Veterinary care center "Elitevet" Addison's disease is one of the most common pathologies of the endocrine system among young dogs.

Addison's disease in dogs is not rare, but rather not as common as other diseases and is one of the most common pathologies in young dogs. In a large number of cases the symptoms are simply interpreted, but accurate diagnosis I can't deliver. The animal suffers from excruciating pain in the body. He may even be treated long time, but if the diagnosis is made incorrectly, then all medications simply poison the body.

What is this disease?

This is a deviation in work endocrine system which occurs due to disruption of the process of hormone synthesis. This is one of the causes of the disease, but it is not the only one. Another reason for the development of pathology may be long-term use of glucocorticoid drugs. The symptoms of this disease are very vague and therefore difficult to determine. This often leads to a false diagnosis. The disease is congenital, so young dogs suffer from it, or rather it manifests itself in young dogs under 1 year of age.

Probably if veterinarian will begin to remember some symptoms of adrenal diseases, he will understand that the diagnoses could have been made incorrectly, and in some cases Addison's disease could have been diagnosed. This disease is quite secretive and similar to many others. Therefore, its diagnosis is quite complex and requires large quantity accurate analyses.

What, then, are the classic signs of hypoadrenocorticism? If we start to understand the typical form of the disease, then, most likely, we will encounter a young dog that may periodically experience the disorder for a long time gastrointestinal tract. At the same time, the dog will be lethargic and lag behind in body growth and development.

At the first stage of the disease, you can see a deterioration in the dog’s health. At advanced stage Addison's disease is already evident dangerous symptoms. In both the first and second cases, it is necessary to quickly take the dog to veterinary clinic and conduct an inspection with knowledgeable doctor. This disease does not tolerate slowness and procrastination.

Symptoms of Addison's disease in dogs

Classic signs of Addison's disease initial stages its development:

• diarrhea and vomiting,
• depression and poor appetite,
• frequent urination, thirst and rapid decline weight.

Active development of the disease leads to the following symptoms:

• barely perceptible pulse and shortness of breath, low temperature body and baldness, pain in the abdominal area and blood in the stool.

The disease does not tolerate long thought and can lead to death. The doctor will definitely prescribe necessary tests and conduct an examination. When the veterinarian not only identifies symptoms of Addison's disease in dogs, but tests also confirm this, he will immediately prescribe required course treatment. In order to be sure of the correct diagnosis, the doctor needs to take blood from the animal for testing. This analysis is one of the most basic and will be carried out regularly at all stages of treatment.

Addison's disease in dogs affects each breed differently. In some it develops once per hundred dogs, while in other breeds every fourth patient suffers. Dogs of the following breeds are very prone to developing this pathology:

• poodle,
• different types of terriers,
• rottweiler,
• Great Danes,
• bearded collies.

The exact causes of the disease have not yet been determined. Scientists all over the world are trying to learn as much as possible about this pathology, but no one has yet given a concrete answer. Diseases of the kidneys and adrenal glands bring great harm the animal's body and severe pain, which the dog cannot cope with on its own. There are several basic possible reasons diseases:

• tumors and neoplasms of the kidneys and adrenal glands that metastasize;
• insufficient production of ACTH;
• taking hormonal medications without a biochemical blood test.

Diagnosis of Addison's disease in dogs

Hypoadrenocorticism in dogs is quite variable in its symptoms. They appear and disappear for a while. In such a situation, it can easily be confused with another disease and Addison’s disease can be detected too late, when irreversible pathological changes. Sometimes there are also relapses of the disease.

At successful treatment at the veterinary clinic, the disease subsided and the dog was completely healthy. But she returns without any problems if there is a reason for it favorable conditions. Often, if the disease returns, it does so with greater force and in a more severe form. During a relapse, a blood test accurately shows kidney disease and anemia. The disease can be diagnosed using an x-ray, but the conclusion of an x-ray is not a 100% positive result. The image shows a decrease in the size of the heart and liver, as a result of prolonged dehydration.

X-rays can also be used to diagnose tumor diseases or other pathologies of the adrenal glands. One more mandatory analysis to identify this disease there is a complete detailed biochemical analysis blood. It shows the level of eosinophils, lymphocytes and potassium in the blood. Checking cortisol levels increases the accuracy of diagnosis. When ACTH is administered to a dog, the hormone levels in the adrenal glands should increase. If this does not happen, then the dog definitely has Addison's disease.

Treatment methods for Addison's disease

Veterinary experts are constantly developing treatment regimens for this disease. The number of sick animals is increasing due to unacceptable keeping of dogs by their owners or due to inconsistency of symptoms. Doctors develop specific treatment methods for each individual phase of the disease.

