Gonadal and sexual function in men treated for childhood cancer

Relander, Thomas; Cavallin‐Ståhl, Eva; Garwicz, Stanislaw; Olsson, Anders; Willén, Marianne

doi:10.1002/1096-911x(200007)35:1<52::aid-mpo9>3.0.co;2-y

Cited by 105 publications

(56 citation statements)

References 26 publications

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“…Almost all survivors who received a cyclophosphamide TCD of 10 g/m 2 or more were at risk for severe spermatogenic dysfunction. These findings support the earlier observations in which a dose-dependent effect of cyclophosphamide was found [20,24]. This dose effect was not found for procarbazine containing regimens, which indicates that this agent might already be gonadotoxic in low concentrations in males.…”

Section: Discussionsupporting

confidence: 91%

“…Although several studies have shown the value of modern fertility markers for prediction of spermatogenesis, studies on gonadal function after chemotherapy and irradiation in large series of adult male cancer survivors, using Inhibin B as a novel serum markers are lacking [5,15,[20][21][22]. Therefore, we performed a study in a full single center cohort of male childhood cancer survivors (n ¼ 248).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of childhood cancer treatment on fertility markers in adult male long‐term survivors

Casteren

Linden

Hakvoort-Cammel

et al. 2008

Pediatric Blood & Cancer

124

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BackgroundAlthough it is accepted that pediatric cancer treatment harbors a risk of gonadal damage, large cohort studies using up‐to‐date fertility markers are lacking.ProcedureThe aim of our study was to evaluate the gonadal toxicity of childhood cancer treatment using fertility markers. We included 248 adult male long‐term survivors of childhood cancer. Median age at diagnosis: 5 years, median age at follow‐up: 24 years, median follow‐up time 18 years. We evaluated patient characteristics, treatment modalities, testicular size, and endocrinological parameters including Inhibin B, luteinizing hormone (LH), follicle‐stimulating hormone (FSH), and testosterone.ResultsThe median value of Inhibin B in the cancer survivor group was 126 ng/L versus 177 ng/L in the control group (P < 0.001). In the survivors, 67% had Inhibin B levels below the normal reference value of 150 ng/L compared with 26% in the control group (P < 0.05). Inhibin B was the most sensitive discriminator between survivors and controls. Significantly decreased Inhibin B levels and increased FSH levels were found in men treated for Hodgkin and non‐Hodgkin lymphoma, acute‐myeloid leukemia, neuroblastoma, and sarcoma as compared to other malignancies. Cumulative dosages of procarbazine and cyclophosphamide were the only independent chemotherapy‐related predictors for decrease of Inhibin B levels and increase of FSH. Age at time of treatment did not influence post‐treatment Inhibin B or FSH levels.ConclusionsSevere gonadal impairment is a risk in a considerable subgroup of childhood cancer survivors based on current fertility markers like Inhibin B. Males receiving gonadotoxic treatment before puberty are not protected from post treatment gonadal dysfunction. Pediatr Blood Cancer 2009;52:108–112. © 2008 Wiley‐Liss, Inc.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Effect of childhood cancer treatment on fertility markers in adult male long‐term survivors

Casteren

Linden

Hakvoort-Cammel

et al. 2008

Pediatric Blood & Cancer

124

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“…Deficits of LH and FSH secretion following irradiation of the hypothalamicpituitary region occur less often than GHD, and generally only occur following doses to the sellar region, O30 to 40 Gy (Sklar & Constine 1995, Relander et al 2000, Byrne et al 2004, Armstrong et al 2009, Green et al 2009). In a report from the CCSS on survivors of childhood CNS tumors, late menarche (defined by the onset of menstrual cycles after 16 years of age) was used as a marker for hypogonadotropic hypogonadism, given that few patients were additionally exposed to alkylating agents (Table 1), known for their ovarian toxicity.…”

Section: Hypogonadotropic Hypogonadismmentioning

confidence: 99%

“…Nonetheless, Leydig cell dysfunction may be observed following treatment with alkylating agent regimens, with some reports indicating that from 10 to 57% of male subjects can develop elevated serum concentrations of LH following treatment (Bramswig et al 1990, Siimes et al 1995, Heikens et al 1996, Mackie et al 1996, Papadakis et al 1999, Sklar 1999, Relander et al 2000, Kenney et al 2001, Romerius et al 2009). When it does occur, chemotherapy-induced Leydig cell dysfunction is generally subclinical (Afify et al 2000, Bakker et al 2004, Sanders 2004.…”

Section: Leydig Cell Dysfunctionmentioning

confidence: 99%

Endocrine complications in long-term survivors of childhood cancers

Chemaitilly

Sklar²

2010

Endocrine-Related Cancer

181

149

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Endocrine disturbances are among the most frequently reported complications in childhood cancer survivors, affecting between 20 and 50% of individuals who survive into adulthood. Most endocrine complications are the result of prior cancer treatments, especially radiotherapy. The objective of the present review is to discuss the main endocrine complications observed in this population, including disorders of the hypothalamic-pituitary axis, disorders of pubertal development, thyroid dysfunction, gonadal dysfunction, decreased bone mineral density, obesity, and alterations in glucose metabolism with a special focus on recent findings reported from the Childhood Cancer Survivor Study.

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“…Leydig cell dysfunction may be observed following treatment with alkylating agent regimens. Ten to 57% of male patients can develop elevated serum concentrations of LH following treatment, but chemotherapyinduced Leydig cell dysfunction is generally subclinical (Bramswig et al 1990, Kenney et al 2001, Mackie et al 1996, Relander et al 2000, Romerius et al 2009, Sklar 1999). …”

Section: Leydig Cellsmentioning

confidence: 99%