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Letters to the Editor |
1 Departments of Clinical Chemistry, and Laboratory Medicine
2 Internal Medicine, Isala Klinieken Zwolle, The Netherlands.
aAddress correspondence to this author at: Postbus 10.500, 8000 GM Zwolle, The Netherlands. Fax 31-38-424-2676; e-mail jaremijn{at}gmail.com.
To the Editor:
Hyperparathyroidism is a potentially serious complication in patients with advanced renal insufficiency (1). As renal mass dwindles and phosphate excretion gets more difficult, synthesis of 1,25-dihydroxycholecalciferol is impaired, and concentrations of fibroblast growth factor-23 increase (2), leading to low serum calcium concentrations and an initially appropriate response of the parathyroids: parathyroid hormone (PTH) synthesis increases. Subsequently, however, parathyroid hypertrophy gradually develops. After a period of time, the calcium-sensing receptor is reset, the calcium x phosphate product increases, soft tissues and vessels become calcified, and bone is destroyed. Eventually, down-regulation of PTH synthesis declines and the parathyroid hypertrophy is transformed into an autonomous nodular hyperplasia, which can be resolved only by parathyroidectomy (3). Several tactics for parathyroidectomy have been employed: (a) subtotal (3
) parathyroidectomy, (b) total parathyroidectomy with immediate partial autotransplantation, e.g., in the forearm, and (c) total parathyroidectomy with cryopreservation and elective/delayed autotransplantation (4)(5).
In the present report we describe a 43-year-old man with hyperparathyroidism due to long-standing renal failure. After failure of his first renal transplant, the patient returned to hemodialysis. At that time, total parathyroidectomy was performed with partial autotransplantation of parathyroid tissue into his right forearm (method b). A second kidney transplant was life-sustaining; subsequently, the patient maintained a stable serum creatinine concentration of 110 µmol/L (
1.2 mg/dL). Large fluctuations of PTH were observed, however (Table 1
). The PTH concentrations were inconsistent with serum calcium and alkaline phosphatase (AP) values. The fluctuations of PTH were probably not due to our analytical methods, because they were confirmed with several different intact PTH immunoassays: Elecsys® PTH Immunoassay (Roche Diagnostics GmbH), Immulite® (Diagnostic Products Corp.), and Advantage® (Nichols Institute Diagnostics). We hypothesized that the fluctuating PTH concentrations might be due to preanalytical differences, i.e., which arm was used for blood collection. Therefore, we measured PTH in blood samples simultaneously drawn from the left and right arms. Interestingly, the left-arm sample had a measured PTH of 4.1 pmol/L, whereas the right-arm sample yielded a PTH of 235 pmol/L (Table 1
: t = 9). These results confirm our theory that the increased PTH concentrations were due to sampling of blood downstream of the transplanted parathyroid gland. The short half-life of intact PTH (2–4 min) explains the normal values measured in the left arm, which represent the "true" systemic PTH concentrations.
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In conclusion, in a patient with a parathyroid graft in a forearm, PTH must be measured in blood collected from the contralateral arm.
References
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