced osteoporosis. Zoledronic acid has been shown to reduce incidence of vertebral fracture in a study by Boonen et al. (Boonen S, Reginster JY, Kaufman JM, et al. Fracture risk and zoledronic acid therapy in men with osteoporosis. N Engl J Med. 2012;367(18):1714–23.) which evaluated 1199 men ages 50 to 85 with primary and hypogonadism-associated osteoporosis, men who received zoledronic acid 5mg at baseline and then at 12 months had a 67% risk reduction in any new morphometric vertebral fracture. Given the history and symptoms of this patient, the treatment with zoledronic acid would be indicated. 

Although risendronate and denosumab are effective in improving BMD regardless of age and gonadal function, the data are not extensive and to day there is no solid evidence demonstrating that beside increasing BMD these medications also reduce the incidence of vertebral fracture in men. 

 

Vitamin D supplementation is not indicated as this patient does not have deficiency and the data does not show that its use in men with osteoporosis reduces vertebral fracture. Finally, testosterone is not indicated because the patient does not have hypogonadism-associated osteoporosis and testosterone replacement is reserved for patients with demonstrated deficiency.   

Bone/Parathyroid Case 3

A 67-year-old Caucasian woman with vitamin D deficiency presents for follow-up of osteopenia. She has no history of vertebral, radius, or pathological fracture or family history of osteoporosis. A recent DXA scan revealed a bone mineral density with a T-score of -1.7 in the spine, and -2.0 in the left femoral neck. She takes calcium and vitamin D supplementation. She denies bone pain, history of kidney stones, anorexia, change in concentration, peptic ulcer disease or pancreatitis in the past. 

Laboratory test results at the time of the visit:  

Serum calcium = 11.2 mg/dL (8.2-10.2 mg/dL) (SI: 2.8 [2.1-2.6 mmol/L]) 

Serum phosphate = 2.8 mg/dL (2.3-4.7 mg/dL) (SI: 0.9 [0.7-1.5 mmol/L]) 

Serum creatinine = 0.80 mg/dL (0.6-1.1 mg/dL) (SI: 70.7 [53.0-97.2 µmol/L]) 

Glomerular filtration rate (estimated) > 60 mL/min per 1.73 m2 

Serum 25-hydroxyvitamin D = 30 ng/mL (30-80 ng/mL [optimal] (SI 74.9 nmol/L [74.9-199.7 nmol/L]) 

Serum intact PTH = 85 pg/mL (10-65 pg/mL) (SI: 85 ng/L [10-65 ng/L]) 

Serum albumin = 4.0 g/dL (3.5-5.0 g/dL) (SI: 4.0 g/L [35-50 g/L]) 

Serum magnesium, normal 

Urinary calcium = 450 mg/24 h (100-300 mg/24 h) (SI: 11.2 [2.5-7.5 mmol/d]) 

Urinary creatinine = 1.2 g/24 h (1.0-2.0 g/24 h) (SI: 10.6 [8.8-17.7 mmol/d]) 

Urinary volume = 1600 mL/24 h  

Question 1

Which of the following is the correct next step in management?

A. Continue to monitor calcium, 25-hydroxyvitamin D, PTH every 3-6 months.
B. Increase vitamin D supplementation, repeat calcium, 25-hydroxyvitamin D, PTH in 3 months.
C. Refer to surgery for preoperative localization and parathyroidectomy.
D. Start cinacalcet 30 mg daily and repeat calcium, albumin, creatinine and PTH in 2 weeks.
E. Refer to medical genetics for assessment of Familial Hypocalciuric Hypercalcemia (FHH).
Incorrect!
Correct!
Correct Answer
C. Refer to surgery for preoperative localization and parathyroidectomy.

This patient presents with a clinical constellation of hypercalcemia, elevated PTH with a replete 25-hydroxyvitamin D level, that is suggestive of primary hyperparathyroidism. Additionally, she has clear evidence of hypercalciuria with a fractional excretion of calcium [FeCa] = 0.026; FeCa = (urine calcium x serum creatinine)/(serum calcium x urine creatinine), which further supports a diagnosis of primary hyperparathyroidism rather than familial hypocalciuric hypercalcemia (FHH). The fractional excretion of calcium, also termed the urine calcium to creatinine ratio, can be used to distinguish primary hyperparathyroidism and FHH. A FeCa < 0.01 in a vitamin D-replete individual is highly suggestive of FHH rather than primary hyperparathyroidism (ratio usually > 0.02 in primary hyperparathyroidism. In an analysis of five large studies combining 165 patients with FHH and 197 patients with primary hyperparathyroidism, a FeCa < 0.01 had a sensitivity for FHH of 85% and a specificity of 88% with a positive predictive value (PPV) of 85% (1-3). This effectively rules out answer E.  

