Schistosomiasis and the developing child: Impacts on growth, puberty, and endocrine health across disease phenotypes

Background: Schistosomiasis remains highly prevalent in children and adolescents in endemic regions and contributes significantly to growth failure, delayed puberty, and endocrine dysfunction. The severity of these outcomes varies across intestinal, urogenital, and hepatosplenic disease phenotypes, with hepatic fibrosis posing the greatest risk. Despite emerging evidence, an integrated synthesis linking clinical, endocrine, and mechanistic pathways remains limited.

Objectives: To evaluate the effects of schistosomiasis on growth, puberty, endocrine axes, and reproductive health, and to synthesize mechanistic pathways and potential interventions to prevent long-term sequelae.

Methods: A structured narrative review with systematic elements was conducted using PubMed, Scopus, Web of Science, and Google Scholar (1990–2025). Inclusion criteria encompassed human or mechanistic studies reporting anthropometric, GH–IGF-1, endocrine, pubertal, or fertility outcomes in S. mansoni, S. haematobium, or S. japonicum infection. Studies were screened, extracted, and quality-assessed using NOS, RoB 2, SYRCLE, and AMSTAR-2 tools. Findings were synthesized descriptively due to methodological heterogeneity.

Results: Twenty-one studies met all inclusion criteria. Growth impairment was the most consistent finding, with stunting strongly associated with higher egg burdens and chronicity of infection. Children with hepatosplenic disease showed the most severe deficits, often with height-for-age z-scores below –2 and persistent impairment despite treatment. Three studies demonstrated marked suppression of IGF-1 and IGFBP-3, and one study identified blunted GH secretory responses in children with hepatic fibrosis. In contrast, intestinal or bladder-limited disease produced milder growth effects, and IGF-1 levels were generally preserved unless infection intensity was high.

Pubertal abnormalities were linked primarily to chronic hepatosplenic disease, with delayed pubertal progression attributed to low IGF-1, inflammatory stress, nutritional compromise, and environmental enteric dysfunction. Reinfection studies showed that puberty and rising DHEA-S can reduce susceptibility to infection, suggesting a reciprocal relationship between endocrine maturation and disease dynamics.

Reproductive sequelae were predominantly observed in urogenital schistosomiasis. Male genital schistosomiasis was associated with reduced semen volume, increased sperm apoptosis, and occasional testosterone suppression. Female genital schistosomiasis produced cervicovaginal lesions, contact bleeding, subfertility, miscarriage, and altered estrogen-like parasite metabolites. These effects were attributable to direct genital tract pathology rather than systemic endocrine axis disruption.

Mechanistic pathways identified across studies included egg-driven granulomatous inflammation, hepatic fibrosis with reduced hepatocyte synthetic function, cytokine-mediated GH resistance, anemia-related catabolism, and parasite-derived estrogenic metabolites affecting reproductive tissues. Praziquantel therapy improved nutritional status and growth—particularly when given before the development of hepatic fibrosis, though IGF-1 recovery was incomplete in severe disease.

Conclusion: Schistosomiasis profoundly affects growth, puberty, and endocrine function, with the most severe forms occurring in hepatosplenic and urogenital disease. Early diagnosis, timely praziquantel treatment, nutritional support, routine growth and pubertal monitoring are essential to prevent irreversible developmental and reproductive consequences.