Percutaneous ethanol (PEIT) and calcitrol (PCIT) injection therapy are ineffective in treating severe secondary hyperparathyroidism.

BACKGROUND

Secondary hyperparathyroidism (2HPT) is a frequent complication of long-term dialysis treatment and, despite recent advances in medical therapy, surgical parathyroidectomy (PTX) is required in a considerable number of uraemic patients. Recently, other modalities of therapy, such as ultrasound-guided percutaneous parathyroid injection of ethanol (PEIT) or of calcitriol (PCIT), have been used to treat refractory 2HPT. Our objectives were to evaluate the efficacy of these therapeutic modalities and to analyse their effects on parathyroid cell proliferation.

METHODS

Nineteen haemodialysis patients with severe 2HPT were studied. Ten underwent PEIT (Group I) and nine underwent PCIT (Group II). After treatment, five patients in each group were submitted to PTX. Parathyroid cell proliferation was appraised at the beginning and at the end of the study by fine-needle aspiration biopsy, making use of immunocytochemical testing for Ki-67. The surgically removed glands were submitted to histopathological analysis and cellular proliferation was evaluated.

RESULTS

Both PEIT and PCIT proved inefficient in controlling 2HPT. Comparing study onset with day 60, both groups showed a significant decrease in serum-ionized calcium: 5.3+/-0.3 vs 5.1+/-0.5 mg/dl (P = 0.03) in Group I and 5.5+/-0.4 vs 5.4+/-0.3 mg/dl (P = 0.03) in Group II. Other laboratory parameters were unchanged. There was a significant, although transitory, enlargement in glandular volume in Group II at day 30 when compared with study onset (1.5+/-0.6 vs 1.7+/-0.7 cm(3), P = 0.02). When comparing the two groups, Group I showed a glandular volume smaller than that of Group II at days 30 (1+/-0.5 vs 1.7+/-0.7 cm(3), P = 0.003), 60 (0.8+/-0.4 vs 1.5+/-0.9 cm(3), P = 0.006) and 90 (0.8+/-0.5 vs 1+/-0.7 cm(3), P = 0.02). Cellular proliferation, which was equally elevated in both groups at the beginning of the study, could not be evaluated at the end due to lack of material. The majority of glands obtained through PTX presented intensive cellular proliferation and contained areas of nodular hyperplasia, even those glands with a volume of <0.5 cm(3).

CONCLUSION

In our experience, both PCIT and PEIT were unable to control severe 2HPT in chronic haemodialysis patients. We believe that the severity of the 2HPT in the study patients, in conjunction with the fact that we excluded from treatment parathyroid glands with a volume of <0.5 cm(3), were the most important causes of this failure.