Nephrol Dial Transplant (2003) 18: III62-III64
© 2003 European Renal Association-European Dialysis and Transplant Association
Original Article
Intervention for recurrent secondary hyperparathyroidism from a residual parathyroid gland
Department of Nephroendocrinology, Kojinkai Central Hospital, Sendai, Japan
 |
Abstract |
|---|
 Top Abstract IntroductionMethods and resultsReferences |
|---|
There is a significant recurrence rate of secondary (renal) hyperparathyroidism after total parathyroidectomy (PTx) with forearm autograft. The lesions responsible for recurrent hyperparathyroidism are mainly the parathyroid autografts, but in some cases there are previously undetected residual or ectopic parathyroid glands. In Kojinkai hospitals, 155 haemodialysis out-patients had total PTx and forearm autograft for severe renal hyperparathyroidism and, during the past 18 years, 40 of them developed recurrent or persistent renal hyperparathyroidism. Five patients were treated by percutaneous ethanol injection therapy (PEIT): four patients had residual parathyroid glands and one patient had an ectopic parathyroid gland. The results of PEIT depended on the functioning of the parathyroid autografts. In two patients with non-functioning autografts, the effect of PEIT was remarkable; both showed ‘hungry bone’ syndrome and became hypoparathyroid. In the three patients with functioning autografts, the clinical course after PEIT was mild, but resection of the autograft was required in one patient. When an echo-guided approach is possible, PEIT for residual parathyroid glands is an effective intervention for the management of recurrent renal hyperparathyroidism; however, there is a risk of hypoparathyroidism in patients with non-functioning parathyroid autografts. As parathyroid autografts consist of multiple nodules, echo-guided injection of ethanol or calcitriol to each nodule is almost impossible and therefore resection of the autograft is indicated for autograft-dependent recurrent renal hyperparathyroidism.
Keywords: ectopic parathyroid gland; PEIT; persistent secondary hyperparathyroidism; recurrent secondary hyperparathyroidism; residual parathyroid gland
|
Introduction |
|---|
|
TopAbstractIntroductionMethods and resultsReferences |
|---|
In haemodialysis (HD) patients with severe secondary (renal) hyperparathyroidism (2HPT) refractory to medical treatment, such as intravenous pulse therapy with calcitriol or maxacalcitol, total parathyroidectomy (PTx) with forearm autograft is the preferred procedure [1]. It is important to remove all parathyroid glands, including supernumerary glands, at the initial operation and to choose appropriate and adequate parathyroid tissue for the autograft to prevent persistent or recurrent 2HPT [2]. However, the recurrence or persistence of renal hyperparathyroidism caused by enlarged parathyroid autografts in graft-dependent patients is
30% at 7 years after the initial operation [1]. Residual or ectopic parathyroid glands can also be the cause. When an echo-guided approach to locate residual or ectopic parathyroid glands is possible, it has been reported that percutaneous ethanol injection therapy (PEIT) and percutaneous calcitriol injection therapy (PCIT) are suitable treatments [3,4]. |
Methods and results |
|---|
|
TopAbstractIntroductionMethods and resultsReferences |
|---|
Intervention for recurrent renal hyperparathyroidism
Of 729 HD out-patients of Kojinkai hospitals (Kojinkai Central Hospital, Kimachi Hospital, Nagamachi Clinic and Ishinomaki Clinic), 155 had PTx with forearm autograft between March 15 1984 and July 2 2002. Of these, 40 developed recurrent or persistent renal hyperparathyroidism: 21 recurrences in autograft-dependent patients (15 for intervention), 14 recurrences because of residual parathyroid gland(s) (six for intervention) and five because of ectopic parathyroid gland(s) (two for intervention). Even when at least four parathyroid glands had been removed at the initial operation, there were still eight patients with recurrent renal hyperparathyroidism because of residual gland(s), and three patients with ectopic parathyroid gland(s), suggesting the existence of supernumerary glands (Table 1
).
|
In most cases, there is only one residual or ectopic parathyroid gland responsible for the recurrent hyperparathyroidism, which is similar to renal hyperparathyroidism caused by a single gland in which only one nodular hyperplasic parathyroid gland is responsible and the other glands are undetectable by ultrasonic examination. Such cases are a good indication for selective parathyroid PEIT.
Case reports
Case 1 represents the typical clinical course of PEIT in a patient with single gland involvement (Figure 1). The 50-year-old man began HD treatment in 1986, and in 1989 his parathyroid function tests were serum calcium concentration adjusted by serum albumin concentration (adjusted Ca) 10.8 mg/dl, phosphate 6.2 mg/dl and intact PTH (i-PTH) 630 pg/ml. Ultrasonic examination of the neck in July 1999 showed enlargement of the left lower (LL) parathyroid gland (1900 mm3). The other three glands were undetectable. Selective parathyroid PEIT for the LL parathyroid gland was performed in August 1999, and 1 week later the adjusted Ca and i-PTH had decreased to 7.8 mg/ml and 160 pg/ml, respectively, and the phosphate concentration was 5.5 mg/dl. At the end of the study period in February 2000, adjusted Ca was 9.9 mg/dl, phosphate 5.0 mg/dl and i-PTH 73 pg/ml.
|
In 40 patients with recurrent or persistent renal hyperparathyroidism from the Kojinkai hospitals, 23 had interventions: five had PEIT, four of them had residual glands and one patient had an ectopic parathyroid gland. The effect of PEIT for residual or ectopic parathyroid glands depends on the function of the parathyroid autografts. If the autograft is not functioning, there is a risk of hypoparathyroidism.
