2023 AAHA Selected Endocrinopathies of Dogs and Cats Guidelines.

Canine and feline endocrinopathies reflect an endocrine gland disease or dysfunction with resulting hormonal abnormali ties that can variably affect the patient's wellbeing, quality of life, and life expectancy. These guidelines provide consensus recommendations for diagnosis and treatment of four canine and feline endocrinopathies commonly encountered in clini cal practice: canine hypothyroidism, canine hypercortisolism (Cushing's syndrome), canine hypoadrenocorticism (Addi son's disease), and feline hyperthyroidism. To aid the general practitioner in navigating these common diseases, a stepwise diagnosis and treatment algorithm and relevant background information is provided for managing each of these diseases. The guidelines also describe, in lesser detail, the diagnosis and treatment of three relatively less common endo crinopathies of cats: feline hyperaldosteronism, feline hypothyroidism, and feline hyperadrenocorticism. Additionally, the guidelines present tips on effective veterinary team utilization and client communication when discussing endocrine cases.

Hyperadrenocorticism treatment of a dog with high dilution: case report

Hyperadrenocorticism is a common endocrinopathy in dogs, associated to an excessive production or administration of cortisol.Aims:Report the evolution of homeopathic treatment in spontaneous hyperadrenocorticism analyzing with basal and post-acth stimulation cortisol values of a yorkshire male dog with 10 years old, diagnosed from the suppression test with low dose of dexamethasone and stimulation with ACTH, as well as complementary tests.Methodology: Homeopathic treatment was chosen, based on the principle of similitude usingIgnatia amarabecause the patient presents repertorized mental symptoms such as separation anxiety syndrome, docility, annoyances and jealousy and also because it is efficient and less harmful. It was associated to cortisol biotherapy to inhibit cortisol production and adrenal biotherapy to control the response of excess of the cortisol producted by the gland. The exposed information is consented by the tutor.Results:The dog was in convencional treatment with trilostane but didn't response to the therapy, showing 5,41 µg/dL of basal result and 11,8 µg/dL of post-acth result and the symptoms were worst on 12/12/2021, presenting lethargic, panting, more evident alopecia and severe muscle weakness which the patient unable to stand. Therefore, the protocol was recommended for 3 months, included 3 globules ofIgnatia amara30cH orally, every 12 hours, 3 globules of cortisol biotherapy 30 cH and also of adrenal biotherapy 6 cH every 24 hours. On 03/28/2022 the basal and post-acth stimulation results was 3,71 µg/dL e 5,79 µg/dL respectively and the patient was more active, the skin was better and even with difficulty it was movingand having more independence.Conclusion: Homeopathic treatment with high dilution was effective, keeping the indices with the recommended range of post acth between 2.0 and 5.0, confirming an adequate therapeutic monitoring and symptomatic improvement.

Old Problem, New Concerns: Hypercortisolemia in the Time of COVID-19.

The ongoing coronavirus disease 2019 (COVID-19) pandemic forced a change in the way we provide medical treatment. Endocrinology in the era of COVID-19 had to transform and reduce its vast potential to the absolute necessities. Medical professionals needed to update their clinical practice to provide their patients as much support and as little harm as possible in these increasingly difficult times. International expert statements were published to offer guidance regarding proper care. It was suggested to simplify the diagnostic scheme of hypercortisolemia and to modify the approach to treatment. Hypercortisolemic patients with COVID-19 and iatrogenic hypercortisolemia due to glucocorticoid use are important clinical scenarios - we aimed to provide a cohesive summary of issues to consider.

Feline comorbidities: Recognition, diagnosis and management of the cushingoid diabetic.

PRACTICAL RELEVANCE: Diabetes mellitus (DM) is a common feline endocrinopathy, and is often driven by underlying insulin resistance with associated pancreatic beta (ß)-cell dysfunction. Although spontaneous hyperadrenocorticism (HAC) with hypercortisolemia (hypercortisolism) is relatively uncommon in cats, it is a well-established cause of insulin resistance and is routinely associated with DM in this species. CLINICAL CHALLENGES: Many of the clinical signs associated with feline HAC are subtle and may be attributed to concurrent DM or the aging process. Failure to recognize HAC in the diabetic cat can impact patient wellbeing and predispose the patient to progressive compromise. Unfortunately, it can be difficult to establish a diagnosis of HAC, as test results may be influenced by poor diabetic regulation, and protocols are different to those used in canine patients. Treatment options depend on the underlying cause, and often require careful, ongoing assessment and modulation of both adrenal function and insulin requirements. However, various approaches have been shown to either improve glycemic control in cats with sustained insulin dependence, or facilitate diabetic remission. EVIDENCE BASE: This review summarizes the current literature on feline HAC, with a particular focus on cats with concurrent DM. The clinical findings that suggest HAC are discussed, along with an outline of diagnostic options and their limitations. Published outcomes for various medical options, surgical procedures and radiation therapy are provided. The authors also share their thoughts on the safe and effective management of cats with HAC and DM, with an emphasis on the anticipation and recognition of changing insulin requirements.