This patient currently does not have any symptoms to suggest primary hyperparathyroidism, but does meet surgical criteria for parathyroidectomy. For asymptomatic individuals who meet the Fourth International Workshop on Asymptomatic Primary Hyperparathyroidism guidelines, surgical intervention is recommended as opposed to observation (4, 5). Therefore, answers A, B, and D are incorrect. 

Patients need to meet only one of the following criteria for surgery (with our patient’s findings in bold):  

  • Serum calcium concentration of 1.0 mg/dL (0.25 mmol/L) or more above the upper limit of normal 

  • Skeletal indications:  

  • Bone density at the hip, lumbar spine, or distal radius htat is more than 2.5 standard deviations below peak bone mass (T-score < -2.5) 

  • Previous asymptomatic vertebral fracture (by radiograph, computed tomography [CT], magnetic resonance imaging [MRI], or vertebral fracture assessment).  

  • Renal indications: 

  • Estimated glomerular filtration rate (eGFR) < 60 mL/min 

  • Twenty-four-hour urinary calcium > 400 mg/day (> 10 mmol/day).  

  • Nephrolithiasis or nephrocalcinosis by radiograph, ultrasound, or CT.  

  • Age less than 50 years 

This patient currently has primary hyperparathyroidism by lab studies, and has two indications for parathyroidectomy. It is important to note that she does not have any contraindications to surgery that are mentioned in the question stem, therefore, cinacalcet (answer D) would not be the most appropriate next step in management.  

References: 

1. Sywak MS, Knowlton ST, Pasieka JL, et al. Do the National Institutes of Health consensus guidelines for parathyroidectomy predict symptom severity and surgical outcome in patients with primary hyperparathyroidism? Surgery 2002;132:1013.  

2. Walker MD, McMahon DJ, Inabnet WB, et al. Neuropsychological features in primary hyperparathyroidism: a prospective study. J Clin Endocrinol Metab 2009;94:1951.  

3. Walker MD, Silverberg SJ. Parathyroidectomy in asymptomatic primary hyperparathyroidism: improves “bones” but not “psychic moans”. J Clin Endocrinol Metab 2007;92:1613. 

4. Bilezikian JP, Brandi ML, Eastall R, et al. Guidelines for the management of primary hyperparathyroidism with or without parathyroid surgery after 15 years. J Clin Endocrinol Metab 2008;93:3462. 

5. Silverberg SJ, Clarke BL, Peacock M, et al. Current issues in the presentation of asymptomatic primary hyperparathyroidism: proceedings of the Fourth International Workshop.  J Clin Endocrinol Metab 2014;99:3580.  

This patient presents with a clinical constellation of hypercalcemia, elevated PTH with a replete 25-hydroxyvitamin D level, that is suggestive of primary hyperparathyroidism. Additionally, she has clear evidence of hypercalciuria with a fractional excretion of calcium [FeCa] = 0.026; FeCa = (urine calcium x serum creatinine)/(serum calcium x urine creatinine), which further supports a diagnosis of primary hyperparathyroidism rather than familial hypocalciuric hypercalcemia (FHH). The fractional excretion of calcium, also termed the urine calcium to creatinine ratio, can be used to distinguish primary hyperparathyroidism and FHH. A FeCa < 0.01 in a vitamin D-replete individual is highly suggestive of FHH rather than primary hyperparathyroidism (ratio usually > 0.02 in primary hyperparathyroidism. In an analysis of five large studies combining 165 patients with FHH and 197 patients with primary hyperparathyroidism, a FeCa < 0.01 had a sensitivity for FHH of 85% and a specificity of 88% with a positive predictive value (PPV) of 85% (1-3). This effectively rules out answer E.  

This patient currently does not have any symptoms to suggest primary hyperparathyroidism, but does meet surgical criteria for parathyroidectomy. For asymptomatic individuals who meet the Fourth International Workshop on Asymptomatic Primary Hyperparathyroidism guidelines, surgical intervention is recommended as opposed to observation (4, 5). Therefore, answers A, B, and D are incorrect. 