If the dog already has acute form hypocortisolism occurs, loss of consciousness and state of shock. Very often you can observe signs of hypothermia. Such animals are immediately treated with large doses of Dexamethasone and constant heat. Sometimes it becomes necessary to administer insulin. IN in some cases Dexamethasone injection with dextrose can be administered. Additional treatment symptoms are not necessary in the acute phase of the disease.

When the dog chronic phase Addison's disease and observed low level cortisol, it is necessary to take Prednisone orally in a small but constant amount. At chronic disease there is a need to increase the dose over time. Likewise, when an animal finds itself in stressful situation, the dose also needs to be increased once.

To check the level of cortisol in the animal's body, blood is taken for analysis every six months. The presence of side effects from taking medications is also checked. Most often they are absent, but still, treatment methods are very individual and require strict supervision by specialists. When treating your pet, you must clearly understand that even side effects from treatment are much less dangerous than the symptoms of this disease.

No matter how terrible it may sound, a sick dog will forever remain attached to permanent appointment hormonal drugs. Complete cure from Addison's disease is impossible. Modern therapy eliminates only symptoms and painful sensations for the dog. Taking medications should be strictly controlled and not skipped. If there is a need to change the manufacturer of the drug, this must be discussed in advance with the attending physician. Independent activity completely prohibited, otherwise death inevitable.

During the first month of treatment, there should be regular visits to the veterinary clinic at strictly specified times. The dog's blood will be constantly taken for biochemical analysis in order to adjust the course of treatment if necessary. Usually hormonal drugs are administered once a month, but when there is a need for this, the drug can be administered once every three weeks.

During a blood test, the levels of potassium, magnesium and calcium in the blood must be checked. You need to understand the main thing for yourself, that when proper treatment and caring for your dog, the chance of living to an old age is very high. But it all depends on the owner of the animal. A strict ongoing treatment regimen requires a lot of time, money and human effort. Only with full human responsibility is there a chance to save the dog. Any cessation or pause in treatment will immediately lead to a relapse of the disease.

During regular monitoring of the dog's treatment, the progression of adrenal atrophy is checked. If atrophy progresses, it reduces the effectiveness of the dog’s treatment significantly. If the condition of a sick animal sharply worsens, then it is necessary to take the dog to the clinic for treatment. Some blood transfusions or individual blood components are also possible.

Addison's disease itself is very dangerous and terrible in its incurability. Even with the most correct treatment, if an animal has no desire to live, then it will not live. But in the case of a great desire to survive and proper treatment by people, the dog will be able to live absolutely full life, even despite regular intake hormonal drugs.

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Addison's disease in dogs is a disease characterized by a disorder proper operation adrenal glands

Let us consider in detail the occurrence of the disease. What symptoms are characteristic of this disease? How is this disease treated?

Adrenal function

Paired glands, endocrine. They are located on the top of the kidneys themselves. Thanks to them, the optimal level of hormones in the dog’s body is maintained.

Any disease that affects these glands can have an overall effect on the dog’s entire body. In Addison's disease, the adrenal glands do not produce enough steroid hormones.

For example, cortisol directly affects the metabolism of fats, proteins, and carbohydrates. Consequently, on normal balance blood glucose. Also, adrenal steroids play a role in the exchange of ions in epithelial cells.

The body may lose potassium and retain sodium. Addison's disease in dogs directly affects blood biochemical parameters. Moreover, the accompanying symptoms are not specific to her.

Signs

What you can notice in a dog during the course of the disease:

• refusal to eat;
• weight loss;
• Sopor;
• thirst;

As you can see, these signs are also characteristic of other diseases. For this reason, it is not always possible to detect Addison's disease.

Most of all, such signs of the disease clearly appear under various stresses, or periodically. The disease directly depends on the ongoing processes in immune system, tissue in the adrenal glands is destroyed.

Acute attacks of Addison's disease are characterized by:

• weakness;
• arrhythmia;
• decreased heart rate.

If such symptoms are detected, you must immediately contact a veterinary clinic for timely treatment.

Diagnostics

Gender and breed do not matter; young females are most susceptible. Some breeds have a genetic predisposition. They donate blood for biochemistry to measure the level of cortisol in the blood.

A test is performed for the presence of special hormones. The first blood sample is taken and the hormone is administered. After some time, a second fence is made. Cortisol levels are measured in both fences. The results are compared.

If you have Addison's disease, there will be little cortisol in the tests. During treatment, special steroids are used, administered orally. In some cases intramuscularly.

With proper treatment, all signs of the disease will disappear after a short time. For each dog is prescribed individual course treatment.

Have you ever seen Addison's disease in dogs? What measures were taken?

