| Abstract | Hipoadrenokorticizam, odnosno Addisonova bolest, endokrina je bolest ljudi i životinja koju karakterizira smanjeno izlučivanje hormona kore nadbubrežne žlijezde. Ovo je rijetka, no po život opasna bolest pasa koja zahtijeva doživotnu terapiju. Kora nadbubrežne žlijezde je funkcionalno i strukturalno odvojena od srži, a dijeli se na tri različite zone od kojih svaka izlučuje različitu skupinu hormona. Zona arcuata sintetizira mineralokortikoide, zona fasciculata glukokortikoide, dok zona reticularis izlučuje androgene hormone. Funkciju kore nadbubrežne žlijezde reguliraju CRH i ACTH podrijetlom iz hipotalamusa i adenohipofize.
Hormoni kore nadbubrežnih žlijezdi imaju niz funkcija koje pomažu u održavanju homeostaze. Glukokortikoidi, tj. kortizol, sudjeluju u metabolizmu ugljikohidrata, proteina i masti, te sudjeluju u održavanju krvnog tlaka. Također imaju imunosupresivno i protuupalno djelovanje. S druge strane, mineralokortikoidi, tj. aldosteron, ima glavnu ulogu u održavanju fizioloških vrijednosti elektrolita u plazmi. Istodobno, pridonosi održavanju normalnog volumena krvi i krvnog tlaka povezanog s RAAS sustavom.
Addisonovu bolest karakterizira djelomični ili potpuni gubitak funkcije kore nabubrežne žlijezde. Bolest se dijeli na primarni i sekundarni hipoadrenokorticizam, a primarni se dijeli na češći tipičan i rjeđi atipičan oblik. Primarni hipoadrenokorticizam najčešće je imunoposredovane etiologije, no i tumori, infekcije, upale i sl. mogu biti uzroci nastanka oštećenja kore nadbubrežne žlijezde. Tipičan oblik karakterizira nedostatak glukokortikoida i mineralokortikoida, dok je za atipičnu Addisonovu bolest karakteristično samo manjak glukokortikoida. Sekundarni hipoadrenokorticizam nastaje zbog oštećenja tkiva hipotalamusa ili adenohipofize što posljedično rezultira atrofijom adrenalne kore. Određene pasmine pasa su predisponirane za razvoj adrenalne insuficijencije zbog nasljednih svojstva bolesti, te je pojavnost veća u ženki.
Klinička slika izrazito je promjenjiva i nespecifična, a uključuje znakove gotovo svih organskih sustava. Dijeli se na akutni oblik (adisonska kriza) i češći kronični oblik. Najčešći simptomi uključuju letargiju, proljev s ili bez krvi, povraćanje, slabost mišića, anoreksiju, gubitak na težini, poliuriju/polidipsiju, bradikardiju i dehidraciju/hipovolemiju. U laboratorijskim nalazima može biti prisutna anemija, neprisutnost „stresnog leukograma“, hiponatrijemija, hipokloremija, hipoglikemija, hipoproteinemija, acidoza, povišena ureja i
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kreatinin, povišeni određeni jetreni enzimi itd. Objektivna dijagnoza se postavlja na temelju ACTH stimulacijskog testa. Drugi testovi poput određivanja koncentracija Na i K, omjera Na:K, koncentracija bazalnog kortizola, aldosterona i dr. mogu poslužiti kliničaru u postavljanju sumnje na hipoadrenokorticizam.
Pacijentima u adisonskoj krizi potrebno je korigirati hipovolemiju, riješiti elektrolitske abnormalnosti u plazmi, te osigurati nadomjestak glukokortikoida. Također je iznimno važna i simptomatska terapija. Kronični hipoadrenokorticizam se liječi doživotnom terapijom glukokortikoida i mineralokotikoida. Najvažniji sintetski mineralokortikoidi koji se koriste u terapiji su DOCP i fludrokortizon acetat, dok su najčešći glukokortikoidi prednizon, prednizolon, hidrokortizon i deksametazon. Prognoza pacijenata s Addisonovom bolesti je odlična ukoliko je doza lijekova pravilno određena za svakog psa individualno, te ukoliko vlasnici kontinuirano daju psu terapiju i dovode istog na redovite pretrage. |
| Abstract (english) | Hypoadrenocorticism, also known as Addison's disease, is an endocrine disease affecting both humans and animals alike, characterized by a decreased secretion of hormones by the adrenal gland. It is a rare, but a life-threatening disease in dogs that requires a lifelong therapy. The adrenal cortex is functionally and structurally separated from the marrow. It is divided into three different zones, each of which secretes a different group of hormones. The zona arcuata synthesizes mineralocorticoids, the zona fasciculata glucocorticoids, while the zona reticularis secrets androgen hormones. The function of the adrenal cortex is regulated by CRH and ACTH, originating from the hypothalamus and adenohypophysis.
The hormones of the adrenal cortex have a number of functions that help maintain homeostasis. Glucocorticoids, i.e. cortisol, are involved in the metabolism of carbohydrates, proteins and fats, and are also involved in maintaining blood pressure. Alongside that, they also have immunosuppressive and anti-inflammatory effects. On the other hand, mineralocorticoids, i.e. aldosterone, play a major role in maintaining the physiological values of plasma electrolytes. At the same time, they contribute to the maintenance of normal blood volume and blood pressure associated with the RAAS system.
Addison's disease is characterized by partial or complete loss of function of the adrenal cortex. The disease is divided into primary and secondary hypoadrenocorticism, having the primary one divided into the more common typical and the less common atypical form. Primary hypoadrenocorticism is most often of immune-mediated etiology, but at the same time, tumors, infections, inflammation, etc. can be the cause of damage to the adrenal cortex. The typical form is characterized by a deficiency of glucocorticoids and mineralocorticoids, while atypical Addison's disease is characterized only by a deficiency of glucocorticoids. Secondary hypoadrenocorticism occurs due to damage to the tissue of the hypothalamus or adenohypophysis, resulting in atrophy of the adrenal cortex. Certain breeds of dogs are predisposed to develop adrenal insufficiency due to hereditary traits of the disease, with the incidence being higher in females.
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The clinical picture is markedly variable and nonspecific, and includes signs of almost all organ systems. It is divided into the acute form (addisonian crisis) and the more common chronic form. The most common symptoms include lethargy, diarrhea with or without blood, vomiting, muscle weakness, anorexia, weight loss, polyuria/polydipsia, bradycardia, and dehydration/hypovolemia. Laboratory findings may include anemia, absence of "stress leukogram", hyponatremia, hypochloremia, hypoglycemia, hypoproteinemia, acidosis, elevated urea and creatinine, elevated certain liver enzymes, etc. Objective diagnosis is made based on ACTH stimulation test. Other tests such as determining Na and K concentrations, Na: K ratios, basal cortisol, aldosterone concentrations, etc. may serve the clinician in raising the suspicion of hypoadrenocorticism.
Patients in an addisonian crisis need to have their hypovolemia corrected, resolve their plasma electrolyte abnormalities, and they need a glucocorticoid replacement. Symptomatic therapy is also extremely important. Chronic hypoadrenocorticism is treated with lifelong glucocorticoid therapy and mineralocorticoids. The most important synthetic mineralocorticoids used in therapy are DOCP and fludrocortisone acetate, while the most common glucocorticoids are prednisone, prednisolone, hydrocortisone, and dexamethasone. The prognosis of patients with Addison's disease is excellent if the dose of medication is correctly determined for each dog individually, as well as if the owners continuously give therapy to the dog and bring them to regular examinations. |