Patients need to meet only one of the following criteria for surgery (with our patient’s findings in bold):  

  • Serum calcium concentration of 1.0 mg/dL (0.25 mmol/L) or more above the upper limit of normal 

  • Skeletal indications:  

  • Bone density at the hip, lumbar spine, or distal radius htat is more than 2.5 standard deviations below peak bone mass (T-score < -2.5) 

  • Previous asymptomatic vertebral fracture (by radiograph, computed tomography [CT], magnetic resonance imaging [MRI], or vertebral fracture assessment).  

  • Renal indications: 

  • Estimated glomerular filtration rate (eGFR) < 60 mL/min 

  • Twenty-four-hour urinary calcium > 400 mg/day (> 10 mmol/day).  

  • Nephrolithiasis or nephrocalcinosis by radiograph, ultrasound, or CT.  

  • Age less than 50 years 

This patient currently has primary hyperparathyroidism by lab studies, and has two indications for parathyroidectomy. It is important to note that she does not have any contraindications to surgery that are mentioned in the question stem, therefore, cinacalcet (answer D) would not be the most appropriate next step in management.  

References: 

1. Sywak MS, Knowlton ST, Pasieka JL, et al. Do the National Institutes of Health consensus guidelines for parathyroidectomy predict symptom severity and surgical outcome in patients with primary hyperparathyroidism? Surgery 2002;132:1013.  

2. Walker MD, McMahon DJ, Inabnet WB, et al. Neuropsychological features in primary hyperparathyroidism: a prospective study. J Clin Endocrinol Metab 2009;94:1951.  

3. Walker MD, Silverberg SJ. Parathyroidectomy in asymptomatic primary hyperparathyroidism: improves “bones” but not “psychic moans”. J Clin Endocrinol Metab 2007;92:1613. 

4. Bilezikian JP, Brandi ML, Eastall R, et al. Guidelines for the management of primary hyperparathyroidism with or without parathyroid surgery after 15 years. J Clin Endocrinol Metab 2008;93:3462. 

5. Silverberg SJ, Clarke BL, Peacock M, et al. Current issues in the presentation of asymptomatic primary hyperparathyroidism: proceedings of the Fourth International Workshop.  J Clin Endocrinol Metab 2014;99:3580. 

Bone/Parathyroid Case 2

A 76 year-old woman is referred for evaluation of multiple non-traumatic vertebral compression fractures developing over the past year. She was initially diagnosed with osteoporosis at age 58 years, with her lowest T-score of -3.2 at her lumbar spine. She was treated with alendronate for one year, but because of significant gastroesophageal irritation, she switched to intravenous zoledronic acid once a year for the next three years without symptoms, followed by a 6-year drug holiday.

Once her bone density began to decrease after 6 years off treatment, she received a second three-year course of intravenous zoledronic acid, again without symptoms.  After completing her second course of zoledronic acid, her bone density did not increase as much as it did with her first course, and her primary care physician switched her to denosumab 60 mg subcutaneously every six months. Because her bone density increased significantly after four years of denosumab treatment, her physician discontinued denosumab. One year after her last dose of denosumab, she developed severe back pain without a fall or other injury, and her spine films showed new vertebral compression fractures at L1, L3, and L4.

Question 1

The most likely reason for the patient's multiple atraumatic vertebral compression fractures over the last year is which of the following?

A. Stopping denosumab therapy without starting other therapy
B. Lack of adequate calcium and vitamin D supplementation
C. Loss of previous antiresorptive effect of zoledronic acid
D. Persistent low bone mineral density after treatment
E. An unrecognized secondary cause for bone loss
Incorrect!
Correct!
Correct Answer
A. Stopping denosumab therapy without starting other therapy

Bisphosphonate therapies give long-lasting protection against postmenopausal bone loss.  Oral bisphosphonate therapies are typically given for three to five years, followed by up to a five-year drug holiday as long as the femoral neck bone density is above -2.5 and the patient has not had a fracture while on therapy. Intravenous zoledronic acid is given once yearly for up to three years and then followed by a three-year drug holiday, unless the patient has femoral neck bone density less than -2.5 or has sustained a low-trauma fracture on therapy. Bisphosphonate therapy is not usually stopped if the post-treatment T-score is less than -2.5 or a fracture has occurred while on therapy.

Antiresorptive osteoporosis therapies other than bisphosphonates lose their effect soon after therapy is discontinued. Because of this, bone formation and resorption typically increase toward baseline within the next several months after stopping therapy, leading to higher turnover bone loss if nothing else is given. Phase 2 clinical trial data showed that markers of bone formation and bone resorption both rebound above baseline within 6 to 12 months of stopping denosumab. High bone turnover may allow perforation of bony trabeculae and rapid bone loss leading to vertebral structural weakness and subsequent vertebral fractures. As a result of an increased risk of multiple vertebral fractures. 