Hypoadrenocorticism - endocrine disease, characterized by disruption of the adrenal glands, deficiency of vital hormones (glucocorticoids, mineralcorticoids).

Adrenal glands - paired endocrine glands located next to the kidneys. Each gland consists of two layers - the cortex (outer layer) and the medulla (inner layer). The adrenal glands produce 2 vital important hormone, which regulate internal metabolic processes and ensure the normal functioning of the body as a whole. Thus, the hormone cortisol (stress hormone) is formed in the outer layer, and aldosterone is formed in the brain layer.

Cortisol is the main hormone of the glucocorticosteroid class, acts on almost any tissue of the body, regulates glucose metabolism, protein, lipoprotein metabolism, stimulates the formation of red blood cells, regulates blood pressure, counteracting stress, suppresses inflammatory reactions.

Aldosterone is the main hormone of the mineralcorticosteroid class, provides regulation of potassium, sodium, controls water balance in organism.

In Addison's disease, in most cases, the production of both hormones is impaired, however, there are animals that have a deficiency of either mineralocorticoids or glucocorticoids. The adrenal glands are also responsible for the production of androgens and estrogens (sex hormones), but their deficiency in this disease is not clinically significant.

Causes

In most cases, the pathology develops against the background of autoimmune damage to gland cells and severe tissue destruction. Clinically, the lack of hormone production manifests itself when more than 90% of the organ is destroyed. Less common causes include injury or infection of the adrenal glands.

The most typical symptoms:

• diarrhea;
• lethargy, depression, decreased exercise tolerance;
• weight loss;
• general weakness.

The dog's condition may temporarily worsen or improve as the disease progresses. Typically, symptoms increase when the patient is stressed.

It should be remembered that the disease can develop into Addison's crisis - a life-threatening condition accompanied by a fall blood pressure, violation heart rate, pronounced electrolyte imbalance. Therapy is possible only in a hospital setting. Intravenous infusion and monitoring of vital signs are indicated.

Diagnostics

The doctor conducts a physical examination, a detailed examination of the patient. Laboratory diagnostics includes clinical and biochemical blood tests. Determination of the level of hormones in the blood and the final diagnosis occurs when performing an ACTH stimulation test. Your doctor measures your cortisol levels before and after you give adrenocorticotropic hormone (ACTH). It is also possible to measure aldosterone levels in the blood.

Treatment

Authors): ON THE. IGNATENKO, candidate of veterinary sciences, member of the European Society of Dermatology, member of the European Society of Endocrinology, Kiev
Magazine: №2 -2017

UDC: 619:616.45:636.7

Hypoadrenocorticism is an uncommon endocrine pathology in dogs. The cause in most cases is idiopathic atrophy of the adrenal cortex. Clinical signs are varied but not typical and include anorexia, apathy, vomiting, diarrhea, collapse, and, in most cases, electrolyte disturbances. Diagnosis is only possible by performing a stimulation test with adrenocorticotropic hormone (ACTH). Therapy should include gluco- and mineralocorticoids. Addison's crisis is a life-threatening condition requiring intensive care. Long-term therapy is successful, the prognosis is favorable.

Hypoadrenocorticism is infrequent endocrine disorders in dogs. The reason in most cases is idiopathic atrophy of the adrenal cortex. Clinical symptoms are varied, but not typical, include anorexia, lethargy, vomiting, diarrhea, collapse, and, in most cases, electrolyte disturbances. Diagnosis can only conduct the stimulations test with ACTH. Therapy should include gluco and mineralocorticoids. Addisoncrisis is a life-threatening condition requiring intensive care. Long-term therapy illness is successful, the prognosis is favorable.

Introduction

Hypoadrenocorticism is an uncommon condition in dogs and is extremely rare disease in cats. His clinical development occurs when more than 80% of the cortical tissue is destroyed and there is a deficiency of gluco- and mineralocorticoids. Clinical picture is not typical, which makes it difficult to recognize, diagnose and treat this condition in dogs.

Etiological factors

Hypoadrenocorticism can be primary, secondary and, extremely rarely, tertiary. In the case of primary hypoadrenocorticism, the cause is hidden in the disruption of the adrenal glands. Depending on the degree of adrenal dysfunction, it can be typical or atypical. In the case of secondary hypoadrenocorticism, either the functioning of the pituitary gland, which produces ACTH, is impaired, or iatrogenic factors disrupt the functioning. In the case of tertiary hypoadrenocorticism, disturbances occur at the level of the hypothalamic-pituitary axis.

Most common cause The development of Addison's disease in dogs and cats, as in humans, is the autoimmune destruction of all three layers of the adrenal cortex or their idiopathic atrophy. IN in rare cases the disease can be associated with the consequences of injury or systemic diseases, such as coagulopathies, amyloidosis, systemic mycoses (cryptococcosis, histoplasmosis, blastomycosis). In humans, tuberculosis is also a common cause of hypoadrenocorticism, leading to granulomatous inflammation and destruction of adrenal tissue.

