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Cavernosal arterial insufficiency and metabolic syndrome probably represent a common pathology of endothelial dysfunction in recipients of high-dose therapy and stem-cell transplantation

Chatterjee, R.; Palla, K.; Kottaridis, P.D.; (2004) Cavernosal arterial insufficiency and metabolic syndrome probably represent a common pathology of endothelial dysfunction in recipients of high-dose therapy and stem-cell transplantation. Journal of Clinical Oncology , 22 (11) pp. 2253-2254. 10.1200/JCO.2004.99.556.

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Abstract

Improved long-term survival of recipients of high-dose myeloablative chemotherapy/radiotherapy (HDC) and stem-cell transplantation (SCT) has led to increased awareness of long-term side effects, including those of multiple endocrinopathy, which can ultimately affect the quality of life in these patients.1 We have previously shown that HDC can cause hypogonadism with germ and Leydig cell insufficiency, as defined by diminished testicular volume, low basal, and human chorionic gonadotropin-stimulated testosterone levels, and cavernosal vascular insufficiency in patients with hematologic malignancies presenting with erectile dysfunction (ED).2 Taskinen et al3 have recently reported a high incidence (39%) of core signs of "X" syndrome (metabolic syndrome) in a small group of 23 survivors of SCT, which includes type II diabetes mellitus, hypertension, and hypertriglyceridaemia. Such information is important as it can contribute to long-term cardiovascular comorbidity and mortality in SCT survivors. Although the exact etiology is unknown, endothelial dysfunction may contribute to X syndrome.3 However, little is known about the association between cavernosal vasculopathy and X syndrome. This is important, as ED may present as a symptom of a serious underlying disease of X syndrome. Here we report two recipients of HDC who developed some of the core signs of X syndrome (impaired glucose tolerance test according WHO criteria, persistent hypertension, and hyperlipidemia)3,4 and ED at 72 and 80 months post-transplant, respectively. Table 1 provides patients' information, including endocrine profile and penile Doppler studies at the time of diagnosis of the X syndrome. Endocrine assays, testicular ultrasonography scan, and color Doppler studies of cavernosal vessels were conducted according to previous published protocols.2 Both patients had fasting lipid profile, endocrine tests at 0900 hours, which was followed by glucose tolerance test. Routine biochemical tests were undertaken in the chemical pathology lab at University College London Hospital (London, UK). Patient 1 had normal weight (body-mass index 21 kg/m2 and hip/waist ratio 0.7), and patient 2 was overweight (body-mass index > 33 kg/m2 and hip/waist ratio > 1) and also had persistent functional hyperplolactinemia with grade 2 gynecomastia. However, he had normal magnetic resonance imaging scan of the pituitary gland and normal thyroid function. Our data suggests a possible common link between endothelial dysfunction, ED, and metabolic syndrome. Even though aging may be an additional contributing factor implicated for the development of hypogonadism, atherosclerosis, and changes in penile blood vessels,5 these findings highlight the fact that endothelial dysfunction manifested as generalized vasculopathy may be an important pathologic link between the metabolic syndrome and the cavernosal arterial insufficiency.

Type: Article
Title: Cavernosal arterial insufficiency and metabolic syndrome probably represent a common pathology of endothelial dysfunction in recipients of high-dose therapy and stem-cell transplantation
DOI: 10.1200/JCO.2004.99.556
Publisher version: http://dx.doi.org/10.1200/JCO.2004.99.556
Language: English
UCL classification: UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Cancer Institute > Research Department of Haematology
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Pop Health Sciences > Inst for Women's Health
URI: http://discovery.ucl.ac.uk/id/eprint/8702
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