Symptoms to Diagnosis

Severe hypercalcemia in a 54-year-old woman

Author and Disclosure Information

 

References

A morbidly obese 54-year-old woman presented to the emergency department after experiencing generalized abdominal pain for 3 days. She rated the pain as 5 on a scale of 10 and described it as dull, cramping, waxing and waning, not radiating, and not relieved with changes of position—in fact, not alleviated by anything she had tried. Her pain was associated with nausea and 1 episode of vomiting. She also experienced constipation before the onset of pain.

She denied recent trauma, recent travel, diarrhea, fevers, weakness, shortness of breath, chest pain, other muscle pains, or recent changes in diet. She also denied having this pain in the past. She said she had unintentionally lost some weight but was not certain how much. She denied tobacco, alcohol, or illicit drug use. She had no history of surgery.

Her medical history included hypertension, anemia, and uterine fibroids. Her current medications included losartan, hydrochlorothiazide, and albuterol. She had no family history of significant disease.

INITIAL EVALUATION AND MANAGEMENT

On admission, her temperature was 97.8°F (36.6°C), heart rate 100 beats per minute, blood pressure 136/64 mm Hg, respiratory rate 18 breaths per minute, oxygen saturation 97% on room air, weight 130.6 kg, and body mass index 35 kg/m2.

She was alert and oriented to person, place, and time. She was in mild discomfort but no distress. Her lungs were clear to auscultation, with no wheezing or crackles. Heart rate and rhythm were regular, with no extra heart sounds or murmurs. Bowel sounds were normal in all 4 quadrants, with tenderness to palpation of the epigastric area, but with no guarding or rebound tenderness.

Laboratory test results

Notable results of blood testing at presentation were as follows:

  • Hemoglobin 8.2 g/dL (reference range 12.3–15.3)
  • Hematocrit 26% (41–50)
  • Mean corpuscular volume 107 fL (80–100)
  • Blood urea nitrogen 33 mg/dL (8–21); 6 months earlier it was 16
  • Serum creatinine 3.6 mg/dL (0.58–0.96); 6 months earlier, it was 0.75
  • Albumin 3.3 g/dL (3.5–5)
  • Calcium 18.4 mg/dL (8.4–10.2); 6 months earlier, it was 9.6
  • Corrected calcium 19 mg/dL.

Findings on imaging, electrocardiography

Chest radiography showed no acute cardiopulmonary abnormalities. Abdominal computed tomography without contrast showed no abnormalities within the pancreas and no evidence of inflammation or obstruction. Electrocardiography showed sinus tachycardia.

DIFFERENTIAL DIAGNOSIS

1. Which is the most likely cause of this patient’s symptoms?

  • Primary hyperparathyroidism
  • Malignancy
  • Her drug therapy
  • Familial hypercalcemic hypocalciuria
Table 1. Initial treatment of hypercalcemia
The increase in this patient’s uncorrected calcium level from 9.6 to 18.4 mg/dL in 6 months indicates some form of increased calcium resorption or retention. Moreover, her hypercalcemia is very severe (Table 1).1 Patients with severe hypercalcemia can present with life-threatening arrhythmias and seizures, as well as volume depletion.2

In total, her laboratory results were consistent with macrocytic anemia, severe hypercalcemia, and acute kidney injury, and she had generalized symptoms.

Primary hyperparathyroidism

A main cause of hypercalcemia is primary hyperparathyroidism, and this needs to be ruled out. Benign adenomas are the most common cause of primary hyperparathyroidism, and a risk factor for benign adenoma is exposure to therapeutic levels of radiation.3

In hyperparathyroidism, there is an increased secretion of parathyroid hormone (PTH), which has multiple effects including increased reabsorption of calcium from the urine, increased excretion of phosphate, and increased expression of 1,25-hydroxyvitamin D hydroxylase to activate vitamin D. PTH also stimulates osteoclasts to increase their expression of receptor activator of nuclear factor kappa B ligand (RANKL), which has a downstream effect on osteoclast precursors to cause bone reabsorption.3

Inherited primary hyperparathyroidism tends to present at a younger age, with multiple overactive parathyroid glands.3 Given our patient’s age, inherited primary hyparathyroidism is thus less likely.

Next Article:

Low-dose steroids for acute exacerbations of COPD in a non-ICU setting: Worth consideration

Related Articles