Enfermedad de Addison

La enfermedad de Addison1 es una deficiencia hormonal causada por dao a la glndula adrenal lo que ocasiona una hipofuncin o insuficiencia corticosuprarrenal primaria. La descripcin original por Addison 2 de esta enfermedad es: languidez y debilidad general, actividad hipocintica del corazn, irritabilidad gstrica y un cambio peculiar de la coloracin de la piel.3 ] La enfermedad de Addison es muy rara, apareciendo a cualquier edad y afectando ms a mujeres que a hombres en relacin de 3 a 1. La insuficiencia suprarrenal secundaria es mucho ms frecuente debido al uso de corticoides y a su supresin brusca. 4 Etiologa y patogenia Destruccin anatmica de la glndula suprarrenal: para que aparezca la Enfermedad de Addison debe destruirse ms del 50% de las glndulas suprarrenales de forma bilateral. Entre las causas de destruccin de las suprarrenales destaca: 1. Infecciones: suelen ser infecciones granulomatosas crnicas tuberculosa, mictica o viral.5 1. Tuberculosis: en las primeras series de pacientes que relataban la insuficiencia suprarrenal, la tuberculosis era la causa del 70 al 90% de los casos.6 A partir de la dcada de 1980, la tuberculosis con afectacin suprarrenal ocurre principalmente en pacientes con sida. 2. SIDA: siempre hay que sospechar una insuficiencia suprarrenal. El citomegalovirus afecta habitualmente a las suprarrenales, produciedo la adrenalitis necrotizante por citomegalovirus. Tambin hay afectacin suprarrenal por el Mycobacterium aviumintracellulare, Cryptococcus, Sarcoma de Kaposi, histoplasmosis, coccidiodomicosis. 3. Sndrome de Waterhouse-Friderichsen: se describe como un shock fulminante debido a la destruccin aguda de las glndulas suprarrenales.7 Ocurre sobre todo en nios pequeos afectos de meningitis meningoccica. En realidad la Enfermedad de Addison es una insuficiencia suprarrenal crnica. Atrofia Idioptica: son de causa desconocida y a partir de la dcada de 1970 es la causa ms frecuente, siendo un mecanismo probablemente autoinmunitario. 1. Mecanismo autoinmunitario: la mitad de los pacientes tienen anticuerpos circulantes contra las glndulas suprarrenales, concretamente contra la P450. Entre las causas autoinmunitarias encontramos al Sndrome autoinmunitario poliglandular de tipo II: caracterizado por presentar dos o ms manifestaciones endocrinas autoinmunitarias en una misma persona como: tiroiditis linfocitaria crnica, insuficiencia ovrica prematura, diabetes mellitus tipo I, hipotiroidismo o hipertiroidismo, anemia perniciosa, vitligo, alopecia, esprue no tropical, y miastenia gravis por produccin de autoanticuerpos. Dentro de las familias se observan muchas generaciones que estn afectadas por una o ms de las enfermedades citadas. Se debe a un gen mutante situado en el cromosoma 6, y se asocia a los alelos B8 y DR3 del HLA. Suele manifestarse en la edad adulta. El Sndrome autoinmunitario poliglandular de tipo I se caracteriza por la combinacin de insuficiencia paratiroidea y suprarrenal y moniliasis mucocutnea crnica. Tambin puede aparecer anemia perniciosa, hepatitis crnica activa, alopecia, hipotiroidismo primario e insuficiecia gonadal prematura. Este sndrome se hereda de forma autosmica recesiva, y no est asociado al HLA. Al contrario que el sndrome tipo II, este sndrome aparece en la niez. Se desconoce los mecanismos por los que interacta la predisposicin gentica y la autoinmunidad en estos procesos. Aunque la mayora de los autoanticuerpos suprarrenales producen destruccin de las glndulas, algunos ocasionan insuficiencia suprarrenal al provocar bloqueo de la unin de la ACTH a sus receptores por autoanticuerpos. Otro

2.

3.

4. 5. 6.

proceso es la insuficiencia suprarrenal familiar autosmico recesivo que produce una falta de reactividad a la ACTH secundaria a mutaciones del receptor de la ACTH. 2. Adrenoleucodistrofia: produce una desmielinizacin intensa y la muerte prematura en nios, y la adrenomieloneuropata se asocia a una neuropata mixta, motora y sensorial, con parapleja espstica en los adultos. Ambos procesos cursan con niveles circulantes elevados de cidos grasos de cadenas muy largas que provocan insuficiencia suprarrenal. Hemorragias bilaterales de las suprarrenales: ocurren sobre todo en pacientes tratados con anticoagulantes, en los que tienen anticoagulantes circulantes y en los estados de hipercoagulabilidad, como ocurre en el sndrome antifosfolpido. Invasin de las suprarrenales: ocurre en las metstasis tumoral, sobre todo en el cncer de pulmn, en la amiloidosis y sarcoidosis. Extirpacin quirrgica Fallo metablico de la produccin hormonal 1. Hiperplasia suprarrenal congnita 2. Inhibidores enzimticos: la metirapona, ketoconazol, aminoglutetimida, rifampicina, fenitona y opiceos, pueden causar o potenciar una insuficiencia suprarrenal. 3. Agentes citotxicos: mitotano.

Sintomatologa y signos clnicos[editar] La insuficiencia corticosuprarrenal por destruccin lenta de las glndulas suprarrenales tiene un comienzo insidioso, donde la identidad de la enfermedad en las primeras fases es muy difcil, siendo fcil de diagnsticar en los casos avanzados. Se caracteriza por: Astenia o debilidad: aparece casi constantemente en la Enfermedad de Addison en el 99% de los casos. Al principio puede ser espordica y ms frecuente en momentos de estrs, pero a medida que la funcin suprarrenal se deteriora, el paciente est continuamente fatigado y necesita reposo en cama. Hiperpigmentacin cutnea y de mucosas: ocurre en el 98% de los casos. Normalmente aparece como un oscurecimiento difuso de color moreno, pardo o bronceado en ciertas regiones como los codos o los surcos de las manos, y en las zonas que estn normalmente pigmentadas como las aureolas mamarias. En las mucosas pueden aparecer placas de color negro azulado en el 82% de los casos. Algunos pacientes presentan eflides oscuras y a veces paradjicamente reas irregulares de vitligo (9% de los casos). Esta hiperpigmentacin persiste tras la exposicin solar. Se debe a que en el proceso de sntesis de la ACTH se debe sintetizar previamente proopiomelanocortina (POMC). Pptido que, adems de dar lugar a la ACTH, tambin dar -MSH, hormona estimulante de la sntesis de melanina. Prdida de peso o adelgazamiento: ocurre en el 97% de los casos, debido a la anorexia y alteracin de la funcin gastrointestinal. Alteracin de la funcin gastrointestinal: la anorexia, las nuseas y los vmitos aparecen en el 90% de los casos y a veces es la primera manifestacin de la enfermedad. En ocasiones (34% de los casos) puede aparecer un dolor abdominal impreciso, tan intenso que puede confundirse con un abdomen agudo. La diarrea ocurre en el 20% de los casos y el estreimiento en el 19%. Hipotensin arterial: descrita como menor de 110/70, ocurre en el 87% de los casos y se acenta la postura hasta ser menor de 80/50 o menos. El sncope puede ocurrir en el 16% de los casos. Trastornos perceptivos: existe refuerzo de las percepciones sensoriales gustativas, olfatorias y auditivas reversibles con el tratamiento. Tambin puede aparecer cambios en la personalidad como inquietud e irritabilidad excesiva. Prdida de vello: en la mujer puede haber prdida de vello axilar y pubiano por ausencia de andrgenos suprarrenales. Hipertermia: la glndula del hipotlamo no controla la homeostasis del cuerpo por ausencia de secrecin de corticoides

