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Little data has addressed the issue of male fertility on anti TNF Therapy. The recent article by Villiger and colleagues in this journal suggested that sperm quality of patients with spondyloarthritis receiving long term anti TNF inhibition therapy was comparable to that in healthy
controls and imputed reassurance for male patients treated with anti TNF therapy for fatherhood.
We report herein one...
We report herein one of our AS patients whose sperm count decreased precipitously while treated with infliximab, without other DMARDs, correlating with infertility while under treatment.
A 50 years old male was diagnosed 4 years earlier to have AS.
Diagnosis was based on symptoms of inflammatory lower back pain and limitation of spinal motion, with imaging support of sacroilitis on MRI study. After failure of prolonged NSAID treatment he was started on anti TNF therapy. His treatment was changed several times due to incomplete response to treatment. During his treatment period the patient was evaluated at the hospital's IVF unit for suspected infertility and tested for sperm count routinely.
The patient was started first on etanercept 25 mg twice weekly with his first sperm count after 3 months of treatment 6 million/cc. Due to secondary failure, after 16 months treatment was switched to adalimumab 40mg twice monthly, and then after another 6 months to infiximab 400 mg once every 8 weeks. Three months after initiating infliximab the sperm count was 2 million; three months later it had decreased to 0.2 million/cc, and then 0.1 million/cc three months later. At that point infiximab was discontinued, despite a positive clinical response to
treatment, due to suspected effect of the treatment on the sperm count.
Six months after discontinuing infliximab, the sperm count rose to one million and soon thereafter his wife became pregnant without resorting to IVF.
TNF has been shown to have a positive role in the male gonadal tract with an effect on germ cell apoptosis. However at high tissue concentration, adverse effects on spermatogenesis have also been noted.
Villiger et al showed that the sperm quality of patients with inactive disease treated with anti TNF therapy is comparable to that of healthy controls. Yet an earlier letter by La Montagna et al showing no alterations in serum follicle stimulating hormone, luteinising hormone,
prolactin, and testosterone levels testing 3 fertile male patients on anti TNF therapy for treatment of ankylosing spondylitis, described asthenoazoospermia in two patients, potentially related to anti TNF therapy.
The possible negative effect of active inflammatory disease on gonadal dysfunction is appreciated. In the present case, despite successful inhibition of active disease by infliximab, it was discontinuation of the drug which led to increased sperm count which was translated into improved fertility. We believe that caution is advised and the possibility of such an effect should be taken into consideration when male infertility is suspected in patients treated with anti TNF agents.
Further large studies are needed to fully explore the effect of anti TNF agents on male fertility.