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Background Objective Animals Methods Results Conclusions and Clinical Relevance Knowledge about primary hypoadrenocorticism coexisting with immune‐mediated thyroiditis (Schmidt's syndrome) in dogs is limited.To evaluate thyroid function in dogs with naturally occurring hypoadrenocorticism before and during treatment.Sixty‐six client‐owned dogs.Measurement of canine thyroid stimulating hormone (cTSH), total thyroxine (T4), free thyroxine, and autoantibodies against thyroglobulin, T4, and total triiodothyronine.Thirty‐eight dogs were assessed before and 28 during treatment. Follow‐up data were available for 24/38 and 17/28 dogs, with median follow‐up duration of 3.8 years (range, <1.0‐8.8 years) and 4 years (range, 1.1 weeks to 10.5 years), respectively. Canine thyroid stimulating hormone was above the reference range at the time of diagnosis of hypoadrenocorticism in 10 of 38 dogs but decreased into the reference range in 7 for which follow‐up data was available. Hypothyroidism was confirmed in 5 dogs at a median age of 11 years (range, 7‐15 years). In 4 dogs, the condition was diagnosed after a median treatment duration of 5.75 years (range, 2.6‐10 years), while in 1 dog, the diagnosis was made concurrently. One dog had detectable thyroid autoantibodies.Hypothyroidism occurs as a rare concurrent condition in dogs with hypoadrenocorticism, potentially at any phase of treatment. Close monitoring of cTSH levels in these dogs could be beneficial, as early changes might indicate the onset of hypothyroidism. The low prevalence of detectable thyroid autoantibodies suggests that nonimmune mechanisms might contribute to thyroid dysfunction. [ABSTRACT FROM AUTHOR]

Background: The relationship between collapse and a diagnosis of hypoadrenocorticism is not well understood in dogs. Hypothesis: To assess the prevalence of episodes of collapse in dogs screened for hypoadrenocorticism, and to assess the prevalence of confirmed hypoadrenocorticism in dogs presenting with reported collapse. Animals: Seventy‐three client‐owned dogs with resting cortisol concentrations were measured and presented to a University teaching hospital for collapse. Methods: Retrospective review of medical records of dogs at a single center. Results: The prevalence of episodes of collapse in dogs that had a resting cortisol measurement was 73/856 (8.5%; 95% confidence interval [95% CI], 6.7%‐10.6%). Resting cortisol concentration was <2 μg/dL (<55 nmol/L) in 19 dogs. Cortisol concentration after ACTH stimulation was <2 μg/dL (<55 nmol/L) in 1 of the 73 dogs in this cohort, consistent with a diagnosis of hypoadrenocorticism, giving a prevalence estimate of hypoadrenocorticism of 1.3% (95% CI, 0.15%‐6.2%). In 8 dogs with an initial resting cortisol concentration <2 μg/dL (<55 nmol/L), hypoadrenocorticism was excluded based on a repeat resting cortisol concentration >2 μg/dL (>55 nmol/L). The most common diagnosis was vasovagal syncope (10/73), followed by sick sinus syndrome and third‐degree atrioventricular block (2/73). The final diagnosis was unknown in 24/73 dogs. Conclusions and Clinical Importance: Hypoadrenocorticism was the final diagnosis in 1 of 73 dogs presented to a teaching hospital either in a collapsed state or with a previous history of episodes of collapse. No dog presenting as cardiovascularly stable for intermittent collapse was found to have hypoadrenocorticism. [ABSTRACT FROM AUTHOR]