Survival analysis of 219 dogs with hyperadrenocorticism attending primary care practice in England.

BACKGROUND: Hyperadrenocorticism is an endocrine disease routinely encountered within primary care practice; however, few studies evaluating survival beyond diagnosis have studied this population. METHODS: This retrospective cohort study analysed the electronic patient records of 219 cases of hyperadrenocorticism from a sample of dogs attending primary care practices in England. Kaplan-Meier plots examined the cumulative survival and Cox proportional hazard regression modelling identified factors associated with the hazard of all-cause mortality. RESULTS: In the analysis, 179/219 (81.7 per cent) hyperadrenocorticism cases died during the study period with a median survival time from first diagnosis of 510 days (95% CI 412 to 618 days). Trilostane was used in 94.1 per cent of cases and differentiation between pituitary-dependent and adrenal-dependent disease was made in 20.1 per cent of cases. In the multivariable analysis, dogs weighing greater than or equal to 15 kg (HR 1.51, 95% CI 1.06 to 2.15, P=0.023) and those diagnosed greater than or equal to 13 years of age (HR 3.74, 95% CI 2.29 to 6.09, P<0.001) had increased hazards of all-cause mortality. Dogs that had their initial trilostane dose increased had a favourable prognosis (HR 0.49, 95% CI 0.32 to 0.76, P=0.015). CONCLUSION: This study shows that survival from diagnosis of hyperadrenocorticism appears fair for many dogs and provides primary care practitioners with relatable benchmark prognostic figures.

Physiolgic hypercortisolism at onset of celiac disease in a girl: A case report.

RATIONALE: Celiac disease (CD) is an autoimmune disorder induced by dietary gluten in genetically predisposed subjects. Activation of the hypothalamic-pituitary-axis (HPA) can occur in patients with CD; however, this condition has never been described in overweight/obese CD children. PATIENT CONCERNS: A 12-year-old girl with CD was admitted with mild acanthosis nigricans of the armpits, groin and neck. Recently, extra fat appeared around the neck, and moon face was observed. The abdomen was globular and meteoric, treatable and not aching. She weighed 64 kilos (75°-97° percentile) and was 146 centimeters tall (3°-25° percentile) with a body mass index of 30 kg/mq. Laboratory tests revealed hypertriglyceridemia and positive anti-transglutaminase IgA. Cortisoluria was determined. Serum ACTH was normal. DIAGNOSES: This paper reports a case of a girl with CD in which both obesity and activation of HPA activity were noted. INTERVENTIONS: During follow-up, anti-transglutaminase IgA increased to 201.5 UI/mL. The patient was positive for anti-endomysium antibodies, and the HLA DQ2 haplotype was identified, confirming a diagnosis of CD. OUTCOMES: Despite a gluten-free diet, obesity and hyperadrenalism persisted, and anti-transglutaminase antibodies remained elevated. In addition, high cortisoluria persisted. A high-dose suppression dexamethasone test (8 mg) produced negative results with a morning cortisol value of 1 ng/mL, suggesting the diagnosis of pseudo-Cushing's syndrome. LESSONS: This case highlights that the first manifestation of CD could be being overweight, and this finding seems to support the need to prescribe laboratory tests for CD not only to children with failure to thrive, as commonly recommended, but also to those with increased body weight.

Peculiarities of feline hyperadrenocorticism: Update on diagnosis and treatment.