En algunos casos la enfermedad de Addison comienza con sntomas psiquitricos, pero esta presentacin no es tan frecuente como en los cuadros tiroideos y el sndrome de Cushing. En la mayora de los casos las

alteraciones mentales suelen aparecer en forma de cambios de conducta y de personalidad.8 Por este motivo es fcil el diagnstico errneo de trastorno de la personalidad y trastorno somatomorfo de caractersticas hipocondracas. Los sntomas psicolgicos de aislamiento, apata, fatiga, trastorno del estado de nimo, afectacin de la memoria y pobreza global del pensamiento tambin suelen ser de inicio precoz, por lo que se puede confundir la enfermedad de Addison con una demencia o con una depresin. En la crisis suprarrenal aguda puede desarrollarse un sndrome cerebral con psicosis (alucinaciones) y delirium. 8 Diagnstico[editar] 1. Datos necesarios de laboratorio Hiponatremia: los niveles sricos bajos de sodio se debe a su prdida por la orina por dficit de aldosterona y al desplazamiento del sodio hacia el compartimento intracelular. Esta prdida de sodio extravascular reduce el volumen plasmtico y acenta la hipotensin. Hiperkalemia: aumento de los niveles sricos de potasio. Se debe a los efectos combinados del dficit de aldosterona, la reduccin del filtrado glomerular y la acidosis. Hipocortisolemia: los niveles de cortisol y aldosterona son bajos y no aumentan con la administracin de ACTH. Hipercalcemia: aumento de los niveles sricos de calcio. Ocurre en un 10-20% de los pacientes de causa desconocida. Cambios electrocardiogrficos: suelen ser inespecficos, aunque con lentificacin generalizada del trazado. Hemograma: puede haber anemia normoctica, linfocitosis relativa y eosinofilia moderada. Prueba de estimulacin de ACTH: prueba principal que confirma el diagnstico de insuficiencia suprarrenal, al evaluar la capacidad de las suprarrenales para producir esteroides, que suelen estar ausentes o disminuidos tanto en sangre como en orina tras la estimulacin de ACTH. Determinacin de la ACTH: en la insuficiencia suprarrenal primaria o Enfermedad de Addison, la ACTH y sus pptidos afines, estn elevados en plasma ante la prdida del mecanismo de retroalimentacin del eje hipotlamo-hipfisario-suprarrenal. hipertermia: la hormona del hipotlamo no controla la homeostasis

2. 3. 4. 5. 6. 7.

8.

9.

Tratamiento[editar] El tratamiento de la insuficiencia suprarrenal es el tratamiento hormonal sustitutivo basado en el cortisol o hidrocortisona (glucocorticoide) y fludrocortisona (mineralcorticoide). Dosis de hidrocortisona: la dosis en los adultos es entre 20 a 30 mg al da. Dosis de fludrocortisona: De 0,05 a 0,1 mg por va oral a da, junto con un aumento de la ingesta de sal diaria de 3 a 4 g Forma de administracin: el corticoide se debe administrar en las comidas, tomando dos tercios de la dosis por la maana y un tercio al finalizar la tarde. Monitorizacin del efecto de la medicacin: se debe conocer los niveles de sodio, potasio, urea y creatinina en sangre, junto con la toma de presin arterial que no se debe modificar en el cambio postural, adems de la brando mejora de todos los sntomas y control del peso corporal. Consideraciones especiales: todos los pacientes con insuficiencia suprarrenal crnica deben llevar una tarjeta identificativa que alerte al personal mdico ante un ingreso hospitalario o atencin mdica urgente, debido a que en situaciones de estrs, como ejercicio, fiebre, intervencin quirrgica, debe duplicarse o triplicarse la dosis de corticoides, y si no es posible administrarla por va oral, debera ser por va intravenosa a una dosis de 10 mg/h 250-300 mg/da, para ir disminuyendo de un 2030% de la dosis diariamente, cuando la situacin estresante ceda. A partir de 100 mg/da de hidrocortisona, no es preciso administrar fludrocortisona. Efectos secundarios: el principal es la gastritis por exceso de acidez gstrica y trastornos de la mucosa del estmago, que se soluciona con anticidos. Si apareciera insomnio, irritabilidad o excitacin mental al comienzo del tratamiento habra que disminuir la dosis.

Definicin y Causas de la Enfermedad de Addison La enfermedad de Addison, forma extrema de la hipoadrenia, fue descrita por primera vez por Thomas Addison, de quien recibe su nombre. Se trata de un desorden hormonal o endocrino que puede tener lugar a cualquier edad, afectando a ambos sexos, y que provoca la progresiva destruccin de la corteza suprarrenal causando una deficiente secrecin de hormonas adrenocorticales, es decir, de hormonas esteroides. Tambin se conoce como insuficiencia suprarrenal primaria, insuficiencia corticoadrenal primaria, insuficiencia adrenal primaria, etctera. La enfermedad es mortal si no es tratada. Desgraciadamente, no siempre se diagnostica rpidamente debido a la gran variedad de sntomas que presenta y a la falta de informacin que existe al respecto. Cuando ms del 90% de la corteza suprarrenal se encuentra afectada, es decir, en los casos ms avanzados de la enfermedad, el diagnstico es ms sencillo, ya que apenas existe capacidad adrenal. Sin embargo, su progresin puede ser rpida o lenta (avanzando durante 20 aos o ms) por lo que no es necesario llegar a sufrir tal afectacin de la corteza suprarrenal para padecer una insuficiencia suprarrenal primaria. En la insuficiencia suprarrenal primaria, y en la Enfermedad de Addison, se pueden perder las hormonas glucocorticoides y, a menudo, las mineralocorticoides, y es causada por la destruccin anatmica de la glndula por el sistema inmunolgico del cuerpo. Esta destruccin puede ser debida a varias causas, incluida la tuberculosis o una infeccin fngica, otras enfermedades infiltradas en las glndulas adrenales y una hemorragia. Tambin puede ser debido a un fallo metablico (por ejemplo, una produccin insuficiente de hormonas). Este fallo puede ser el resultado de una hiperplasia adrenal congnita, inhibidores enzimticos o agentes citotxicos. Thomas Addison (1793-1860). Afamado mdico y cientfico britnico, no slo fue quien descubri la enfermedad de Addison, sino que tambin describi una amplia gama de enfermedades, entre ellas el sndrome de Addison-Schilder (conocido como adrenoleucodistrofia), enfermedad de Alibert, sndrome de Allgrove, enfermedad de Rayer Entre otras causas menos frecuentes se encuentran las siguientes: clulas cancergenas en el organismo, la extraccin quirrgica de las glndulas suprarrenales, SIDA, sangrado en las glndulas suprarrenales, defectos genticos en el desarrollo de las glndulas suprarrenales, la inhabilidad de responder al ACTH o un defecto en la produccin de la hormona adrenal, etc. ser La insuficiencia adrenal primaria a su vez, puede completa (afectando a los 3 esteroides

