Oestrogen‐induced bone marrow aplasia in a dog with a Sertoli cell tumour

Abstract

A 10-year-old male Drahthaar dog with unilateral cryptorchidism was examined because of feminisation and myelotoxicity. Radiography and ultrasonography revealed an abdominal mass which was surgically removed. The mass was identified as a Sertoli cell tumour on histological examination. Findings on bone marrow examination were compatible with aplasia due to the oestrogens secreted by the tumoral cells. Treatment with fluids, antibiotics, whole blood transfusions, corticosteroids and lithium carbonate was unsuccessful. Survival time was 22 days after surgery.

Seminoma with Hyperesterogenemia in a Yorkshire Terrier

“…The development of seminoma in dogs can be traced from the seminiferous tubules, where it arises from spermatogenic epithelium [2]. Testicular tumors may cause feminization in dogs, which is characterized by gynaecomastia, atrophy of the contralateral testis, a pendulous prepuce and attractiveness to other male dogs, as well as fatal bone marrow depression in severe case [3,5]. Feminization is attributed to the secretion of excessive amounts of estrogens by the tumor.…”

Bone marrow bi-hypoplasia in a dog with a sertoli cell tumor

“…In all reports of hematological changes induced by high levels of estrogen, bone marrow hypoplasia was found in all hematopoietic lineages (Sherding et al, 1981;Suess et al, 1992;Sanpera et al, 2002;Sontas et al, 2009); some cases were initially bi-hypoplastic, with granulocytic or megakaryocytic cells, but became widely hypoplastic after several weeks (Sherding et al, 1981, Suess et al, 1992. In contrast, in the present case, erythroid precursor cells in the bone marrow were preserved, although there were no reticulocytes in the circulating blood.…”

“…The myelotoxicity of high levels of estrogen, endogenous or exogenous, is widely described in dogs and other animals such as ferrets. However, the action mechanism of this hormone in bone marrow is not well known (Sanpera et al, 2002). Several hypotheses have been considered: a reduction in the number of hematopoietic stem cells, an inhibition of the differentiation of these cells, changes in the utilization of iron by erythroid precursors, and a reduction of the bone marrow response to erythropoietin (Brockus, 1998).…”

“…Animals with a Sertoli cell tumor may present hyperestrogenism with a bilateral symmetrical alopecia, hyperpigmentation, gynecomastia, galactorrhea, pendulous prepuce, and atrophy of the penis and the contralateral testicle (Peters et al, 2001). Additionally, high serum levels of estrogen are considered myelotoxic in dogs because they cause bone marrow hypoplasia with pancytopenia (Sherding et al, 1981;Suess et al, 1992;Sanpera et al, 2002;Sontas et al, 2009). The prognosis for a bone marrow hypoplasia secondary to hyperestrogenism varies from reserved to unfavorable because dogs tend to not respond well to treatment and may also present with generalized secondary infections and hemorrhages (Sherding et al, 1981;Sanpera et al, 2002).…”

“…Additionally, high serum levels of estrogen are considered myelotoxic in dogs because they cause bone marrow hypoplasia with pancytopenia (Sherding et al, 1981;Suess et al, 1992;Sanpera et al, 2002;Sontas et al, 2009). The prognosis for a bone marrow hypoplasia secondary to hyperestrogenism varies from reserved to unfavorable because dogs tend to not respond well to treatment and may also present with generalized secondary infections and hemorrhages (Sherding et al, 1981;Sanpera et al, 2002). The present report describes the changes caused by the myelotoxic action of the hyperestrogenism secondary to a Sertoli cell tumor in a cryptorchid dog.…”