Documentos de Académico
Documentos de Profesional
Documentos de Cultura
en la anorexia nerviosa
R.K. St0ving, J. Hangaard, M. Hansen-Nord, C. Hagen
Resumen.
La anorexia nerviosa es un síndrome de etiología desconocida. Se asocia con múltiples anormalidades endo-
crinas. Las monoaminas hipotalámicas (especialmente la serotonina), los neuropéptidos (especialmente el neuro-
péptido Y y la colecisto-quinina) y la leptina participan en la regulación del apetito humano, y se transforman de
diversas formas en la anorexia nerviosa. Sin embargo, aún queda por clarificar si la alteración de la regulación del
apetito es secundaria o etiológica. Parece que el hambre trae como consecuencia un aumento en la secreción de la
hormona de emisión de corticotropina y propiomela-nocortina, no obstante, hay evidencias de que puede mantener
e intensificar la anorexia, la actividad física excesiva y la amenorrea. La amenorrea hipotalámica, que es un criterio
de diagnóstico en la anorexia nerviosa, tiene otras implicaciones y no únicamente el bajo peso y el ejercicio. La
resistencia de la hormona del crecimiento con una baja producción del factor de crecimiento I similar a la insulina
y una secreción de la hormona de crecimiento elevada reflejan una insuficiencia nutricional. La terapia nutricional
de los pacientes con anorexia nerviosa puede mejorarse con la administración de un agente anabólico como la hor-
mona del crecimiento o el factor I de crecimiento similar a la insulina. Hasta ahora, no se ha demostrado que nin-
guna de las anormalidades endocrinas sea primaria, sin embargo, hay una evidencia creciente de que alguna de ellas
puedan formar parte de ese círculo vicioso.
Hipotalamico Monoaminas Catecolaminas Dato contradictorio van Binsbergen et al., 1991; Grossetal.,
1979; Barry y Klawans, 1976 Dopamina
Dato contradictorio Johnston et al., 1984; Kaye et al, 1984b;
Gillberg, 1983
Serotonina Dato contradictorio Hassanyeh y Marshall, 1991; Kaye et al.,
1991; Brewertonet al., 1987
Opiáceos β-endorfina Dato contradictorio Brambillaet al., 1991; de Marinis et al.,
1994; Baranowska, 1990
Corticotropina Liberada Incrementado Hotta et al., 1986; Smith et al., 1989
Hormonas Hormona
Gonadotropina Liberada Disminuido van Binbergen et al., 1990; Marshall
Hormona y Kelch, 1979; Ceda et al., 1981
Crecimiento hormona liberada Incrementado Scacchi et al., 1997
hormonas
Tireotropina hormona Liberada Disminuido Kiriike et al., 1987; Bando et al., 1989
Hormonas
Gastrointestinal Colecistokinina Dato contradictorio Harty eí al., 1991; Phillip et al., 1991
peptidos Geracioti, Jr. et al., 1989
Pituitario anterior Peptidos Adrenocorticotropina Dato contradictorio Gwirtsman et al., 1989; Gold et al., 1986
Brambillaet al., 1993
serum (Hebebrant et al, 1995) y de CSF (Mantzoros et al., némica entre los pacientes anoréxicos, y que unas tasas
1997) como reflejo de la baja reserva de grasa. Sin cognitivas moderadas en los comedores moderados se
embargo, Hebebrant et al (1995) descubrieron que había relacionaban con el nivel de leptina independientemente
escasa relación entre el nivel de leptina y el BMI, lo que del porcntaje de grasa en el cuerpo (vonPritz et al., 1997).
sugería que podía deberse a una subpoblación hiperlepti- El conocimiento sobre las proteínas de enlace de leptina y
El 'síndrome de baja T3' caracterizado por un des- Únicamente en el margen de una semana se aña-
censo notable de la triodotironina (T3), la tiroxina nor- den nuevos e interesantes datos al gran conjunto de
mal o debajo de lo normal (T4) y el nivel de tirotropi- literatura sobre trastornos endocrinos en la AN.
na basal normal (TSH) es una constante en la AN Obviamente, existen aún muchos problemas metodo-
(Kiyohara et al., 1989; Bannai et al., 1988; Croxson e lógicos a considerar a la hora de interpretar las obser-
Ibbertson, 1977), y es un estado que se conoce bien en vaciones endocrinológicas. Los modelos de anorexia
otras formas de nutrición deficiente(Turkay et al., en animales, el aumento de la actividad motora, y la
1995). Se ha observado una hipotireosis inducida por disminución en la receptividad sexual no tienen nece-
yodido en casos de AN (Haraguchi et al.,1986), pero es sariamente que ser modelos adecuados para la AN.
infrecuente. El hipotrio-dotiroidismo se atribuye en Las concentraciones de serum de monoa-minas y pép-
primer lugar a una de-yodiza-ción periférica disminui- tidos reflejan la secreción pituitaria, pero pueden ser
da del T4, y un aumento de formación simultáneo del un mal indicador de lo que ocurre en las fisuras sináp-
metabolito inactivo inverso T3(rT3). No obstante, el ticas. El valor de los parámetros de CSF está limitado
nivel de T3 alto no va siempre acompañado de un rT3 tanto como que no puede conocerse la contribución de
elevado, lo cual sugiere que debe de haber otros meca- la médula espinal. En pacientes con AN las variacio-
nismos involucrados. Hay evidencia de que un nivel nes pequeñas de peso van unidas a respuestas rele-
bajo de IGF-I (Jorgensen et al., 1994) al igual que la vantes en las catecolaminas de serum (Lessem et al.,
hipercortisolemia (Bannai et al., 1988; Hangaard et al., 1989), en la lepti-na (Hebebrand et al., 1997), el cor-
1996) contribuyen a ese estado. Aunque el triodotiroi- tisol (Fitcher et al, 1982), la gonadotropina (Katz et
dismo es reversible (Tamai et al., 1986) y probable- al., 1977), y la GH (Argente et al., 1997) lo cual indi-
mente adaptativo, no se puede excluir la presencia de ca que el tiempo en que se realizaron las respectivas
una desregulación simultánea del TRH central. En investigaciones es de una importancia crítica y puede
varios estudios de AN se ha observado una respuesta ser la causa de discrepancias en algunos trabajos. Y
embotada y atrasada de TSH al TRH administrado por último, aunque igual de importante, la mayoría de
exógenamente (Matsubayashi et al., 1988; Kiriike et los modelos describen sólo uno o dos sistemas especí-
al., 1987; Bandi et ak.,1989) así como en pacientes de ficos entre todos los que hay, con lo que tenemos un
peso normal con buli-mia (Gwirtsman et al., 1983) o conocimiento limitado sobre las interacciones entre
con enfermedades de depresión (Loosen, 1985). Así estos sistemas. Anteriormente, hemos tratado algunos
pues, el bajo nivel de T3 puede deberse tambión a la sistemas interactivos, pero parece ser un problema
disminución de secreción tiroi-dal en respuesta al casi irresoluble trazar el mapa de la suma de las nume-
TSH, que es indicativo de una perturbación hipotalá- rosas vías interactivas.
mica-pituitaria-tiroidal. Esta hipótesis se apoya ade- Las dos preguntas más importantes son:
más en el descubrimiento de que en la AN, la TSH 1) ¿desempeñan algún papel las anormalidades
puede ser estimulada por una prohormona TRH que endocrinas en la etiología?,
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