Hypotension is a common complication during hemodialysis that develops due to high ultrafiltration rate and sometimes requires intravenous fluid replacement. Intradialytic hypotension may reduce the effectiveness of dialysis and contributes to hemodialysis‐related morbidity and mortality. Adrenal insufficiency is one of the causes of hypotension in the community. Our case was diagnosed with end‐stage renal failure and was undergoing routine hemodialysis with a central venous catheter 3 days a week. Upon the patient's hypotension attacks during the dialysis sessions and hypoglycemia attacks in the follow‐ups, the morning cortisol was 6.2 μg/dL. Adrenocorticotropic hormone was 39 pg/mL, and testosterone was 0.0442 ng/mL. Adrenocorticotropic hormone stimulation test was performed on the patient with 250 mcg tetracosactide. The patient did not show adequate cortisol response, was detected to have partial empty sella on pituitary magnetic resonance imaging, and was diagnosed with secondary adrenal insufficiency, and then the hemodialysis hypotension improved with prednisolone treatment. We present a case of adrenal insufficiency, which is a rare cause of hypotension in patients on routine hemodialysis. [ABSTRACT FROM AUTHOR]

Objectives Rheumatic diseases may impair reproductive success and pregnancy outcomes, but systematic evaluations across diseases are lacking. We conducted a nationwide cohort study to examine the impact of rheumatic diseases on reproductive health measures, comparing the impacts with those of other immune-mediated diseases (IMDs). Methods Out of all of the 5 339 804 Finnish citizens, individuals born 1964–1984 and diagnosed with any of the 19 IMDs before age 30 (women) or 35 (men) were matched with 20 controls by birth year, sex, and education. We used data from nationwide health registers to study the impact of IMDs on reproductive health measures, such as reproductive success and, for women, ever having experienced adverse maternal and perinatal outcomes. Results Several of the rheumatic diseases, particularly SLE, JIA, and seropositive RA, were associated with higher rates of childlessness and fewer children. The risks for pre-eclampsia, newborns being small for gestational age, preterm delivery, non-elective Caesarean sections, and need of neonatal intensive care were increased in many IMDs. Particularly, SLE, SS, type 1 diabetes, and Addison's disease showed >2-fold risks for some of these outcomes. In most rheumatic diseases, moderate (1.1–1.5-fold) risk increases were observed for diverse adverse pregnancy outcomes, with similar effects in IBD, celiac disease, asthma, ITP, and psoriasis. Conclusion Rheumatic diseases have a broad impact on reproductive health, with effects comparable with that of several other IMDs. Of the rheumatic diseases, SLE and SS conferred the largest risk increases on perinatal adverse event outcomes. [ABSTRACT FROM AUTHOR]

Oral hormone replacement therapy has been and continues to be the cornerstone of adrenocortical insufficiency management. However, the introduction of continuous subcutaneous hydrocortisone infusion (CSHI) shows great potential for advancing the management of adrenocortical insufficiency. It resembles the circadian rhythm of physiological cortisol secretion and was shown to have a promising outcome in terms of quality of life (QOL) and clinical outcomes in the literature. We conducted a systematic search strategy including MEDLINE, Web of Science, Cochrane Central Register of Controlled Trials (CENTRAL), and the online trials registers at ClinicalTrials.gov without geographic restrictions. Research investigations where self-reported quality of life (QOL) was assessed as a variable in adult individuals with confirmed adrenal disease, treated by CSHI, and results were presented in English. All articles included were published between 2014 and 2023, even though we had no timeframe limitations in our inclusion criteria. A total of six studies were included, with 63 subjects enrolled, and the average age was 40 years, a study showed a significant reduction in the average total daily dose of HC from 47.5 mg to 31.4 mg on CSHI, while other two studies estimated a reduction in the hospitalization rate due to adrenal crisis from 2.6 to 1.3 admissions per year on CSHI. Most of the studies on subjective well-being and quality of life have shown significant improvement. Overall, CSHI shows great potential as a treatment method for Adrenal insufficiency. It improves the quality of life and lowers hospitalization rates, resulting in increased patient satisfaction and acceptance. Additional comprehensive research is necessary to strengthen these discoveries, gain a deeper understanding of the effectiveness and safety of this treatment approach, and provide guidance for medical practitioners. [ABSTRACT FROM AUTHOR]

