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Jemcov TK, Petakov M, Bogdanovic A, Djukanovic L, Lezaic VD. Parathyroidectomy and Improving Anemia. Arch Surg. 2008;143(1):97–98. doi:10.1001/archsurg.2007.26
We have read with great interest the article written by Chow and coworkers1 showing that anemia improved after total parathyroidectomy (PTX), especially in the patients who received therapy with human recombinant erythropoietin. As the mechanisms for the improvement were not considered in the article, we would like to share our results concerning increased erythropoiesis after PTX, even though they were obtained from an investigation of a small patient group.
Nine patients (5 men; mean [SD] age, 45.0 [15.4] years) who had been receiving regular hemodialysis for 76.8 [43.8] months were included in the study after subtotal PTX. All of them gave informed consent to participate in the study. Indication for PTX was based on clinical, biochemical, and radiological criteria.2 Three patients (patients 6, 7, and 8 in the Table) were positive for hepatitis virus B or C. None of the patients had iron deficiency anemia or blood loss, and none of them were treated with human recombinant erythropoietin before or after PTX. Histological examination found hyperplasia in all extirpated glands. The following laboratory analyses were done before and 6 months after PTX in all patients: hemoglobin, serum calcium, phosphorus, alkaline phosphatase, intact parathormone (iPTH) (radioimmunoassay; Nichols Institute Diagnostics, San Juan Capistrano, California) (normal values, 10-55 pg/mL), erythropoietin (Epo) (enzyme-linked immunosorbent assay 500; Medac, Wedel, Germany) (normal values for healthy nonanemic adults, 4-25 mU/mL), bone marrow burst-forming units erythroid (BFU-E)
(assayed by methyl cellulose culture technique in vitro3), and bone marrow cellularity.
Six months after PTX, serum iPTH levels were 10 to 69 times lower than the initial value in all but 1 patient (Table). In the first 8 patients presented in the Table, mean (SD) iPTH levels decreased significantly (1453.7 [634.2] vs 71.0 [75.8] pg/mL, P = .02) after successful PTX. This was accompanied by increases of mean (SD) hemoglobin level (88.5 [19.4] vs 99.2 [10.7] g/L, P = .31) and mean (SD) serum Epo level (23.54 [21.1] vs 31.1 [22.5] IU/mL, P = .04) and a decline in mean (SD) BFU-E number (40.1 [12.5] vs 26.2 [10.6], P = .14). Individual data showed that serum Epo concentration increased after successful PTX in 6 of 8 patients. In 2 patients who were positive for hepatitis virus, serum Epo levels were higher than the normal range even before PTX. The increase of serum Epo levels was accompanied by greater hemoglobin values and increased bone marrow cellularity from proliferation of erythroblasts, which lowered the myeloid to erythroid ratio in the bone marrow (4.4:1 before and 1.8:1 after PTX). Numbers of BFU-E were decreased in all the patients with successful PTX (including the patient with high initial Epo).
The results presented show erythropoiesis stimulation after successful PTX by an increase in serum Epo, which suggests a direct inhibitory effect of PTH on Epo synthesis. These data are in concert with those obtained by others4 and confirm that even in patients with end-stage renal disease and without excretory kidney function, increase of erythropoietin synthesis could occur. Increased serum Epo before PTX found in 2 of our patients who were positive for hepatitis is in agreement with our previous results.5 However, in all patients with successful PTX, including these 2, bone marrow cellularity improved and BFU-E numbers decreased. That indicated that more efficacious erythroid maturation after successful PTX resulted not only from the increase of Epo synthesis but also from a decrease of bone marrow suppression. The role of PTH as a uremic toxin and inhibitor of erythropoiesis was described 2 decades ago.6
Successful PTX in 8 of 9 patients was followed with a manifold decrease of serum iPTH levels, increase of serum Epo level, more efficient maturation of the erythroid line, and alleviation of anemia.
Correspondence: Dr Jemcov, Clinic of Nephrology, Clinical Center of Serbia, Pasterova 2, 11000 Belgrade, Serbia (firstname.lastname@example.org).
Author Contributions:Study concept and design: Jemcov and Lezaic. Analysis and interpretation of data: Jemcov, Petakov, Bogdanovic, Djukanovic, and Lezaic. Drafting of the manuscript: Petakov and Bogdanovic. Critical revision of the manuscript for important intellectual content: Djukanovic and Lezaic. Statistical analysis: Jemcov and Lezaic. Study supervision: Petakov, Djukanovic, and Lezaic.
Financial Disclosure: None reported.
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