Described in dogs clinical case the occurrence of hypoadrenocorticism against the background of infiltration of the adrenal glands by lymphoma cells.

People often have a combination of several endocrine pathologies: More than 50% of people with Addison's disease have additional endocrine pathology. The most common is a combination of hypoadrenocorticism, hypothyroidism and diabetes mellitus. A combination of hypoadrenocorticism and hypothyroidism, Schmidt's syndrome, also occurs in dogs, but much less frequently than in humans, about 4% of cases. It should be suspected in dogs with Addison's disease and markedly elevated cholesterol levels, bradycardia, and symmetrical noninflammatory alopecia. All these signs are not typical for hypoadrenocorticism.

With primary typical hypoadrenocorticism, electrolyte disturbances will be pronounced.

With primary atypical hypoadrenocorticism, electrolyte disturbances will not be detected at the time of diagnosis. "Atypical Addison" without electrolyte disturbances occurs in 10% of patients with primary hypoadrenocorticism. However, over time (sometimes over several years), these patients may develop symptoms of mineralocorticoid deficiency.

Iatrogenic primary hypoadrenocorticism can occur with the use of drugs that act on the adrenal cortex - mitotane and trilostane, which have a selective cytotoxic effect on this area. The zona fasciculata of the adrenal glands is more susceptible to the influence of mitotane (trilostane), however, in some cases, the use of these drugs has a significant effect on the zona glomerulosa, which leads to a lack of mineralocorticoids - Addison's symptoms. When necrosis of all three layers of the adrenal cortex occurs, animals require lifelong therapy with both glucocorticoids and mineralocorticoids. Vetoril is a more selectively acting drug on the adrenal cortex, however, its use can lead to necrosis of the adrenal cortex (it can be reversible and irreversible) and lifelong replacement therapy gluco- and mineralocorticoids.

Secondary hypoadrenocorticism occurs as a result of insufficient ACTH secretion. This leads to atrophy of the zona fasciculata and reticularis and the absence of glucocorticoid secretion; the zona glomerulosa (and mineralocorticoid secretion) remains intact. The cause may be trauma, neoplasms of the pituitary gland, secondary destruction due to the inflammatory process.

The cause of secondary iatrogenic hypoadrenocorticism may be sudden steroid withdrawal syndrome when they are used. long-term use or high-dose glucocorticoid therapy.

In very rare cases, idiopathic isolated defect ACTH secretion. In these cases, no electrolyte disturbances are observed since aldosterone secretion remains normal.

Tertiary hypoadrenocorticism, caused by a breakdown in the secretion of CRH (corticotropin-releasing hormone) from the hypothalamus, is extremely rarely reported in humans. In dogs, CRH deficiency leads to ACTH deficiency and provokes secondary hypoadrenocorticism. Isolated aldosterone deficiency alone is rare in humans and to date only one case report has been reported in one dog.

Clinical picture

Hypoadrenocorticism can occur in dogs of any age and gender, but young and middle-aged animals, more often females, are more predisposed to it (in 69% of cases according to most researchers). Animals aged 4 to 6 years are most often susceptible to hypoadrenocorticism, but the disease can occur in both young one-year-old animals (hypoadrenocorticism has been described in a 2-month-old puppy) and in older dogs over 10 years old. The most susceptible breeds are Collies, Great Danes, Poodles, West Wyland Terriers, Border Collies, Rottweilers and Basset Hounds. Genetic predisposition proven in standard poodles, Leonbergers and border collies. Obviously, there is no relationship between the size of the breed and the incidence of the disease.

The clinical signs of this disease are not characteristic; they can occur in many other pathologies, which very often misleads the doctor general practice who does not routinely treat endocrine patients. Patients pass through like animals who suffer from gastrointestinal disorders or renal failure. Another point that differs from most commonly encountered endocrine pathologies, in which the disease tends to steadily progress (hyperadrenocorticism, hypothyroidism, diabetes etc.), – in 25–43% of cases the disease will be intermittent. Clinical signs will appear, disappear, and appear again after some time, again misleading the veterinarian regarding chronic infection Gastrointestinal tract or kidney disease. Suddenness of manifestation clinical signs and the severity also varies from patient to patient.

