Introducción: la deficiencia de testosterona es un síndrome clínico y bioquímico asociado con alteraciones sexuales, metabólicas, musculoesqueléticas y reproductivas. En varones en edad fértil, la administración de testosterona exógena induce supresión del eje hipotálamo–hipófiso–gonadal por retroalimentación negativa, con disminución de LH y FSH, reducción de la testosterona intratesticular y potencial deterioro de la espermatogénesis. Entre 2021 y 2026, la literatura ha aportado evidencia relevante sobre los efectos clínicos de la terapia de reemplazo con testosterona (TRT) y sobre alternativas terapéuticas dirigidas a preservar la fertilidad.
Objetivo: evaluar sistemáticamente la evidencia publicada entre enero de 2021 y febrero de 2026 acerca de los beneficios clínicos de la TRT y de las estrategias terapéuticas orientadas a optimizar el estado androgénico sin comprometer la función reproductiva.
Métodos: se realizó una revisión sistemática conforme a la guía PRISMA. Se efectuó búsqueda en PubMed/MEDLINE, Scopus y Web of Science para el período 2021–2026. Se incluyeron ensayos clínicos, estudios observacionales, revisiones sistemáticas, metaanálisis y guías internacionales que reportaran desenlaces en función sexual, composición corporal, densidad mineral ósea, estado anímico, perfil metabólico, parámetros hormonales, parámetros seminales y eventos adversos.
Resultados: en varones con hipogonadismo bioquímicamente confirmado, la TRT se asocia con mejoría significativa de la libido, función eréctil, masa magra, densidad mineral ósea y calidad de vida. En poblaciones específicas, como síndrome de Klinefelter, enfermedad de células falciformes e hipogonadismo secundario, se describen beneficios clínicos bajo seguimiento protocolizado. La evidencia reciente no demuestra incremento concluyente del riesgo prostático ni cardiovascular cuando la indicación es adecuada y existe monitorización hematológica. Desde el eje reproductivo, la TRT y el uso de esteroides anabólico-androgénicos se asocian con supresión gonadotrópica y deterioro de parámetros seminales; la recuperación tras la suspensión es variable. En varones con deseo de paternidad, la hCG (sola o combinada con FSH), los moduladores selectivos del receptor de estrógeno y, en casos seleccionados, los inhibidores de aromatasa permiten aumentar la testosterona sérica preservando la función intratesticular y mejorar parámetros seminales en subgrupos específicos. Las intervenciones sobre obesidad y comorbilidades metabólicas se asocian con reversibilidad parcial del hipogonadismo funcional y mejoría reproductiva.
Conclusiones: la evidencia publicada entre 2021 y 2026 respalda la TRT como tratamiento eficaz en hipogonadismo correctamente diagnosticado. Sin embargo, en varones en edad reproductiva es imprescindible evaluar el deseo de paternidad antes de iniciar terapia androgénica. Las estrategias basadas en estimulación del eje gonadal y el abordaje de factores metabólicos permiten optimizar el estado androgénico preservando la integridad funcional del eje hipotálamo–hipófiso–gonadal y la espermatogénesis.
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