Effects of H2-Receptor Antagonists on Male Reproductive Health

Histamine H2-receptor antagonists, widely prescribed for peptic ulcer disease and gastro-oesophageal reflux, have been shown to influence male reproductive function through antiandrogenic pathways. By blocking H2 receptors expressed in Leydig cells, Sertoli cells and smooth muscle layers of the epididymis and vas deferens, these agents can disrupt steroidogenesis, reduce serum testosterone and alter intratesticular hormone conversion. Empirical studies in animal models have documented impairment of spermatogenesis, increased germ cell apoptosis and structural damage to the seminiferous tubules and peritubular tissue. Such changes may lead to reduced sperm count, motility and fertilising potential. Given the global prevalence of H2-receptor antagonist use, understanding these reproductive effects is critical for risk assessment, counselling of patients of reproductive age and exploration of protective interventions.

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Effects of H2-Receptor Antagonists on Male Reproductive Health publication trend

The graph below shows the total number of articles in effects of h2-receptor antagonists on male reproductive health across all publications each year (not limited to Nature Index journals).

Technical terms

H2-receptor antagonist: A drug that inhibits histamine binding to H2 receptors, commonly used to reduce gastric acid secretion.

Steroidogenesis: The biochemical process by which steroid hormones, including testosterone, are synthesised in Leydig cells.

Apoptosis: Programmed cell death characterised by DNA fragmentation, cell shrinkage and membrane blebbing.

Androgen receptor (AR): A nuclear receptor activated by binding of androgens, regulating gene expression crucial for male reproductive development.

Seminiferous tubules: Coiled structures within the testis where germ cells undergo mitotic and meiotic divisions to form mature spermatozoa.

References

1. Vitamin B12 Prevents Cimetidine-Induced Androgenic Failure and Damage to Sperm Quality in Rats. Frontiers in Endocrinology (2019).
2. NF-kB overexpression and decreased immunoexpression of AR in the muscular layer is related to structural damages and apoptosis in cimetidine-treated rat vas deferens. Reproductive Biology and Endocrinology (2013).
3. Enhanced ERbeta immunoexpression and apoptosis in the germ cells of cimetidine-treated rats. Reproductive Biology and Endocrinology (2009).
4. Morphological evidences indicate that the interference of cimetidine on the peritubular components is responsible for detachment and apoptosis of Sertoli cells. Reproductive Biology and Endocrinology (2008).