Abstract Background The relationship between collapse and a diagnosis of hypoadrenocorticism is not well understood in dogs. Hypothesis To assess the prevalence of episodes of collapse in dogs screened for hypoadrenocorticism, and to assess the prevalence of confirmed hypoadrenocorticism in dogs presenting with reported collapse. Animals Seventy‐three client‐owned dogs with resting cortisol concentrations were measured and presented to a University teaching hospital for collapse. Methods Retrospective review of medical records of dogs at a single center. Results The prevalence of episodes of collapse in dogs that had a resting cortisol measurement was 73/856 (8.5%; 95% confidence interval [95% CI], 6.7%‐10.6%). Resting cortisol concentration was 2 μg/dL (>55 nmol/L). The most common diagnosis was vasovagal syncope (10/73), followed by sick sinus syndrome and third‐degree atrioventricular block (2/73). The final diagnosis was unknown in 24/73 dogs. Conclusions and Clinical Importance Hypoadrenocorticism was the final diagnosis in 1 of 73 dogs presented to a teaching hospital either in a collapsed state or with a previous history of episodes of collapse. No dog presenting as cardiovascularly stable for intermittent collapse was found to have hypoadrenocorticism.

Primary adrenal insufficiency (PAI) is a rare medical condition, characterized by a deficiency in adrenal hormones. Although rare, PAI is a life-threatening disease requiring prompt recognition and treatment. However, symptoms of PAI are often non-specific and diagnosis can be challenging, causing frequent diagnostic delays. In adults, autoimmunity is the most common cause of PAI in industrialized countries, whereas in children, the most frequent etiology is represented by congenital defects of steroidogenesis and, in particular, by congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency. A few recent case series from different countries have reported that autoimmunity is the second most common etiology of PAI in the pediatric age group. However, data on autoimmune PAI in children are still scant and the exact epidemiology, clinical manifestations, and long-term outcomes of this condition have yet to be defined. The scope of this review is to summarize the current knowledge on the etiology, presentation, and treatment of autoimmune PAI in childhood and to increase physicians' awareness of the signs that should raise an early suspicion of this condition. [ABSTRACT FROM AUTHOR]

The article presents a case study of an 18-year-old male with adrenal insufficiency, characterized by dizziness, shortness of breath, and weight loss. Topics discussed include the diagnosis of primary adrenal insufficiency, treatment with glucocorticoids and mineralocorticoids, and the importance of screening for additional autoimmune endocrine disorders.

This manuscript seeks to describe diagnostic considerations in individuals with diabetes mellitus presenting to the ED with abdominal pain. It highlights the importance of early investigation with computerised tomography to differentiate aetiologies that compel early surgical intervention from those which may be treated conservatively. [ABSTRACT FROM AUTHOR]

Recognizing the limitations of current therapies for Addison's disease, novel treatments that replicate dynamic physiologic corticosteroid secretion, under control of ACTH, are required. The aim of these experiments was to evaluate the feasibility of adrenocortical cell transplantation (ACT) in a large animal model, adapting methods successfully used for intracutaneous pancreatic islet cell transplantation, using a fully biodegradable temporizing matrix. Autologous porcine ACT was undertaken by bilateral adrenalectomy, cell isolation, culture, and intracutaneous injection into a skin site preprepared using a biodegradable temporizing matrix (BTM) foam. Hydrocortisone support was provided during adrenocortical cell engraftment and weaned as tolerated. Blood adrenocortical hormone concentrations were monitored, and the transplant site was examined at endpoint. Outcome measures included cellular histochemistry, systemic hormone production, and hydrocortisone independence. Transplanted adrenocortical cells showed a capability to survive and proliferate within the intracutaneous site and an ability to self-organize into discrete tissue organoids with features of the normal adrenal histologic architecture. Interpretation of systemic hormone levels was confounded by the identification of accessory adrenals and regenerative cortical tissue within the adrenal bed postmortem. Corticosteroids were unable to be completely ceased. ACT in a large animal model has not previously been attempted, yet it is an important step toward clinical translation. These results demonstrate rhe potential for ACT based on the development of adrenal organoids at the BTM site. However, the inability to achieve clinically relevant systemic hormone production suggests insufficient function, likely attributable to insufficient cells through delivered dose and subsequent proliferation. [ABSTRACT FROM AUTHOR]