suprarrenales) o parcial. Dependiendo de la funcin de las suprarrenales que se ha visto afectada, del grado de susceptibilidad del individuo, as como del grado de afectacin, la persona puede no manifestar ningn sntoma y sufrir una crisis repentina, tener sntomas dispares, o mostrar una gran variedad de sntomas, aparentemente dispares y no relacionados entre s.

Pero, la enfermedad de Addison no es una condicin de o todo o nada. Aunque se producen ms de 50 esteroides en las glndulas adrenales, el cortisol y la aldosterona son los ms activos y abundantes. En las fases iniciales de la enfermedad, muchos individuos todava pueden producir cortisol y aldosterona suficientes. En cuanto a la forma clsica de la enfermedad, es producida por una disminucin de ambas hormonas; cortisol y aldosterona, debido a la total o casi total destruccin de ambas glndulas adrenales. A esta condicin tambin se le denomina hipocorticolismo. La causa ms comn del hipoaldosteronismo es la insuficiencia adrenal primaria. La insuficiencia adrenal secundaria suele describirse como Addison, aunque tiene una causa muy distinta. Por lo general suele suceder debido a un traumatismo sufrido en la cabeza en el pasado, incluso puede haber sucedido hace muchos aos, y puede que el paciente desconozca

que esa es la causa de sus problemas. En aproximadamente un 3% de los casos la causa de la insuficiencia adrenal secundaria ha sido un tumor en la pituitaria. Etiologa y patogenia

Destruccin anatmica de la glndula suprarrenal: para que aparezca la Enfermedad de Addison debe destruirse ms del 50% de las glndulas suprarrenales de forma bilateral. Entre las causas de destruccin de las suprarrenales destaca: Infecciones: suelen ser infecciones granulomatosas crnicas tuberculosa, mictica o viral.[5] Tuberculosis: en las primeras series de pacientes que relataban la insuficiencia suprarrenal, la tuberculosis era la causa del 70 al 90% de los casos.[6] A partir de la dcada de 1980, la tuberculosis con afectacin suprarrenal ocurre principalmente en pacientes con SIDA. SIDA: siempre hay que sospechar una insuficiencia suprarrenal. El citomegalovirus afecta habitualmente a las suprarrenales, produciedo la adrenalitis necrotizante por citomegalovirus. Tambin hay afectacin suprarrenal por el Mycobacterium avium-intracellulare, Cryptococcus, Sarcoma de Kaposi, histoplasmosis, coccidiodomicosis. Sndrome de Waterhouse y Friderichsen: se describe como un shock fulminante debido a la destruccin aguda de las glndulas suprarrenales.[7] Ocurre sobre todo en nios pequeos afectos de meningitis meningoccica. En realidad la Enfermedad de Addison es una insuficiencia suprarrenal crnica. Atrofia Idioptica: son de causa desconocida y a partir de la dcada de 1970 es la causa ms frecuente, siendo un mecanismo probablemente autoinmunitario. Mecanismo autoinmunitario: la mitad de los pacientes tienen anticuerpos circulantes contra las glndulas suprarrenales, concretamente contra la P450. Entre las causas autoinmunitarias encontramos al Sndrome autoinmunitario poliglandular de tipo II: caracterizado por presentar dos o ms manifestaciones endocrinas autoinmunitarias en una misma persona como: tiroiditis linfocitaria crnica, insuficiencia ovrica prematura, diabetes mellitus tipo I, hipotiroidismo o hipertiroidismo, anemia perniciosa, vitligo, alopecia, esprue no tropical, y miastenia gravis por produccin de autoanticuerpos. Dentro de las familias se observan muchas generaciones que estn afectadas por una o ms de las enfermedades citadas. Se debe a un gen mutante situado en el cromosoma 6, y se asocia a los alelos B8 y DR3 del HLA. Suele manifestarse en la edad adulta. El Sndrome autoinmunitario poliglandular de tipo I se caracteriza por la combinacin de insuficiencia paratiroidea y suprarrenal y moniliasis mucocutnea crnica. Tambin puede aparecer anemia perniciosa, hepatitis crnica activa, alopecia, hipotiroidismo primario e insuficiecia gonadal prematura. Este sndrome se hereda de forma autosmica recesiva, y no est asociado al HLA. Al contrario que el sndrome tipo II, este sndrome aparece en la niez. Se desconoce los mecanismos por los que interacta la predisposicin gentica y la autoinmunidad en estos procesos. Aunque la mayora de los autoanticuerpos suprarrenales producen destruccin de las glndulas, algunos ocasionan insuficiencia suprarrenal al provocar bloqueo de la unin de la ACTH a sus receptores por autoanticuerpos. Otro proceso es la insuficiencia suprarrenal familiar autosmico recesivo que produce una falta de reactividad a la ACTH secundaria a mutaciones del receptor de la ACTH. Adrenoleucodistrofia: produce una desmielinizacin intensa y la muerte prematura en nios, y la adrenomieloneuropata se asocia a una neuropata mixta, motora y sensorial, con parapleja espstica en los adultos. Ambos procesos cursan con niveles circulantes elevados de cidos grasos de cadenas muy largas que provocan insuficiencia suprarrenal. Hemorragias bilaterales de las suprarrenales: ocurren sobre todo en pacientes tratados con anticoagulantes, en los que tienen anticoagulantes circulantes y en los estados de hipercoagulabilidad, como ocurre en el sndrome antifosfolpido. Invasin de las suprarrenales: ocurre en las metstasis tumoral, sobre todo en el cncer de pulmn, en la amiloidosis y sarcoidosis. Extirpacin quirrgica Fallo metablico de la produccin hormonal

