Resistance to Human Recombinant Erythropoietin in Hypothyroidism
Author(s) -
Cem Sungur,
Tomris Erbaş,
Tekin Akpolat,
Nurol Arık,
Ünal Yasavul,
Çetin Turgan,
Şali Çaḡlar
Publication year - 1992
Publication title -
acta haematologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.574
H-Index - 56
eISSN - 1421-9662
pISSN - 0001-5792
DOI - 10.1159/000204676
Subject(s) - erythropoietin , recombinant dna , medicine , endocrinology , immunology , biology , genetics , gene
Resistance to Human Recombinant Erythropoietin in Hypothyroidism C. Cem Sungur T. Tomris Erbas T. Tekin Akpolat N. Nurol Arik Ü. Ünal Yasavul Ç. Çetin Turgan Ş. Şali Çaḡlar Dr. Cem Sungur, Nephrology Unit, Department of Internal Medicine, Hacettepe Medical School, TR-06100 Sihhiye, Ankara (Turkey) respectively (fig. 1). The target level of Hct was achieved within 6 weeks. The dose of hrEPO was reduced to 4,000 units once weekly and was administered subcutaneously. Her Hb and Hct levels have been maintained with the same regimen up till now. These findings not only prove that underlying hypothyroidism may be a cause of resistance to hrEPO treatment but also suggest that an euthy-roid state is essential for the action of erythropoietin on the bone marrow. References Larsson SD: Anemia and iron metabolism in hypothyroidism. Acta Med Scand 1967;157: 349-354. Carmel A, Spencer CA: Clinical and subclinical thyroid disorders associated with pernicious anemia. Arch Intern Med 1982;142:1465-1469. Normochromic normocytic anemia is a common laboratory finding in hypothyroidism [1]. Several mechanisms have been implicated as the cause of anemia of the hypothyroid patient [2]. We have observed a hypothyroid hemodialysis patient with diminished response to human recombinant erythropoietin (hrEPO). The patient is a 37-year-old female who was accepted to our hemodialysis unit in 1979. Apart from 4.5 years with a functioning renal allograft, she was treated thrice weekly with regular hemodialysis. HrEPO treatment was instituted by the beginning of 1991 as a part of her renal replacement therapy together with oral iron supplementation. At the beginning she received 4,000 units of hrEPO thrice weekly which was administered intravenously. Her hemoglobin was 7.6 g/dl and haematocrit 24.7% at the initiation of therapy. She failed to respond to this treatment within 3 months. The route of administration was switched to subcutaneous injections, and the dose regimen was again 4,000 units thrice weekly. The expected he-matological response was not observed within 12 weeks. In order to define the underlying mechanism for hrEPO resistance she underwent a hematological survey which yielded the following results: Hb, 8.6 g/dl; Hct,
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