Poor appetite, recurrent vomiting, regurgitation, lethargy, apathy, weight loss, tremors, symptoms of polydipsia-polyuria (PD-PU), pain abdominal wall upon palpation, these are signs of hypoadrenocorticism. They may not be constantly present, but pass in the background symptomatic therapy and come back again. Some patients may experience progression of the disease. All of the listed manifestations will be characteristic of atypical hypoadrenocorticism, which occurs without electrolyte disturbances, and it will be even more difficult to identify it. A change in lifestyle, a move, an exhibition, studying at a “dog school” or even a visit to a veterinarian - all events causing stress, can provoke the manifestation of the disease. Hemorrhagic gastroenteritis, shock and collaptoid states, convulsions have also been described in patients with hypoadrenocorticism. Bradycardia in a patient presenting with symptoms of shock is a reason to suspect hyperkalemia and, accordingly, Addison's crisis.

The researchers compared patients with “typical” hypoadrenocorticism with electrolyte abnormalities (mineralocorticoid deficiency) with patients with “atypical” hypoadrenocorticism (glucocorticoid deficiency) without electrolyte abnormalities and observed no differences in disease presentation or incidence of clinical signs. But patients with glucocorticoid deficiency were, on average, older than patients with mineralocorticoid deficiency.

Hypotension, which is common in 90% of people suffering from Addison's disease, is very rarely seen in dogs, mostly presenting with symptoms of severe shock. However, it is necessary additional research patients with hypoadrenocorticism.

Table 1 shows the symptoms encountered in patients with hypoadrenocorticism, in descending order of frequency of manifestations.

It follows from the table that all these signs are not unique to this disease; moreover, they will be more common with gastrointestinal disorders– vomiting and diarrhea, heart disease, kidney disease, in the case of hepatitis and pancreatitis.

TABLE 1. Clinical manifestations

hypoadrenocorticism in dogs

in order of frequency of occurrence

Table 1. Clinical manifestations of hypoadrenocorticism in dogs in order of frequency of occurrence according to Kirk

Laboratory abnormalities

It is very important to collect blood for testing before infusion therapy, and, especially, before using steroids.

Laboratory abnormalities in patients with hypoadrenocorticism are shown in Table 2.

Table 2. Laboratory abnormalities in patients with hypoadrenocorticism according to Kirk

The “classic” laboratory abnormalities characteristic of hypoadrenocorticism are hyperkalemia and hyponatremia. The ratio of these electrolytes is Na:K<27 наблюдается более чем у 80% пациентов с болезнью Аддисона. Электролитные нарушения, такие, как гиперкалиемия, гипонатриемия, гипохлоремия, гиперкальциемия могут наблюдаться независимо друг от друга. При первичном гипоадренокортицизме гипонатриемия и гиперкалиемия прежде всего, объясняются дефицитом альдостерона, что вызывает нарушение работы почек, пытающихся сохранить натрий и вывести калий. При вторичном гипоадренокортицизме гипонатриемия является следствием потерь в организме, возникающих из-за анорексии и нарушений работы желудочно-кишечного тракта. Наиболее опасными для жизни последствиями гиперкалиемии являются изменения в миокарде, связанные со снижением возбудимости, уменьшением проводимости миокарда, которые могут привести к остановке сердца. Соотношение уровней натрия и калия может не совпадать в различных лабораториях, поэтому желательно вывести это соотношение в каждой лаборатории, занимающейся исследованиями электролитов. Следует также помнить, что эритроциты собак некоторых японских пород (акита ину, шиба ину) содержат большое количество калия, гемолиз сыворотки и разрушение эритроцитов может вызвать гиперкалиемию in vitro, не in vivo, псевдогиперкалиемию. Гиперкалиемия может также наблюдаться у животных, принимающих в качестве терапии гепарин. Также любые метаболические нарушения, ассоциированные с ацидозом, лейкоцитозом, тромбоцитозом, могут быть ассоциированы с гиперкалиемией.

Details of diseases that can cause hyperkalemia and/or hyponatremia are presented in Table 3.

Table 3. Differential diagnosis of hyperkalemia and (or) hyponatremia

(Feldmen at all)

Most patients with hypoadrenocorticism will have sodium levels below 135 mmol/L and potassium levels above 5 mmol/L. Na:K ratios<25, <24, <23 являются «подозрительными» на предмет гипоадренокортицизма. В одном исследовании только у 25% собак с соотношением Na: K <25 был в действительности гипоадренокортицизм. У других исследователей две трети пациентов с соотношением Na: K <20 были больны гипоадренокортицизмом. У пациентов с болезнью Аддисона может не быть электролитных нарушений, если:

The disease was detected in the early stages;

Transient dysfunction of the zona glomerulosa of the adrenal cortex was observed;

These dogs often have a “long history of illness” and are older in age, with significant hypocholesterolemia and hypoalbuminemia.