Hiperplasia suprarrenal congnita Inhibidores enzimticos: la metirapona, ketoconazol, aminoglutetimida, rifampicina, fenitona y opiceos, pueden causar o potenciar una insuficiencia suprarrenal. Agentes citotxicos: mitotano. Sintomatologa y signos clnicos La insuficiencia corticosuprarrenal por destruccin lenta de las glndulas suprarrenales tiene un comienzo insidioso, donde la identidad de la enfermedad en las primeras fases es muy difcil, siendo fcil de diagnsticar en los casos avanzados. Se caracteriza por: Astenia o debilidad: aparece casi constantemente en la Enfermedad de Addison en el 99% de los casos. Al principio puede ser espordica y ms frecuente en momentos de estrs, pero a medida que la funcin suprarrenal se deteriora, el paciente est continuamente fatigado y necesita reposo en cama. Hiperpigmentacin cutnea y de mucosas: ocurre en el 98% de los casos. Normalmente aparece como un oscurecimiento difuso de color moreno, pardo o bronceado en ciertas regiones como los codos o los surcos de las manos, y en las zonas que estn normalmente pigmentadas como las areolas mamarias. En las mucosas pueden aparecer placas de color negro azulado en el 82% de los casos. Algunos pacientes presentan eflides oscuras y a veces paradjicamente reas irregulares de vitligo (9% de los casos). Esta hiperpigmentacin persiste tras la exposicin solar. Se debe a la hiperproducin de ACTH, que contiene un pptido responsable de la produccin de melanina. El pptido se llama PROOPIOMELANOCORTINA (POMC) Prdida de peso o adelgazamiento: ocurre en el 97% de los casos, debido a la anorexia y alteracin de la funcin gastrointestinal. Alteracin de la funcin gastrointestinal: la anorexia, las nuseas y los vmitos aparecen en el 90% de los casos y a veces es la primera manifestacin de la enfermedad. En ocasiones (34% de los casos) puede aparecer un dolor abdominal impreciso, tan intenso que puede confundirse con un abdomen agudo. La diarrea ocurre en el 20% de los casos y el estreimiento en el 19%. Hipotensin arterial: descrita como menor de 110/70, ocurre en el 87% de los casos y se acenta la postura hasta ser menor de 80/50 o menos. El sncope puede ocurrir en el 16% de los casos. Trastornos perceptivos: existe refuerzo de las percepciones sensoriales gustativas, olfatorias y auditivas reversibles con el tratamiento. Tambin puede aparecer cambios en la personalidad como inquietud e irritabilidad excesiva. Prdida de vello: en la mujer puede haber prdida de vello axilar y pubiano por ausencia de andrgenos suprarrenales. hipertermia:la glandula del hipotalamo no controla la homeostasis del cuerpo por ausencia de secrecion de corticoides En algunos casos la enfermedad de Addison comienza con sntomas psiquitricos, pero esta presentacin no es tan frecuente como en los cuadros tiroideos y el sndrome de Cushing. En la mayora de los casos las alteraciones mentales suelen aparecer en forma de cambios de conducta y de personalidad.[8] Por este motivo es fcil el diagnstico errneo de trastorno de la personalidad y trastorno somatomorfo de caractersticas hipocondracas. Los sntomas psicolgicos de aislamiento, apata, fatiga, trastorno del estado de nimo, afectacin de la memoria y pobreza global del pensamiento tambin suelen ser de inicio precoz, por lo que se puede confundir la enfermedad de Addison con una demencia o con una depresin. En la crisis suprarrenal aguda puede desarrollarse un sndrome cerebral con psicosis (alucinaciones) y delirium.[8]

Diagnstico

Datos de laboratorio Hiponatremia: los niveles sricos bajos de sodio se debe a su prdida por la orina por dficit de aldosterona y al desplazamiento del sodio hacia el compartimento intracelular. Esta prdida de

sodio extravascular reduce el volumen plasmtico y acenta la hipotensin. Hiperkalemia: aumento de los niveles sricos de potasio. Se debe a los efectos combinados del dficit de aldosterona, la reduccin del filtrado glomerular y la acidosis. Hipocortisolemia: los niveles de cortisol y aldosterona son bajos y no aumentan con la administracin de ACTH. Hipercalcemia: aumento de los niveles sricos de calcio. Ocurre en un 10-20% de los pacientes de causa desconocida. Cambios electrocardiogrficos: suelen ser inespecficos, aunque con lentificacin generalizada del trazado. Hemograma: puede haber anemia normoctica, linfocitosis relativa y eosinofilia moderada. Prueba de estimulacin de ACTH: prueba principal que confirma el diagnstico de insuficiencia suprarrenal, al evaluar la capacidad de las suprarrenales para producir esteroides, que suelen estar ausentes o disminuidos tanto en sangre como en orina tras la estimulacin de ACTH. Determinacin de la ACTH: en la insuficiencia suprarrenal primaria o Enfermedad de Addison, la ACTH y sus pptidos afines, estn elevados en plasma ante la prdida del mecanismo de retroalimentacin del eje hipotlamo-hipfisario-suprarrenal. hipertermia: la hormona del hipotalamo no controla la homeostasis

Tratamiento

El tratamiento de la insuficiencia suprarrenal es el tratamiento hormonal sustitutivo basado en el cortisol o hidrocortisona (glucocorticoide) y fludrocortisona (mineralcorticoide). Dosis de [[]]: la dosis en los adultos es entre 20 a 30 mg al da. Dosis de fludrocortisona: De 0,05 a 0,1 mg por va oral a da, junto con un aumento de la ingesta de sal diaria de 3 a 4 g Forma de administracin: el corticoide se debe administrar en las comidas, tomando dos tercios de la dosis por la maana y un tercio al finalizar la tarde. Monitorizacin del efecto de la medicacin: se debe conocer los niveles de sodio, potasio, urea y creatinina en sangre, junto con la toma de presin arterial que no se debe modificar en el cambio postural, adems de la mejora de todos los sntomas y control del peso corporal. Consideraciones especiales: todos los pacientes con insuficiencia suprarrenal crnica deben llevar una tarjeta identificativa que alerte al personal mdico ante un ingreso hospitalario o atencin mdica urgente, debido a que en situaciones de estrs, como ejercicio, fiebre, intervencin quirrgica, debe duplicarse o triplicarse la dosis de corticoides, y si no es posible administrarla por va oral, debera ser por va intravenosa a una dosis de 10 mg/h 250-300 mg/da, para ir disminuyendo de un 20-30% de la dosis diariamente, cuando la situacin estresante ceda. A partir de 100 mg/da de hidrocortisona, no es preciso administrar fludrocortisona. Efectos secundarios: el principal es la gastritis por exceso de acidez gstrica y trastornos de la mucosa del estmago, que se soluciona con anticidos. Si apareciera insomnio, irritabilidad o excitacin mental al comienzo del tratamiento habra que disminuir la dosis. Publicado por Jessica Hinojoza en 12:13

