Objective: To test the hypothesis that progression of secondary hyperparathyroidism from normocalcaemia to hypercalcaemia occurs because of development of monoclonal parathyroid tumours after the inactivation of a tumour suppressor gene on chromosome 11q13.
Design: Experimental study.
Setting: University hospital, Sweden.
Subjects: 13 Patients with secondary hypercalcaemic hyperparathyroidism.
Interventions: 48 Parathyroid glands were removed, 39 of which were analysed using Southern blot hybridisation and polymerase chain reaction.
Main outcome measures: Loss of heterozygosity on several loci on chromosome 11, including 11q13, which carries the presumed gene for multiple endocrine neoplasia type 1 (MEN1).
Results: Monosomy for chromosome 11 was found in one tumour.
Conclusions: It seems unlikely that the MEN1 gene is of importance in the progression of secondary hyperparathyroidism.