Practical relevance: Hyperadrenocorticism (HAC) is a relatively uncommon endocrinopathy of older cats, with a mean age at diagnosis of 10 years. In addition to pituitary-dependent and adrenal-dependent hypercortisolism, clinical signs of HAC can result from adrenal sex steroid-producing tumours. Clinical challenges: While HAC in cats has many similarities to canine HAC, there are key differences in presentation, diagnosis and response to therapy. Most, but not all, cats with HAC have concurrent diabetes mellitus, which is often insulin resistant. Up to a third of cats with HAC have extreme skin fragility and are at high risk of debilitating iatrogenic skin tears during diagnostic or therapeutic interventions. Infections of the skin and nail beds, and urinary, respiratory and gastrointestinal tract, secondary to cortisol-induced immune suppression, are also common. Cats respond differently to dogs to adrenal function tests including adrenocorticotropic hormone (ACTH) stimulation and dexamethasone suppression tests; a 10-fold higher dose of dexamethasone is recommended in cats to screen for HAC. Curative treatment options include adrenalectomy or transsphenoidal hypophysectomy. Radiation or medical treatment may improve clinical signs. The response to mitotane therapy is poor. While trilostane is the medical treatment of choice based on retrospective studies, investigations into the pharmacokinetics of this drug in cats are lacking. Global importance: Feline HAC occurs worldwide and is not associated with any purebreed predisposition. Although uncommon, adrenal sex steroid-producing tumours have a higher prevalence in cats than in dogs. Evidence base: The information in this review is drawn from over 180 reported cases of feline HAC. Reports investigating clinical presentation, clinicopathological findings and treatment outcomes are observational, retrospective multiple case series (EBM grade III) or single case reports (EBM grade IV). While most endocrine testing studies for diagnosis are cohort controlled analytical studies (EBM grade III), prospective, randomised, placebo-controlled studies have been performed (EBM grade I).

Pituitary tumour-transforming gene (PTTG) and pituitary senescence.

Pituitary tumours account for 15% of intracranial neoplasms and are benign monoclonal neoplasms that may be clinically silent or secrete hormones, including prolactin, growth hormone, adrenocorticotrophic hormone or, rarely, thyroid-stimulating hormone or gonadotrophins. These adenomas account for clinical infertility, growth disorders and hypercortisolism or metabolic dysfunctions associated with hypopituitarism. We explored the role of disordered pituitary cell proliferation control in the pathogenesis of these invariably benign adenomas, studying the mechanisms underlying pituitary aneuploidy, premature proliferative arrest (senescence), markers of cell proliferation and tumorigenesis in single, double or triply mutant transgenic mice with mutations of Rb, Pttg and/or p21. Our results provide further insights into the role of cell-cycle control and growth constraints on experimental and human pituitary tumours, which underlie their failure to progress to malignancy. These results improve our understanding of pituitary syndromes associated with infertility, growth disorders, hypercortisolism or adrenal, thyroid and gonadal failure due to abrogated pituitary function.

Hyperadrenocorticism associated with sex steroid excess.

Diagnosis of sex steroid excess or hyperadrenocorticism in dogs may be challenging. Unlike Cushing's disease, sex steroid excess may have a multitude of manifestations that differ from standard hyperadrenocorticism. In particular, the clinical scenario of a dog with sex steroid imbalance involves one of three systems: dermatologic, reproductive, or hepatic. The history of a dog with hyperadrenocorticism manifesting as sex steroid imbalance often lacks the classical clinical signs of polydipsia and polyuria. Dogs with sex steroid imbalance will often be of specific breeds such as miniature poodles and exhibit trunkal hair loss as the only sign. There is often involvement of the reproductive system, manifested as the growth of perianal adenomas in neutered male or female dogs. The most common laboratory findings consist of elevations in serum alkaline phosphatase and serum alanine transferase. The following article reviews the etiology, common signalment, clinical signs, and laboratory findings associated with atypical hyperadrenocorticism caused by sex steroid imbalance and then explores the medical, surgical, and radiation treatment options.

[Endocrine myopathies]. / Myopathies endocrines.

Disturbances in the endocrine system induce a myopathy by acting on protein synthesis or on energetic metabolic pathways. Thus, a proximal myopathy is seen in hypercorticism, hyper- or hypothyroidism and acromegaly. On the other hand, endocrine disorders modify the transsarcolemmal balance in electrolytes, inducing generalized paresia, as in adrenal insufficiency or in thyrotoxic periodic paralysis. The diagnosis is usually easy if a muscle disorder occurs in a complete clinical feature of endocrinopathy but a myopathy may reveal it. Moreover, the steroid myopathy induced by iatrogenic glucocorticoid excess may lead to confusion in patients treated for an inflammatory myopathy. The treatment of endocrine myopathies is based on the correction of the hormonal disorder.