WHAT IS ADDISONS DISEASE? Addisons Disease affects both humans and canines. This particular pamphlet focuses on Canine Addisons Disease. Addisons Disease is also called Hypoadrenocorticism. It is caused by an insufficient production of the hormones secreted by the adrenal glands. The adrenal glands are two small glands that sit next to the kidneys and essential for life. There are two types of Addisons Disease: 1) Primary (Typical) and 2) Secondary (Atypical). The cause of Primary Addisons Disease is basically the bodys immune system destroying the adrenal tissues. The cause of Atypical Addisons Disease is generally due to problems with the pituitary gland. A number of hormones are produced by the adrenal glands, however the two that are affected in Addisons Disease are: Mineralocorticoids (Aldosterone) and Glucocorticoids (Cortisol). Aldosterone controls the bodys ability to maintain electrolyte and water balance in the body. Cortisol affects almost every tissue in the body: 1) Promotes general well-being, 2) Appetite, 3) Controls blood glucose levels, 3) Helps the kidneys control water and calcium levels in the blood and 4) Helps control the red and white blood cell numbers. Without medication to control the levels of Aldosterone and Cortisol, Canine Addisons Disease is fatal. When a dog has undiagnosed Addisons Disease, it is fatal within 24 hours of the onset o f an Addisonian Crisis. However, if the dog has been diagnosed with Addisons Disease, when (s)he goes into an Addisonian Crisis, the vet can stop the crisis with intravenous hydrocortisone and intravenous fluids.

ARE ALL BREEDS AFFECTED? As more research is being done across the world, more breeds are being diagnosed with Primary Addisons Disease. Generally speaking, the breeds currently known to be more susceptible to this disease are: o o o o o o Standard Poodle Great Dane Labrador Retriever Nova Scotia Duck Trolling Retriever Portuguese Water Dog Rottweiler

o o

Soft-Coated Wheaten Terrier West Highland White Terrier

Addisons Disease is non-discriminate, it can affect any breed of dog. There is a belief that Primary Addisons Disease (AD) could quite possibly b e genetic and many studies are currently being conducted with DNA research collected from all breeds of all dogs including: 1) Diagnosed Primary AD, 2) AD relatives of Diagnosed Primary AD, 3) non-AD relatives of Diagnosed Primary AD and 4) non-AD, non-related dogs. Please bear in mind that many dogs are cross-bred which brings the occurrence of Primary AD to a broader canine population. Atypical AD can affect any breed of dog as it is a secondary development of a different condition. If you are a breeder, please keep records of all your litters to see if Addisons Disease is present in any of the dogs. Keep in touch with adopting families and ask them to let you know if one of the dogs from your litters is diagnosed with AD.

WHAT ARE THE PHYSICAL SYMPTOMS OF AD? o o o o o o o o o o o o o o Weakness Depression Lethargy Anorexia or Poor Appetite Weigh Loss Vomiting Diarrhea Excess Drinking or Urinating Slow Heart Rate Abdominal Pain Hypothermia Changes in Pigmentation of the Skin Seizures due to hypoglycemia Dry, Itchy Skin

Please note that your dog may not present with all of these symptoms. Addisons Disease is called the Great Mimic, as these symptoms are present in many other illnesses. An Addisonian Crisis can mimic other illnesses such as: gastrointestinal disorders (diarrhea), acute renal failure (kidney disease), liver disease, insulinoma (too much insulin), hypothyroidism (underactive thyroid) or hypoglycemia (low blood sugar). Situations such as illness or excessive stress can cause an Addisonian Crisis. If your dog presents with any of these symptoms, please consider asking your vet to do a full laboratory panel to confirm or eliminate AD.

LABORATORY TESTS TO CONFIRM DIAGNOSIS

Primary Addisons Disease can be diagnosed sometimes as early as 6 months of age. It is the authors experience, discussing with other families of Addisonian dogs, that many were diagnosed between 6 months and 2 years of age. If your dog presents with any abnormalities in the blood panel between 6 months and a year, it is a possibility that (s)he has AD and comparison blood work will confirm a diagnosis. If however, at any time during your dogs life (s)he displays any of the above symptoms, it is never too late to do the blood work and if a positive diagnosis is confirmed, begin the regimen of medication. The alternative is not a choice! Your vet can test for Addisons Disease using a blood panel that includes the following: o o o o o o o o o o o Increased Lymphocyte (a type of white blood cell) numbers Anemia Increase Serum Potassium Decreased Serum Sodium Altered Sodium/Potassium ratio (Na:K): <27 Increased Serum Phosphorus Increased Serum Calcium Decreased Blood Glucose Increased BUN & Creatinine (indicators of kidney function) Acidosis (upset in body's acids/base balance) Low Blood Cortisol Levels

Additionally, an ACTH (Adrenocorticotropic Hormone) stimulation test must be performed in order to confirm a suspected diagnosis based on the results of the original blood panel. A normally working pituitary gland releases adrenocorticotropic hormone (ACTH) to signal the adrenal glands to produce cortisol. The ACTH stimulation test stimulates the pituitary gland to release the hormone. If the adrenal glands are working normally, the cortisol levels should rise.

THE ACTH STIMULATION TEST o o o A blood test is taken to determine the baseline cortisol levels An injection of ACTH is given An hour or two later, another blood test is taken and the cortisol levels are measured.

Normally, the dog will produce cortisol in response to the ACTH injection, an AD dog will not. The ACTH is the only test that will give your vet a confirmed diagnosis of Addisons Disease. An X-Ray will also show if the heart is smaller than normal due to the volume of circulating fluid in the body being reduced by Addisons Disease.

TREATMENT FOR ADDISONS DISESASE If your dog is diagnosed prior to an Addisonian crisis, (s)he will begin maintenance therapy which supplements the missing hormones. Your dog will be on medication every day for the rest of his/her life, however, closely monitored, the dog can live a full life.

DURING AN ADDISONIAN CRISIS A dog in the midst of an Addisonian Crisis will generally be extremely weak, unable to walk or only just a few feet with assistance, disoriented, abnormal heart rate, diarrhea, vomiting and loss of bladder, depending on the stage of the Crisis. During an Addisonian Crisis, the dog must be cared for immediately by a vet as AD is fatal without proper medication. Even if your dog is on medication, there is a possibility (s)he may go into an Addisonian Crisis and will require emergency veterinary care. Generally speaking, the following four medications are used during the emergency care of an Addisonian Crisis, although it may vary with your dog and (s)he may not require all of these medications: o o o o IV Saline Solution to help replace lost electrolytes and other minerals. This can also help to dilute high levels of potassium in the blood IV Prednisolone Sodium Succinate or Dexamathasone Sodium Phosphate to replace glucocorticoids Percorten-V or Florinef to replace missing mineralcorticoids IV Calcium Gluconate to treat life-threatening heart arrhythmias

MAINTENANCE TREATMENT FOR PRIMARY AD A dog with Primary Addisons Disease will require cortisol and aldosterone replacements everyday of his/her life. There are two drug options: 1) Fludrocortisone (marketed under the name Florinef) and 2) DOCP (Percorten-V) and Predisone. Fludrocortisone replaces both cortisol and aldosterone and may provide all that your dog needs. It comes in pill form and is given each day, however, this drug is costly and could cost several hundreds of dollars each month for a large dog. The other option is to use Percorten-V which replaces aldosterone and is given monthly by injection. Some vets teach you to give the dog the injection yourself, while others insist that it only be done at the vets office. If your vet is willing to show you how to do the injection, it can save you a lot of money, as you can order the medication online. If you choose to use the Percorten-V, your dog will also require a daily dose of Prednisone to replace cortisol, which is given in pill form.

