After hospital discharge, the patient was referred to the outpatient clinic of internal medicine. Single-photon emission computed tomography with ¹²³I/⁹⁹mTc-sestamibi revealed an active parathyroid adenoma (figure 2). Recent cytology of the largest nodus (3.9 cm) in his multinodular goitre revealed a benign nodus (Bethesda 2). A dual-energy X-ray absorptiometry showed signs of osteoporosis with a bone mineral density T-score of -1.3 for the lumbar spine and -3.6 for the femoral column. Because of persistent high serum calcium levels >3.0 mmol/l and osteoporosis, the patient underwent parathyroidectomy after which he completely recovered. Pathological examination confirmed the diagnosis of a parathyroid adenoma and a multinodular goitre of the right thyroid gland. The thyroid function remained normal.

Discussion
The exact mechanism of postoperative graft spasm is still unknown, but it is thought to be an extreme form of vasoconstriction. Both mechanical and nerve stimulation provoke vasoconstriction as well as spasmogens such as prostaglandins, α-drenoceptor agonists (e.g. norepinephrine and phenylephrine) and platelet-derived substances (e.g. 5-hydroxytryptamine). These factors influence calcium influx through the calcium channels located in the membrane and release of calcium from the intracellular sarcoplasmic reticulum. The rise of intracellular calcium ultimately facilitates actin and myosin filament binding resulting in contraction. On the other hand, different endothelium-erived relaxing factors such as nitric oxide, prostacyclin and endothelium-derived hyperpolarising factor are released by the intact endothelium in order to maintain balance between vasoconstriction and vasodilatation.[2] Retrospectively, the patient had hypercalcaemia within the first hour of surgery and no spasmogens or α-adrenoceptor agonists were administered during surgery. We presume that the hypercalcaemia already existed preoperatively and could have been the sole cause of the graft spasm. Noradrenaline was administered postoperatively after arrival to the ICU. Despite hyperhydration, diuretics and bisphosphonate, the calcium levels remained high accompanied by intermittent graft spasm with cardiac damage reaching its peak 14 hours after the coronary angiography. After enough calcium channel blockade was reached, further graft spasm disappeared despite elevated plasma calcium levels.

To our knowledge, there are no previous reports of patients with perioperative graft spasm due to hyperparathyroidism with hypercalcaemia. Oguchi et al. reported a patient with coronary artery spasm during spinal anaesthesia with hyper-parathyroidism.[3] Hong et al. described a patient admitted to hospital with coronary artery spasm and hyperparathyroidism.[4] Furthermore, Rasool et al. presented a 27-year-old female with hyperparathyroidism and cerebral vasospasm resulting in ischaemic stroke.[5] All these reports suggest a relation between hypercalcaemia due to hyperparathyroidism and vasospasm.

Primary hyperparathyroidism is the most common cause of hypercalcaemia and is the result of excessive secretion of PTH by one or more of the parathyroid glands. Commonly this is a single, benign, parathyroid adenoma. The secretion of PTH is modulated by serum calcium, phosphorus and vitamin D through negative and positive feedback loops. The PTH acts in the kidney to increase renal calcium reabsorption, stimulate the conversion 25-hydroxyvitamin D3 to the active 1,25-dihydroxyvitamin D and decrease phosphate reabsorption. In the bones it leads to osteoclastic bone resorption in order to release both calcium and phosphorus from the skeleton. The production of 1,25-dihydroxyvitamin D stimulates the absorption of calcium and phosphorus in the intestines.