Bisphosphonate therapies give long-lasting protection against postmenopausal bone loss.  Oral bisphosphonate therapies are typically given for three to five years, followed by up to a five-year drug holiday as long as the femoral neck bone density is above -2.5 and the patient has not had a fracture while on therapy. Intravenous zoledronic acid is given once yearly for up to three years and then followed by a three-year drug holiday, unless the patient has femoral neck bone density less than -2.5 or has sustained a low-trauma fracture on therapy. Bisphosphonate therapy is not usually stopped if the post-treatment T-score is less than -2.5 or a fracture has occurred while on therapy.

Antiresorptive osteoporosis therapies other than bisphosphonates lose their effect soon after therapy is discontinued. Because of this, bone formation and resorption typically increase toward baseline within the next several months after stopping therapy, leading to higher turnover bone loss if nothing else is given. Phase 2 clinical trial data showed that markers of bone formation and bone resorption both rebound above baseline within 6 to 12 months of stopping denosumab. High bone turnover may allow perforation of bony trabeculae and rapid bone loss leading to vertebral structural weakness and subsequent vertebral fractures. As a result of an increased risk of multiple vertebral fractures. 

Bone/Parathyroid Case 1

A 34 year-old woman comes to the emergency department for evaluation and management of postsurgical hypoparathyroidism. Her serum calcium is 6.8 mg/dL (normal, 8.9 to 10.1 mg/dL) two days after undergoing subtotal thyroidectomy for a unicentric 2.5-cm right thyroid lobe papillary cancer, without evidence of metastatic lymph nodes. She tolerated her surgery without difficulty but developed mild symptoms of tingling paresthesias at her fingertips, toe tips, and lips, and muscle cramps, beginning about six hours after surgery. She was sent home on calcium carbonate 500 mg twice daily, but her tingling paresthesias worsened over the next 24 hours. Her laboratory studies during her emergency department evaluation showed her serum phosphate increased at 6.4 mg/dL (normal, 2.5 to 4.5 mg/dL), serum creatinine normal at 1.0 mg/dL, and parathyroid hormone (PTH) undetectable.

Question 1

What treatments should be offered acutely to this patient with newly diagnosed symptomatic hypoparathyroidism?

A. Infusion of calcium gluconate given by diluting 10 mL of 10% calcium gluconate solution in 100 mL D5W (5% dextrose in water) over 5-10 minutes and repeat as needed
B. Begin oral calcium citrate 600 mg elemental calcium two tablets twice daily as soon as she can begin oral intake
C. Begin magnesium oxide 400 mg twice daily
D. Begin calcitriol 0.25 mg twice daily
E. All of the above
Incorrect!
Correct!
Correct Answer
E. All of the above

Patients with new-onset postsurgical hypoparathyroidism commonly present to the emergency department within several days of surgery with hypocalcemia, hyperphosphatemia, normal serum creatinine, and a low or undetectable parathyroid hormone level. Most patients with acute hypoparathyroidism are symptomatic, like this patient, with tingling paresthesias around their fingertips, toe tips, and lips, and experience muscle cramps or tetany.

Chvostek's sign, Trousseau's sign, and prolonged QT interval on their electrocardiogram may be seen. Repletion of their deficiencies with supplementation of intravenous calcium followed by oral calcium, both active and nutritional vitamin D, and magnesium, if needed, is usually sufficient to minimize their symptoms and signs. Doses are titrated up every few days until serum calcium is in the 8.0 to 8.5 mg/dL range, with improved symptoms, serum 25-hydroxyvitamin D are in goal range, and serum magnesium is normal.

Patients with new-onset postsurgical hypoparathyroidism commonly present to the emergency department within several days of surgery with hypocalcemia, hyperphosphatemia, normal serum creatinine, and a low or undetectable parathyroid hormone level. Most patients with acute hypoparathyroidism are symptomatic, like this patient, with tingling paresthesias around their fingertips, toe tips, and lips, and experience muscle cramps or tetany.

Chvostek's sign, Trousseau's sign, and prolonged QT interval on their electrocardiogram may be seen. Repletion of their deficiencies with supplementation of intravenous calcium followed by oral calcium, both active and nutritional vitamin D, and magnesium, if needed, is usually sufficient to minimize their symptoms and signs. Doses are titrated up every few days until serum calcium is in the 8.0 to 8.5 mg/dL range, with improved symptoms, serum 25-hydroxyvitamin D are in goal range, and serum magnesium is normal.