LEARNING TO WORK WITH THE MEDICATIONS As with all medications, there are side effects to each of the above medications that could present in your dog. Often this may just mean that the vet will need to adjust the dosage of the medication. Often the side effects may mimic symptoms of AD, so it is very important to have regular blood panels to make sure the medication dosages are correct. Do not change any dosages without first consulting your vet.

MAINTENANCE TREATMENT FOR ATYPICAL AD A dog with Atypical Addisons Disease only requires Cortisol replacement. Generally, Prednisone, Hydrocortisone, Dexamethasone or a similar replacement medication is prescribed. The dosage may need to be changed, so again, it is important to have regular blood panel to know that the dosage is accurate.

STRESS MANAGEMENT An Addisonian dog cannot produce stress hormones, so it is best to be prepared prior to a potentially stressful situation to administer extra prednisone to keep his/her levels even. Stress can include illness, hospitalization, issues of trauma, travelling, unfamiliar experiences (such as large family gatherings), thunderstorms, fireworks, etc. Always make sure you are prepared for any situation. If you are away from home, make sure you know where the nearest emergency veterinary care programs are during your travels. Always keep extra medication with you in a thermal cooler as well as lots of extra water. If you are flying with your dog, make sure that the crate has a clear label on it, listing that the dog has Addisons Disease. Include the medications (s)he is taking, your home address, your home vet contact information, your place of destination and the nearest vet clinic at your place of destination. Carry a letter from your vet with detailed explanations of AD, the medication the dog is taking as well as clearly defined instructions on what to do in the event of an emergency. Carry the extra medication with you in a thermal cooler, make sure your dog has adequate water for the trip and ask that your dog stay with you until you board the plane (or other mode of transportation where your dog and you will be separated). Immediately upon reuniting with your dog at your destination, take time to make sure (s)he is doing alright and make sure (s)he drinks a lot of water to balance out the system. Most likely, (s)he will need to rest when you arrive at your destination so plan ahead to have a little bit of down-time before you begin your travel business.

LIVING WITH CANINE ADDISONS DISEASE It is not easy to live with Canine Addisons Disease, both emotionally and financially. It is ideal to keep a small binder that includes copies of all the blood panel results as well as a detailed chart of the dosage of medication given each day. This will help you keep on top of your dogs condition as well as provide all the information you need should you require an emergency visit to a vet other than your own. There are a number of websites with information about Addisons Disease. Even the websites for AD humans will provide you a lot of information that is useful to you when dealing with Canine Addisons Disease. You can also find online support groups for Canine AD families and make use of the search engines such as Google and Yahoo to comparison shop for medications online. Some may require a fax of the prescription from your vet which no doubt is easy enough to do. Also, I have heard that there are regular pharmacies now who will fill a vet prescription for Prednisone and other medications. Look around and ask questions, the best way to provide you with peace of mind and financial sustainability is to keep reading more information about Canine Addisons Disease and talking with other families. Addisons Disease in Your Dog Treating Hypoadrenocorticism

Enlarge and explain my image

You can read an extensive veterinary review of Addison's disease here

Some dogs develop just the opposite problem, their adrenal glands produce too much cortisol. You can read about that problem here.

Ron Hines DVM PhD Lots of my articles are plagiarized and altered on the web to market products and services. There are never ads running or anything for sale with my real articles - other than my time. Try to stay with the ones that begin with http://www.2ndchance.info/ in the URL box or find all my articles at ACC.htm. What Is Addisons Disease (Hypoadrenocorticism) ? I am going to tell you some things about hypoadrenocorticism it is a long word for a comparatively simple, but very serious, disease. Dr. Addison recognized its symptoms well over a hundred years ago. We call the problem Addisons because it is so much easier to say. ( If you are a history buff, you can read the good Dr.s diaries here) Both you and your pet have two, lima bean-shaped , creamy-pink organs just above (or ahead) of the kidneys. They are your adrenal glands . Although they are quite small, they have two critical functions. Their outer layers, or cortex, produces cortisol (a glucocorticoid) hormone which one must have to deal with stress; and a second hormone, aldosterone (a mineralcorticoid) , which one must have to regulate the amount of salt in your body. Cortisol also decreases inflammation, increases blood sugar, suppress the immune system, increase the production of fat and decrease the number of certain white blood cells called lymphocytes that are involved in immunity. The adrenals produce more cortisol in times of stressful situations (both physical and mental stress). Cortisol has a number of other functions as well - all of which allow us to dealing with stress better. The aldosterone, or salt-regulating hormone that the outer adrenal layers also produce regulates the amount of sodium and potassium in your pets blood. Both these salt ions have to be kept in very tight limits in order for your pets body to function correctly. The inner layers of the adrenal gland are called the medulla. They play no part in Addisons disease. The medulla (medullary portion) produces the epinephrine we all need to deal with sudden stresses. (like realizing youre an hour late for your pets veterinary appointment or your pets terror when it realizes thats where you both are going !) Is This A Common Problem In Dogs ? Addisons disease is not a common disease in pets or humans. Its mirror image, Cushings disease , is much more common. But veterinarians think and talk about Addisons alot. That is because pets with Addison's come through our clinic doors pretending to have so many other health issues. It quite often it takes repeated office visits, frustrated clients and perplexed veterinarians , before the light bulb comes on in our head and the word, Addisons !!! , flashes through our minds. Once that happens, the diagnosis and treatment of your pet are usually quite straightforward. Addisons disease occurs in both sexes. It appears to be a bit more common in female dogs. Dogs that develop the problem are usually over 5.5 years of age when major signs are first noticed. But the destructive tissue processes that lead to Addisons disease occur slowly and these pets were in the process of loosing their adrenal gland function considerably before that. Occasionally, an elderly dog will develop Addisons disease as part of a malignancy situation. (ref) Are Certain Dogs More Susceptible ? Yes, some breeds do develop this disease more commonly than others. That is because of genetic predisposition. Genetic predisposition occurs when a breed or a line of dogs relies on too few ancestors. That is, all dogs in the breed or line are too closely related. These high-incidence breeds include Portuguese Water dogs , Duck-trolling retrievers , Standard Poodles , Wheaten terriers, Great Danes, and the Westies (like the one