An increase in calcium levels is usually closely related to an increase in potassium levels. There is an increase in both total and ionized calcium. However, in cases where hypoadrenocorticism is associated with hypoalbuminemia, total calcium levels may be reduced, but ionized calcium will remain normal.

Hypoadrenocorticism may cause increased levels of ALT, AST, and azotemia, which are also common findings in many infectious diseases such as leptospirosis. A decrease in liver size, hypoalbuminemia, and rarely ascites may also be observed. The exact cause of the increase in transaminases is unknown, but it is assumed that this is a violation of tissue perfusion. Hypotension, deterioration of myocardial contractility and conductivity can lead to such changes. Also, autoimmune liver diseases can lead to such abnormalities, especially in the absence of a stress leukogram.

Prerenal azotemia is a common finding and is caused primarily by dehydration, hypovolemia, and decreased tissue perfusion. In this case, we observe a significantly greater increase in urea than in creatinine. Gastrointestinal bleeding also increases urea levels. Sodium loss leads to a decrease in the specific gravity of urine. Despite severe degrees of dehydration in patients with hypoadrenocorticism, the specific gravity of urine often does not rise above 1010-1025.

In a CBC hemogram, similar to the decreased sodium to potassium ratio, the classic findings would be lymphocytosis and eosinophilia. Identification of these abnormalities gives reason to the specialist to suspect adrenal insufficiency, however, this can also be observed in only 20% of patients with Addison's disease.

A list of other diseases that can lead to severe eosinophilia is presented in Table 4.

Dirofilariasis;

4. Mastocytomas, as well as other neoplasms.

5. Hypoadrenocorticism (Addison's disease).

6. Eosinophilic myositis.

7. Eosinophilic rhinitis/conjunctivitis/pneumonitis.

8. Eosinophilic enterocolitis (allergic colitis).

9. Eosinophilic leukemia.

10. Feline eosinophilic granuloma complex.

11. Eosinophilic vasculitis.

12. Drug reaction.

Insufficient stimulation of the bone marrow by steroids can lead to the development of normocytic normochromic non-regenerative anemia, which can be “masked” by dehydration and, as a consequence, hemoconcentration. Anemia can also occur with gastrointestinal bleeding. The absence of a stress leukogram in a seriously ill animal should also cause concern to a veterinary specialist and provides grounds for further research to exclude hypoadrenocorticism.

Hypoglycemia is also an uncommon but possible finding that is directly related to insufficient levels of steroids in the body.

Visual diagnostic methods

Visual diagnostic methods are not decisive for identifying hypoadrenocorticism. A chest x-ray can reveal microcardia, a decrease in the size of the liver, which occurs due to a decrease in the volume of circulating fluid. Dilatation of the esophagus and megaesophagus have been described in a small number of animals with hypoadrenocorticism; the exact mechanism is unknown, but the effects of hyperkalemia have been suggested leading to impaired neuromuscular function.

Using an abdominal ultrasound, an experienced visual diagnostic doctor can detect a decrease in the size of the adrenal glands.

Diagnostics

Determination of basal cortisol levels alone is not sufficient to establish hypoadrenocorticism. Low basal cortisol levels can occur in animals suffering from any severe systemic disease. However, it can be a good rule-out test: a basal cortisol level greater than 2 mg/dL (57 mmol/L) is highly likely to rule out hypoadrenocorticism. If the level of basal cortisol is 2 mg/dl or lower, then the “gold standard” for diagnosis is a stimulation test with ACTH, despite the fact that determining only basal cortisol will be significantly cheaper. Previously, it was recommended to measure basal cortisol, then administer 250 mcg (and 125 mcg for animals weighing less than 5 kg) of synthetic ACTH (intravenously or intramuscularly) and repeat the cortisol level 1–2 hours after stimulation. Lower doses of synthetic ACTH have been observed to produce similar hormonal stimulation. Therefore, synacthen is most often administered at a dosage of 5 mcg/kg, with a maximum of 250 mcg per animal. There are various synthetic ACTH preparations: synacthen - cosinotropin solution, synacthen gel, and synacthen depot. The dosage of synacthen gel is 2.2 units/kg. Some authors recommend that when using a gel or depot preparation, a second cortisol test should be taken 2 hours after administration. However, there have been no studies comparing cortisol levels between different ACTH drugs. Synacthen can be administered either intravenously or intramuscularly, but its absorption when administered intramuscularly may be slowed in animals entering a state of crisis due to dehydration. In this case, intravenous administration is the best option. But it should be remembered that depot preparations and synacthen gel can only be administered intramuscularly.

The cosinotropin remaining after opening the ampoule can be stored in the refrigerator for up to three weeks without reducing its activity. When frozen to -20 degrees, it can be stored for up to 6 months without loss of activity.