Case 2 is a patient with recurrent renal hyperparathyroidism caused by a residual parathyroid gland. The 61-year-old woman began HD treatment in November 1976, and total PTx with forearm autograft was performed in May 1989, removing four parathyroid glands (RU 1600 mg, RL 300 mg, LU 3500 mg and LL 1200 mg). Parathyroid function test results in November 1992 were adjusted Ca 9.7 mg/dl, phosphate 6.4 mg/dl and i-PTH 567 mg/dl. Ultrasonic examination of the neck revealed an enlarged parathyroid gland (4980 mm3) below the lower pole of the left lobe of the thyroid gland, and the forearm autografts were undetectable. Selective parathyroid PEIT was performed in December 1992, and 1 week later the adjusted Ca, phosphate and i-PTH had decreased to 6.9 mg/ml, 2.8 mg/dl and 33 pg/ml, respectively. The patient had a transient tetany attack suggesting that the parathyroid autografts were not functioning.
Case 3 is a patient with recurrent renal hyperparathyroidism caused by a residual parathyroid gland and enlarged autografts (Figure 2). The 51-year-old man began HD treatment in September 1987 and underwent a total PTx with forearm autograft in October 1995, during which three parathyroid glands were removed (RU 490 mg, LU 1140 mg and LL 60 mg). The results of post-operative parathyroid function tests were adjusted Ca 10.9 mg/dl, phosphate 5.4 mg/dl and i-PTH 440 pg/ml. Ultrasonic examination of the neck revealed an enlarged residual parathyroid gland (RL 820 mm3) and also enlarged autografts (total volume 790 mm3). The Casanova test was negative (before 490 pg/ml, after 370 pg/ml) [5]. Selective parathyroid PEIT was performed in November 2000, and by April 2001 the ultrasonic volume of the RL gland had decreased to 75 mm3 and the autografts had increased to 1050 mm3. Adjusted Ca was 10.5 mg/dl, phosphate 4.1 mg/dl, i-PTH was 310 pg/ml and the Casanova test was positive (before 330 pg/ml, after 88 pg/ml). Resection of the parathyroid autografts was done in July 2001, and two parathyroid clusters, 815 mg and 460 mg, were removed. Four days after surgery, the phosphate concentration was 4.5 mg/dl, and the adjusted Ca and i-PTH concentrations had decreased to 9.4 mg/dl and 25 pg/ml, respectively. The results of parathyroid function tests in March 2002, at the end of the study period, were adjusted Ca 9.2 mg/dl, phosphate 4.7 mg/dl and i-PTH 160 pg/ml.
|
PEIT for enlarged parathyroid autografts is difficult because they consist of multiple nodules, and echo-guided injections of ethanol or calcitriol to each nodule is almost impossible. Resection of autografts is recommended for graft-dependent recurrent renal hyperparathyroidism because the enlarged autografts can be easily removed from the forearm under local anaesthesia [2].
Conclusion
Selective parathyroid PEIT is a good option for patients with recurrent renal hyperparathyroidism caused by residual or ectopic parathyroid glands when an echo-guided approach to these glands is possible. However, PEIT carries a risk of hypoparathyroidism in patients with non-functioning parathyroid autografts.
|
Notes |
|---|
Correspondence and offprint requests to: Shigeru Yumita, Institute, Director, Department of Nephroendocrinology, Kojinkai Central Hospital, 2-1-6, Tsutsujigaoka, Miyagino-ku, Sendai 983-0852, Japan. Email: s_yumita{at}polka.plala.or.jp
|
References |
|---|
|
TopAbstractIntroductionMethods and resultsReferences |
|---|
- Tominaga Y. Surgical management of secondary hyperparathyroidism in uremia. Am J Med Sci 1999; 317:390–397[CrossRef][Medline]
- Tominaga Y, Uchida K, Haba T et al. More than 1,000 cases of total parathyroidectomy with forearm autograft for renal hyperparathyroidism. Am J Kidney Dis 2001; 38 [Suppl 1]:S168–S171[Medline]
- Kitajima K, Fuchinoue S, Agishi T, Hayashi T. Percutaneous ethanol injection therapy (PEIT) for secondary hyperparathyroidism. J Jap Soc Dial Ther 1999; 32:1021–1027
- Kunimatu K, Kakuta T, Fujisaki T et al. A case of secondary hyperparathyroidism in which percutaneous calcitriol injection therapy (PCIT) was effective for ectopic parathyroid gland. J Jap Soc Dial Ther 2001; 34:1501–1504
- De Francisco AL, Amado JA, Casanova D et al. Recurrence of hyperparathyroidism after total parathyroidectomy with autotransplantation: a new technique to localize the source of the hormone excess. Nephron 1991; 58:306–309[Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||