Paciente de mi consulta con TSH inhibida por un hipotiroidismo secundario tras intervención de adenoma de hipófisis, le reduje las hormonas tiroideas un mes por error, el motivo fue seguir rutina habitual en la monitorización de hipotiroidismos primarios el 99% en atención primaria y no pensar la causa.
Cuidado en la rutina del la monitorización de TSH para cambios de tratamiento en los hipotiroidismos, no es lo mismo el seguimiento de un hipotiroidismo primario, el 95 % de nuestra clínica que el de los hipotiroidismo secundarios y terciarios. No usar la TSH en secundarios y terciarios recordemos la fisiopatología.
En el hipotiroidismo primario, al suprimirse el mecanismo de retroalimentación negativa de la hipófisis, asciende las cifras de TSH superiores a las normales y regularmente por encima de a las 10 microunidades. En los hipotiroidismos secundario y terciario baja a menos de 0,20 o no se la detecta en la sangre. La prueba de la TRH-TSH nos sirven en diagnostico diferencial, en el hipotiropidismo terciario existe lesiones hipotalámicas que anulan la secreción de hormona liberadora de tirotrofina razón por la cual la adenohipófisis deja de producir tirotrofina, pero como solo está hipotrófica y aun es capaz de responder al estímulo trófico, al inyectarse la TRH por vía intravenosa, los niveles basales que estaban en cero o menores que 0,20 microunidades, se elevan a más del 100%. En el hipotiroidismo secundario existe lesiones hipofisarias que anulan las células secretoras de TSH, el hipotálamo es normal y funcionante pero no hay respuesta de TSH por falta de células efectoras de modo que si se inyecta la TRH no se producirá modificación de los valores bajos o nulos de la tirotrofina. Debemos recordar que en el hipotiroidismo primario, la hipófisis se encuentra liberada del freno tiroideo de modo que su estimulación con TRH producirá un aumento aun mayor de los valores de TSH basales, es decir que habrá una hiperrespuesta, superior a la que se verifica en la variedad hipotalámica.
Si tenemos en cuenta que desconocemos los límites de normalidad premórbida de cada paciente, es importante valorar el parámetro analítico junto con la sintomatología clínica e intentar conseguir una concentración de TSH normal. Hay que tener en cuenta también, que las determinaciones analíticas tienen su falibilidad y que una TSH en los límites normales en un paciente que se encuentra bien, esté en el límite bajo o alto de la normalidad, no nos tiene por qué obligar a modificar las dosis que el paciente esté recibiendo. Del mismo modo, si el paciente presenta sintomatología atribuible a hipotiroidismo, la dosis de LT4 puede incrementarse hasta conseguir una concentración de TSH en el límite bajo del margen poblacional normal o incluso por debajo de éste, según algunos autores.
Un caso especial es la paciente en edad gestacional, en la que la T4 libre del primer trimestre es esencial para el desarrollo neurológico del embrión. En la paciente con deseo gestacional y tratamiento con LT4 por hipotiroidismo primario, es importante monitorizar la TSH preconcepción y mantenerla inferior a 2 mUI/l, así como recomendar un aumento de dosis de LT4 en cuanto se conozca el estado de gestación.
¿Cómo monitorizamos el hipotiroidismo secundario donde la concentración de TSH no tiene ningún valor?
En el hipotiroidismo central, la T4 libre disminuye por una alteración hipotálamo-pituitaria en la síntesis de TSH. A diferencia del hipotiroidismo primario, la T4 libre baja pero la TSH se mantiene normal, incluso a veces ligeramente elevada debido a la presencia de formas biológicamente inactivas de TSH. Al iniciar el tratamiento con LT4, la TSH se suprime rápidamente y deja de tener valor en la monitorización del tratamiento. Por tanto, en la práctica clínica nos basamos fundamentalmente en las concentraciones de T4 libre para evaluar la idoneidad del tratamiento.
T4 libre, T3 libre o ambas, y qué concentraciones debemos perseguir
La T4 libre es el parámetro individual más valioso en la monitorización del hipotiroidismo central. Ferreti et al estudiaron 37 pacientes con hipotiroidismo central (3 diagnosticados de novo y 34 a los que suspendieron el tratamiento con LT4); la T4 libre fue baja en todos ellos, pero la T3 libre fue normal en un 27% a los 60 días de haber suspendido el tratamiento con LT4, lo que indica que la concentración de T4 libre es más sensible que la T3 libre en la detección de la infradosificación44. No obstante, la determinación de ambas fue superior que la de T4 libre sola en la detección de casos de tratamiento inadecuado. Por tanto, siempre y cuando sea preciso el ensayo para la determinación de T3, la determinación de T3 libre puede añadir información a la de T4 libre en la monitorización del hipotiroidismo central.. El hipotiroidismo central casi nunca se presenta como entidad aislada, sino en el contexto de hipopituitarismo, con otras alteraciones hormonales asociadas. Hay otras hormonas, como los glucocorticoides y la hormona del crecimiento (GH) que afectan la conversión de T4 a T3. La GH, por ejemplo, estimula la conversión de T4 a T3, por lo que teóricamente en la deficiencia de GH no tratada, la concentración teórica de T4 libre para una misma T3 sería mayor que en sujetos control. En pacientes con hipotiroidismo central nosotros hallamos una relación T3/T4 inferior a la de controles, pero no fue distinta a la de sujetos con hipotiroidismo primario estable tratado .
No olvidemos nunca centrarnos en el paciente que tenemos delante y la fisiopatología de la enfermedad , tanto en el diagnostico como en el seguimiento.
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