International Journal of Clinical Case Reports 2017, Vol.7, No.9, 38-41
39
nephrocalcinosis. The parathyroid nodule size varied between 20 and 46 mm, it was palpable in three patients.
Because of the severity of hypercalcemia, all patients received symptomatic treatment before surgical ablation of
parathyroid tumor. These treatments consisted in rehydration with isotonic saline in all patients, bisphosphonates
(zoledronic acid) in three patients, calcitonin in two patients and corticosteroids in one patient. One of our patients
required two sessions of hemodialysis.
While biphosphonates allowed normalization of serum calcium levels in all patients, other treatments had mild
effect on serum calcium levels, with decrease ranging from 0.25 to 0.50 mmol/l.
All patients were operated on. Histological examination had concluded to carcinomas in two cases and to
adenomas in three cases.
In the postoperative period all patients developed hypocalcaemia. The two patients who did not receive
preoperative bisphosphonates experienced severe postoperative hypocalcaemia requiring infusion of high doses of
calcium.
3 Discussion
Primary hyperparathyroidism which was viewed as relatively rare several decades ago and associated with
significant morbidity is now considered a common disorder that is often asymptomatic. Prior to the mid-1970s,
most patients were diagnosed when they presented with specific symptoms of hyperparathyroidism,
nephrolithiasis or bone lesions. Nowadays, most patients are asymptomatic and are usually diagnosed incidentally
when serum calcium is noted to be mildly elevated on a multiphasic chemistry profile (Bilezikian, 2012).
Severe hypercalcemia is rare in primary hyperparathyroidism, it occurs in 1% to 2% of patients with primary
hyperparathyroidism (Kebebew and Clark, 1998). We have identified only 5 cases in our practice. Its presence
increases the possibility of malignancy, as severe hypercalcemia may be seen in 10 to 38% of parathyroid
carcinoma cases, while parathyroid carcinoma represent less than 1% of primary hyperparathyroidism etiologies
(Wermers et al., 2006)
.
40% of our patients had carcinoma.
Clinical manifestations of hypercalcemia depend on the degree of hypercalcemia and the rapidity of its onset. In
general, overt symptoms are rare in patients with serum calcium levels below 12 mg/dL, but at concentrations
above 14 mg/dL most patients are symptomatic (Bilezikian, 1993). Manifestations of hypercalcemia are depicted
in Table 1.
Table 1 Manifestations of hypercalcemia
Neuromuscular
Muscle weakness, lethargy, fatigue, poor recent memory, impaired cognition, confusion, stupor, psychosis,
depression, coma
Gastro-intestinal
Constipation, anorexia, nausea, vomiting, abdominal pain, peptic ulcer disease, pancreatitis
Renal
Decreased ability to maximally concentrate urine, polyuria, polydipsia, dehydration, nephrolithiasis,
nephrocalcinosis, kidney failure
Cardiovascular
Hypertension, shortening of QT interval, arrhythmias, digitalis sensitivity, cardiovascular calcifications
Skeletal
Bone pain, fracture, osteoporosis
Ocular
Band keratopathy
Management of severe hypercalcemia includes medical treatment for rapid lowering of calcium levels and
surgical treatment for the underlying etiology of primary hyperparathyroidism (Ariyan and Sosa, 2004).
Emergency treatment of hypercalcemia must first focus on correcting dehydration, restoring intravascular volume,
and enhancing renal calcium excretion. Restoration of intravascular volume will enhance urinary calcium
excretion by increasing glomerular filtration of calcium and decreasing proximal tubular and loop reabsorption of
sodium. Parenteral fluid resuscitation must be administered cautiously in patients with heart or kidney failure. 500
to 1,000 ml of 0.9 % saline should be infused over the first hour, and then 2 to 5 liters are added over the first 24