in the photo at the top of this page). But any dog has the potential to develop Addisons disease. Is There More Than One Form Of Addison's Disease ? Yes, veterinarians recognize three forms of Addisons disease: Typical ( Primary adrenal form), Secondary (Pituitary form) and an Atypical form. In the majority of pets that develop Addisons disease, the problem is destruction or loss of the cells that produce cortisol and aldosterone in the adrenal cortex. In these pets, their immune system has mistakenly identified these cells as foreign to the pets body - something that shouldnt be there and that needs to be destroyed. This is what occurs in all autoimmune diseases - problems like lupus and rheumatoid arthritis in people or thyroid disease , pemphigus and certain anemias in dogs. You can read all about autoimmune diseases in general here. Less frequently, a messenger hormone, ACTH , that is normally produced in your pets pituitary gland ,ceases to flow adequately. Without ACTH, the cells in its adrenal cortex that normally produce cortisol and aldosterone do not do so. This less-common type of Addisons disease is called secondary or pituitary -based Addisons disease. You can read about some individual cases here. I see Addisons disease more than I should in dogs that have received multiple injections of steroid hormone (Methylprednisolone acetate=Depo) as a quick fix for itchy skin. NEVER allow that form of treatment for allergic skin problems (atopy) in your dog and think twice before attempting to relieve moderate itchy allergies with Atopica. The adrenal cortex is, itself divided into three layers (zona fasciculate, zona reticularis, zona glomerulosa). Usually, but not always, all three layers become dysfunctional together. However, the topmost layer, the zona glomerulosa, is sometimes spared. It is the one most responsible for making aldosterone the hormone that controls body salt concentration (sodium and potassium). The zona glomerulosa will occasionally continues to function while the other two cortisol-secreting layers fail. This is called Atypical Addisons disease. In these atypical cases, the pet only needs to be given cortisol-like drugs (prednisolone, prednisone, etc.) to keep it stable. It is also common for dogs with the pituitary form of Addison's to also continue to make sufficient aldosterone (mineralcorticoid) . Those dogs too can be maintained on a corticosteroid alone. The severe crashes vets see in Addisons dogs are usually in the ones that have major problems in the outermost layer. They are the ones that develop electrolyte imbalances that send them to emergency animal hospitals. When a pet has had an abnormal ACTH stimulation test, there is a very good chance that eventually, all three layers of the adrenal cortex will fail even if the pets blood electrolytes come back normal or close to normal right now. What Are They Symptoms of Addisons Disease ? Addisons disease (hypoadrenocorticism) is a chronic disease. That means it develops gradually, with everincreasing signs. So the first symptoms your dog experiences will probably be written off to something else: Too much exercise or excitement, indigestion, a mild bug caught at the doggy park, etc, etc. Early signs often include listlessness, weakness, vomiting, diarrhea or loss of appetite that come and go. Because early Addisons symptoms are mild and come and go naturally. Vets often treat these cases symptomatically with anti-vomit medications (anti-emetics) anti-diarrheal medications, bland diets and perhaps some antibiotics like metronidazole (Flagyl). The dogs get better, so the complicated diagnostic tests dont get

run. With time, owners often put two and two together. They realize that these health crises occur shortly after stress a big party, guests in the home, rowdy kids, a period at the boarding kennel, etc. Because Addisons disease is progressive, the time will come when the dog becomes quite ill. At that point (often at some nighttime emergency clinic) blood electrolytes do get measured and, if the veterinarian is astute, the possibility of Addisons disease comes up. Those dogs are in what we call an Addsonian crisis. This is a form of shock and collapse of the circulatory system than can be fatal. Some pets do not present with these classical signs. They might be brought in with very low blood sugar levels (hypoglycemia) or seizures or muscle tremors or heart beat irregularities. So they might be misdiagnosed as having reoccurring pancreatitis, kidney or heart disease. The most telling thing about these masquerading cases - the thing that should alert owners and veterinarians alike - is a pet that enters the emergency clinic one night looking like he's on deaths doorstep and leaves the next day looking fit as a fiddle. Occasional cases of Addisons disease present as an inability to fully swallow or a pet that repeatedly regurgitates (link to wordnet) undigested food ( megaesophagus). You can read a little quiz given to veterinarians about Addison's here. Can Addisons Disease Be A Life-threatening Emergency ? Yes, a circulatory collapse (Addisonian crisis) can be fatal if the changes in blood sodium (too low) and potassium (too high) levels are not quickly corrected. This requires substantial amounts of intravenous fluids, supportive care and close monitoring. If the pets blood sugar levels have dropped abnormally low, they need to be elevated. If diarrhea and vomiting have dehydrated the animal, that needs to be quickly corrected as well. Rapidly-acting corticosteroid medications like prednisolone sodium succinate or dexamethasone will also improve the situation. Are There Other Health Problems That Could Be Confused With Addisons Disease ? Yes, after reading this far, you understand that many health issues can be confused with Addisons particularly early in the pets disease. Some Addisons case are at first confused with acute pancreatitis. Others get confused with hypoglycemia, food poisoning, parvovirus enteritis, gastric volvulus, intussuceptions and spinal or joint problems. It is very common for dogs, showing these symptoms to be given intravenous fluids, like lactated ringers solution (LRS) , along with a corticosteroid injection. Just by coincidence, that happens to be quite similar to the specific treatment for an Addisonian crisis. So the pet gets better without the veterinarian really knowing why. For reasons we do not understand, whipworms can affect a dogs sodium and potassium levels much as Addisons disease does. You can read about that here. If you suspect Addisons disease but ACTH tests are normal, giving the pet a monthly heartworm control product or wormer that also controls whipworms might be prudent. What Tests Will My Vet Run To Diagnose The Problem ?

You can read a more complete article on how veterinarians approach an Addison's diagnosis here.