An ACTH test should be performed prior to initiation of therapy, ideally both fluid and steroid therapy. If the animal's condition does not allow this, then dexamethasone should be used for maintenance therapy, since it cross-suppresses the adrenal response to ACTH less than other steroids (prednisolone, methylprednisolone, cortisone, hydrocortisone, etc.). It is described that dexamethasone in the ACTH test suppresses secretion by no more than 35%, which still makes it possible to make a diagnosis of hypoadrenocorticism. If steroid therapy was started as an anti-shock treatment, before diagnosis is made, then in this case it is necessary to wait (the time depends on the steroid with what activity was used) and only then carry out the test.

The ACTH test is quick, easy to perform, does not require much time, and allows for a correct diagnosis. Cortisol is a stable hormone that can be stored and both samples can be transported simultaneously. However, the requirements of the laboratory performing the measurements must always be observed. If there are recommendations on the use of special tubes, delivery conditions, storage periods, they must be followed.

Post-stimulation cortisol levels in dogs with hypoadrenocorticism will not exceed 2 mcg/dL, but most will not exceed 1 mcg/dL.

Differential diagnosis

In the differential diagnosis of young animals with gastrointestinal disorders and symptoms of vomiting and diarrhea, it is necessary, first of all, to exclude obstruction by foreign bodies, dietary disorders, poor nutrition, picking up on the street, food intolerance, infectious (viral, bacterial, fungal, protozoan) etc.) agents that can lead to the development of gastroenteritis. Idiopathic inflammatory bowel syndrome will be accompanied by similar gastrointestinal manifestations. Chemical irritations of the gastrointestinal tract, obstruction, and constipation may also have similar clinical manifestations. Non-gastrointestinal disorders caused by inflammatory processes, such as pancreatitis, peritonitis, cholangiohepatitis, pyelonephritis, pyometra or volvulus of the spleen, may be accompanied by vomiting and diarrhea. Other metabolic and endocrine causes, including uremic stage of renal failure, liver failure, diabetic ketoacidosis, hyperkalemia can provoke vomiting and diarrhea. Intracranial neoplasms, cerebral edema, hydrocephalus and encephalitis in rare cases can provoke vomiting due to an increase in cranial pressure. Otitis media and motion sickness are also accompanied by vomiting.
Abdominal pain, manifested by tenderness on palpation of the abdominal wall, can be caused by emotional stress, inflammatory processes in the stomach and intestines, mechanical obstruction, urolithiasis or visceral expansion of organs - acute dilatation and volvulus of the stomach.

In the differential diagnosis of PD-PU, it is necessary to exclude causes of primary polyuria associated with impaired production or response of antidiuretic hormone; for example, caused by E. coli toxin, hypercalcemia, hyperadrenocorticism, central diabetes insipidus, liver failure; or post-obstructive diuresis, or medications that stimulate diuresis - diuretics, mannitol, glucose. Primary polyuria is much less common; polyuria is often a compensatory process caused by fluid loss. Chronic and acute renal failure can cause the development of polydipsia - polyuria. Primary polydipsia may be caused by hyperthyroidism, renal failure, traumatic brain injury, encephalitis, or psychogenic polydipsia.

Therapy

Treatment approaches should be differentiated between dogs presenting with Addison's crisis and stable patients with hypoadrenocorticism.

Addison's crisis is an acute life-threatening condition in which patients die from hypovolemic shock, electrolyte abnormalities, and hypotension. Therefore, the goal of crisis therapy is the correction of hypovolemia, electrolyte disturbances, especially hyperkalemia, elimination of hypoglycemia (if present), acid-base imbalance, elimination of mineralocorticoid and glucocorticoid deficiency.

Immediately upon admission of the animal, it is necessary to install an intravenous catheter (selection of tests, administration of ACTH), administration of electrolyte solutions (saline solution of sodium chloride and ringer). Solutions are administered at a rate of up to 90 ml/kg per hour during the first hour to stabilize the hypovolemic state, and over the next 24–48 hours, administration of solutions continues at a rate of 40–80 ml/kg/hour. The animal rarely needs glucose solutions. Monitoring diuresis and cardiac activity is mandatory, especially in patients who are already admitted with severe azotemia.

Intensive fluid therapy is usually sufficient to combat hyperkalemia; bolus administration of glucose with insulin is not required for cellular potassium translocation in most cases.

Stabilization of the acid-base balance, as a rule, also occurs against the background of infusion therapy with physiological sodium solution or ringer's solution. The described administration of bicarbonate to combat ketoacidosis is usually not required.

To eliminate severe hyperkalemia, slow (over 20 minutes) intravenous administration of 10% calcium gluconate at a dosage of 0.5–1 mg/kg can also be used. ECG monitoring of such patients is important, and at the slightest sign of arrhythmia, calcium administration should be stopped. But in most cases, intensive infusion therapy is sufficient, without additional calcium administration.

