Hypoadrenokortizismus beim Hund – ein Update zu Pathogenese, Diagnose und Therapie

Zusammenfassung

Ein Hypoadrenokortizismus (HoAK) entsteht durch eine in der Regel primäre (immunmediierte) Entzündung der Nebennierenrinde mit der Folge einer unzureichenden Gluko-und Mineralokortikoidproduktion. Als Sonderform können Patienten mit einem “atypischen” HoAK eine reine Glukokortikoidoder eine Glukokortikoid-und Mineralokorti-koiddefizienz mit dabei stabilen Elektrolytkonzentrationen aufweisen. Das klinische Bild eines HoAK ist beim Hund sehr unspezifisch. Die Symptome reichen von Zittern, Schwäche, milden bis rezidivierenden gastrointestinalen Symptomen bis hin zu Anfällen, hypovolämischem Schock und Kollaps. Die ebenfalls unspezifischen Befunde der Routineuntersuchungen gleichen häufig denen anderer Erkrankungen. Ein fehlendes Stressleukogramm, Eosinophilie, Hyponatriämie, Hyperkaliämie, Azotämie und sonographisch kleine Nebennieren stellen die charakteristischsten Befunde eines HoAK dar. Der ACTH-Stimulationstest gilt als Goldstandard zur Diagnosesicherung. Weitere endokrinologische Tests, wie Bestimmung der endogenen ACTH-Konzentration, der basalen und ACTH-stimulierten Aldosteronkonzentration, des Kortisol:ACTH-Verhältnisses sowie des Aldosteron:Renin-Verhältnisses, helfen bei der Differenzierung zwischen primärem, sekundärem und “atypischem” HoAK. In der akuten Krise bestehen die Eckpfeiler der Therapie in einer aggressiven Flüssigkeitstherapie zur Wiederherstellung der Normovolämie und Korrektur der Elektrolytverschiebungen. Die langfristige Therapie besteht in der Supplementierung von Gluko (Prednisolon) und Mineralokortikoiden (Desoxycortonpivalat) mit dem Ziel stabiler Elektrolytkonzentrationen und eines guten Allgemeinbefindens des Hundes. Die Einstellung eines Patienten unter Desoxycortonpivalat erfolgt anhand der Natrium-und Kaliumkonzentration nach einem standardisierten Protokoll. Beim “atypischen” HoAK sind ebenfalls regelmäßige Kontrollen der Elektrolyte zwingend, um einen späteren Substitutionsbedarf an Mineralokortikoiden möglichst frühzeitig zu erkennen. Mit einer adäquaten Therapie und einer guten Besitzercompliance haben Hunde mit HoAK eine exzellente Langzeitprognose.

Summary

Canine hypoadrenocorticism (HoAC) results from a loss of functional adrenal cortex, the most common etiology of which is an immune-mediated destruction leading to an inadequate production of glucocorticoids and mineralocorticoids. The term “atypical” HoAC is used for a subgroup of dogs with either an isolated glucocorticoid deficiency or a combined glucocorticoid and mineralocorticoid deficiency but normal electrolytes. Dogs with HoAC can present with a large variety of clinical signs, ranging from shaking, weakness, and mild gastrointestinal signs to seizures, hypovolemic shock, and collapse. Routine clinicopathologic and diagnostic imaging findings are usually nonspecific and frequently mimic those of other common diseases. However, the absence of a stress leukogram, eosinophilia, hyponatremia, hyperkalemia, and azotemia and small adrenal glands on abdominal ultrasound are characteristic findings in dogs with HoAC. The ACTH stimulation test is currently the gold standard method for diagnosing HoAC. Other endocrine laboratory diagnostics, including the quantification of endogenous ACTH, basal and ACTH-stimulated aldosterone levels, cortisol:ACTH ratio, and aldosterone:renin ratio, may further aid in differentiating between primary, secondary, and “atypical” HoAC. Aggressive intravenous fluid therapy is the cornerstone of treatment in paients with an acute Addisonian crisis because it restores normovolemia and normal blood electrolytes. Maintenance therapy consists of glucocorticoid (e.g., prednisolone) and mineralocorticoid (e.g., des- oxycortone pivalate) supplementation and aims for stable electrolyte concentrations and a clinically well dog. The optimal dose of desoxy- cortone pivalate for a specific dog is determined based on blood so- dium and potassium concentrations by using a standardized protocol. Regular reevaluation of blood electrolytes is required for early identifi- cation of a mineralocorticoid deficiency in dogs with “atypical” HoAC. The long-term prognosis for dogs with HoAC is excellent provided that patients receive adequate treatment and there is good owner com- pliance.

Schlüsselwörter

Morbus Addison - Glukokortikoiddefizienz - Mineralokortikoiddefizienz - atypischer Morbus Addison - ACTH-Stimulationstest - Aldosteron - Desoxycortonpivalat - Glukokortikoide

Keywords

Addison’s disease - glucocorticoid deficiency - mineralocorticoid deficiency - atypical Addison’s disease - ACTH stimulation test - aldosterone - desoxycortone pivalate - glucocorticoids

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