Abnormally high blood potassium level and abnormally low blood sodium levels can alert veterinarians to the possibility of Addisons disease, but they are not enough to diagnose it. The levels of both can be normal in your pets blood samples when it is between major crises. Low urine specific gr avity (urinalysis too dilute) high levels of metabolic waste in the blood (elevated BUN and Creatinine) and increased body acidity (metabolic acidosis) are also common in Addison's disease; but they also occur in many health problems not related to your pets adrenal glands. You can see what the normals are for these values in your dog here. ACTH Stimulation Test The only current way veterinarians have to diagnose Addisons disease is through an ACTH stimulation test. In this test, a blood sample is taken from your pet and the level of cortisol in it is measured. After that, a small amount of cosyntropin (Cortrosyn, Synacthen ), a product similar to the pituitary hormone ACTH, is injected into your pet. After a period of time, another blood sample is taken from the pet. When the adrenal glands are working normally, that injection will cause your pets blood cortisol levels to rise significantly. When it does not, it is evidence that the pets adrenal glands do not have the reserve capacity to produce added cortisol. This is the definitive test for primary Addison's disease. When pre-test cortisol levels are consistently low, and post test levels rise dramatically, secondary Addison's disease needs to be considered. Those rarer pets still have functional adrenal glands, the glands are just not receiving ACTH messenger chemical from the pituitary gland to stimulate their cortisol production. Low Dose ACTH Stimulation Test In the USA, Cortrosyn is quite expensive. So veterinarians have adapted the test to work with smaller amounts of the drug. You can read about that here. Ideas That Went Nowhere There was some thought that a doppler ultrasound examination of your pet might detect abnormal adrenal glands. An article on that was published in 1997. (ref) 21-Hydroxylase Assay Humans that develop Addisons disease usually develop it as a form of autoimmune disease. That was thought to also be the case in dogs. In humans, a test now exists that measures the amount of antibodies ( or autoimmunity) a person has developed against his own adrenal glands (21OHAb antibodies) . There should not be any. It would be wonderful if we had such a test for dogs. If we did, we could detect the disease in its early stages when the ACTH test results are borderline. Perhaps we could also use such a test to choose which dogs we ought to breed and which ones we shouldnt .

However, the test kits used by human diagnostic labs (Kronus Labs) do not seem to work in dogs. Using these tests to detect 21OHAb in their serum has been consistently negative for their presence. I do not know why. Perhaps the form of Addison's disease that dogs develop is not as similar to the form humans develop as we once thought. A research team at the Veterinary school of Michigan State University, lead by Dr. Markus Rick, is attempting to determine if the test might be modified and applied to dogs. I do not know the current state of his research. Lymphocyte Count and Sodium:Potassium Ratio A recent study found that dogs with Addison's disease tended to have high-end lymphocyte counts along with abnormally low sodium:potassium ratios (less than 27). (ref) The CBC/ WBC and blood chemistry tests that give those values may have already been performed on your dog. Genetic Markers Another group at the veterinary school in Davis CA is attempting to locate genetic markers that might indicate that a dog is prone to develop Addisons disease. This group is led by Dr. Anita Oberbaur. If your pet has been diagnosed with Addison's disease, you can help by having your veterinarian supply her with a blood sample. This is her contact: AMOberbauer"AT"ucdavis.edu Are There Simple Things I Can Do At Home To Monitor My Dog's Treatment Yes, Besides returning to normal blood sodium and potassium concentrations, dogs with Addison's disease that is well controlled should return to producing normal urine volume. Not all dogs with uncontrolled Addison's disease drink and pee excessively - but many do. They do so because they lack cortisol and , in many cases, aldosterone as well. You can read about that here. So dogs that have their Addison's disease well controlled with medications should produce more concentrated urine. It is quite simple for you to measure your dog's urine concentration at home. Many of my clients , dealing with other health conditions, do. To see how the procedure is done, go here. Remember, many things can cause urine to be excessively dilute: the loss of kidney function that occurs in many older dogs, diabetes, etc. So your pet's urine concentration (its specific gravity) needs to be considered in light of the pet's total health picture. Overly-concentrated urine brings its own set of problems. There is a full explaination about urine specific gravity here. Liquorice ??? In 2005, a vet in Touranga, New Zealand wrote a note published in a journal there. It regarded the possible beneficial effects of licorice in pets that suffer from Addison's disease. I know nothing of its use or effect for that purpose. Be cautious about giving anything to your pet in excessive amounts - particularly based on a single article. You can read Dr. Jarret's letter here. What Medications Will My Pet Be Needing ? Most dogs with Addisons disease will need to be medicated for their entire lives. Most will require two forms of medication, one to keep their blood potassium and sodium levels ( blood electrolytes) optimal and another to replace the cortisol that they can no longer produce. The bodys cortisol needs change, depending on stress, exertion, exercise and the pets changing environment. So one dose will not fit all situations your pet will encounter over the years it lives with Addisons disease. If your dog has typical Addisons disease, where both aldosterone and cortisol are deficient, most veterinarians will stabilize the pets with monthly injections of desoxycorticosterone pivalate (DOCP). It is sold under the trade name, Percorten-V. Percorten replaces the mineralcorticoid, aldosterone, that dogs with typical Addisons disease no longer produce in sufficient quantities.

Dogs with typical Addisons disease also need as synthetic corticosteroid to replace the cortisol they no longer produce in sufficient quantities. Oral prednisone or prednisolone is the most common cortisol-substitute that veterinarians give for that. There is a human oral medication, fludrocortisone acetate (Florinef), that replaces both the aldosterone and the cortisol with a single drug. However, it has been quite expensive. So it was not as widely used as the Percorten/prednisolone combination therapy. Fludrocortisone has now gone off-patent and is available in less expensive, generic form. Dogs with secondary or atypical Addisons disease still produce sufficient aldosterone. So they only need a cortisol-substitute , like prednisolone, to maintain their health. Cortisol is a compound that the pets adrenal glands meter into its bloodstream in ever -changing amounts designed to meet its current metabolic needs. So the dose of corticosteroid replacement you give your pet needs to also vary according to the dogs anticipated metabolic needs. It will need more when you anticipate strenuous exercise, boarding, grooming, or any situation that puts excess demands on its body. It will need less when its body is unstressed and at rest. All pets with Addisons disease need periodic monitoring of their blood potassium and sodium levels. Once you know how your pet is reacting to its medications, those tests can be done less frequently. Over time, expect the required dose of each medication to change. Many pet owners have heard that corticosteroid medications, like prednisolone, should not be given every day because they cause adrenal gland suppression ( cause the adrenal glands to get lazy). That is true in dogs with healthy adrenal glands. But dogs that cannot make sufficient natural cortisol need their replacement medication every day. Dont stop just because your dog appears happy for a few days without it. If your pet begins to drink and urinate excessively (in the absence of kidney disease or diuretic medications) ; if it gains considerable weight ; if it is subject to repeat infections ; or if its blood sugar, liver or kidney function tests (BUN, creatinine) results increase, its cortisol replacement dose may need to be lowered. How Long Can My Dog Live With Addisons Disease ? The problems that Addisons disease causes in sodium and potassium levels and a lack of cortisol are straightforward and quite correctable with medications. So your pet has the potential to live a very long life. How long a life depends entirely on how well Addisons disease is managed. Your dog will depend on you to protect it from stress and to tailor its medication dose and frequency to its daily needs. That is not something your veterinarian can do for you on a day-to-day basis. Every dog will be different. But after a period of time on its medications, and after enough blood tests have been run to see how these medications are affecting it, you will be able to make the fine adjustments the pet will need to return to its favorite activities and enjoyments. Concentrate on providing your pet with as low stress a lifestyle as possible, plenty of love, good nutrition, adequate exercise, weight control, and attention to the other health issues that life invariably brings our way. You can read the advice human physicians give to their Addison's patients here. They apply to your pet as well.