We wrote in more detail about methods of treating hyperkalemia in previous issues of our magazine (No. 4, 2014).

Administration of corticosteroids - dexamethasone (depending on the condition of the animal) from 0.1 to 2 mg/kg. It is better to start with small doses, increasing the dosage if necessary and repeating every 8 hours.

Prednisolone can be used at a dosage of 0.1–0.2 (up to 0.4) mg/kg.

Hydrocortisone, a corticosteroid with strong sodium retention, can also be used in the treatment of Addison's crisis. Dosage for dogs: 1.25 mg/kg intravenously - first administration, then 0.5-1 mg/kg every 6 hours for the first 24 hours. On the second day, the dose is reduced to 0.1–0.25 mg/kg every 6 hours. As stabilization occurs, it is transferred to oral administration at a dosage of 0.1–0.25 mg/kg twice a day, while simultaneously adding mineralocorticoid therapy.

Fludrocortisone acetate is a corticosteroid available only in tablet form, so it is generally not used to treat patients in crisis. For maintenance therapy, it can be used at a dosage of 0.01–0.02 mg/kg per day, divided into two doses. This corticosteroid also has pronounced mineralocorticoid activity, it is used as the first choice drug in the treatment of hypoadrenocorticism in humans, and is absorbed much more slowly in dogs than in humans.

Only one of the selected glucocorticoids is used in therapy.

For patients suffering from Addison's crisis, monitoring electrolyte levels is vital, at least twice a day, ideally every 6-8 hours. Monitoring blood gases and glucose levels is also mandatory.

The opinions of various authors differ, but most colleagues today are inclined to begin mineralocorticoid therapy after stabilization of the general condition, when the crisis has passed (after 1-3 days), depending on the severity of the condition. Deoxycortone (deoxycorticosterone) pivalate is optimally suited for this purpose. The dose recommended by the manufacturers is 2.2 mg/kg, which is administered once every 28 days. However, the selection of the dose of deoxycortone is also individual, as is the selection of many drugs used to treat endocrine patients, from Vetoril to insulin. You can start with a lower dose of deoxycortone - 1.5 mg/kg, with mandatory first monitoring after 10-14 days of electrolyte levels. If elevated potassium levels or decreased sodium levels persist, the dose should be increased by 20%. Regular monitoring of electrolyte levels is important in patients taking lifelong therapy and dose reduction when potassium levels decrease. During the maintenance period, prednisolone is also prescribed in parallel at a dosage of 0.1–0.2 mg/kg daily. Determining basal cortisol to adjust the dose of steroids should not be carried out subsequently; a dose reduction is carried out, rather, when symptoms reminiscent of hyperadrenocorticism appear: polydipsia-polyuria, polyphagia, alopecia.

When transferring a patient from fludrocortisone to deoxycortone, it should be remembered that the first drug has glucocorticoid and mineralocorticoid activity, while deoxycortone has only mineralocorticoid activity and requires the addition of prednisolone. Fludrocortisone is administered daily, deoxycortone – once every 25–28 days.

If a patient admitted with Addison's crisis experienced azotemia and increased transaminase levels, then after discharge with further therapy and dose adjustment of mineralocorticoids, their monitoring is also required.

In conclusion, I would like to note that in most cases we are faced with primary hypoadrenocorticism, which requires replacement therapy with both glucocorticoids and mineralocorticoids. In the case of the rare atypical Addison, when no electrolyte disturbances are observed, the opinions of endocrinologists differ: a number of colleagues believe that in the absence of mineralocorticoid deficiency and electrolyte disturbances, mineralocorticoid therapy is not indicated. The second opinion is that mineralocorticoid replacement therapy should still be carried out, since most patients with atypical hypoadrenocorticism also develop mineralocorticoid deficiency over time. It should also be noted that Addison's crisis is an acute condition that requires immediate intensive care. Hypoadrenocorticism is a disease that requires lifelong replacement therapy with adequate regular monitoring.

Forecast

Favorable. Patients who receive adequate mineralocorticoid and glucocorticoid therapy with regular monitoring of electrolyte levels maintain a quality of life and duration comparable to healthy animals.

Literature

1. Feldman EC, Nelson RW l Canine and feline endocrinology. Elsevier Saunders. Fourth edition, 2015

2. Ettinger SJ, Feldman EC (2017) Textbook of veterinary internal medicine: diseases of the dog and the cat. Elsevier Saunders

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6. Klein SC, Peterson ME. Canine hypoadrenocorticism: part II. Can Vet J 2010b; 51: 179-84.

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