Background: Addison's disease and X-linked adrenoleukodystrophy (X-ALD) (Addison's-only) are two diseases that need to be identified. Addison's disease is easy to diagnose clinically when only skin and mucosal pigmentation symptoms are present. However, X-ALD (Addison's-only) caused by ABCD1 gene variation is ignored, thus losing the opportunity for early treatment. This study described two patients with initial clinical diagnosis of Addison's disease. However, they rapidly developed neurological symptoms triggered by infection. After further genetic testing, the two patients were diagnosed with X-ALD. Methods: We retrospectively analyzed X-ALD patients admitted to our hospital. Clinical features, laboratory test results, and imaging data were collected. Whole-exome sequencing was used in molecular genetics. Results: Two patients were included in this study. Both of them had significantly increased adrenocorticotropic hormone level and skin and mucosal pigmentation. They were initially clinically diagnosed with Addison's disease and received hydrocortisone treatment. However, both patients developed progressive neurological symptoms following infectious disease. Further brain magnetic resonance imaging was completed, and the results suggested demyelinating lesions. Molecular genetics suggested variations in the ABCD1 gene, which were c.109_110insGCCA (p.C39Pfs*156), c.1394–2 A > C (NM_000033), respectively. Therefore, the two patients were finally diagnosed with X-ALD, whose classification had progressed from X-ALD (Addison's-only) to childhood cerebral adrenoleukodystrophy (CCALD). Moreover, the infection exacerbates the demyelinating lesions and accelerates the onset of neurological symptoms. Neither the two variation sites in this study had been previously reported, which extends the ABCD1 variation spectrum. Conclusions: Patients with only symptoms of adrenal insufficiency cannot be simply clinically diagnosed with Addison's disease. Being alert to the possibility of ABCD1 variation is necessary, and complete genetic testing is needed as soon as possible to identify X-ALD (Addison's-only) early to achieve regular monitoring of the disease and receive treatment early. In addition, infection, as a hit factor, may aggravate demyelinating lesions of CCALD. Thus, patients should be protected from external environmental factors to delay the progression of cerebral adrenoleukodystrophy. [ABSTRACT FROM AUTHOR]

Primary adrenocortical insufficiency was first described by Dr. Thomas Addison in 1885. At that time the main cause of Addison's disease (AD) was tuberculosis infection. After 1950, autoimmune adrenalitis took precedence. The aim of this review is to consider some new immunological aspects in the pathogenesis of AD. Serum autoantibodies directed against steroidogenic enzymes in the adrenal cortex, most frequently 21-hydroxylase antibodies and less frequently against 17-alpha- and 11-alpha-hydroxylases, are found in nearly 90% of affected patients. In addition, antibodies against interleukin-17F and interleukin-22 can be detected in AD within autoimmune polyglandular syndrome (APS) type 1. A number of studies have shown that other organ-specific autoantibodies are detected in a large proportion of patients with autoimmune adrenalitis, predisposing to the development of concomitant endocrine and extraendocrine autoimmune diseases. Systemic connective tissue diseases may also be seen in association with AD, and it has been hypothesized that, for example, antiphospholipid syndrome may not only be a marker for APS in AD patients but also an etiologic factor for the onset of the disease due to vascular damage to the kidneys. In recent years, immunotherapy with new classes of cancer drugs, immune checkpoint inhibitors (ICIs), which probably mediate autoimmune activation, has been an important cause of AD. In conclusion, the heterogeneous antibody profile against steroidogenic adrenal and gonadal enzymes likely modulates the phenotypic expression of AD. The elevated titer of many organ-specific and cytokine antibodies in patients may predispose to different co-morbidities and treatment needs that should be considered in clinical practice. [ABSTRACT FROM AUTHOR]

Gastric ulcer is a significant clinical issue in dogs, with higher prevalence in mature animals and often occurs secondary to systemic diseases such as hepatic or renal disorders, Addison's disease or shock. This case report highlights a four-and-a-half-year-old intact male Rottweiler presented with persistent vomiting, anorexia, abdominal pain and anemia. Diagnostic imaging, including radiography, ultrasonography and endoscopy, revealed gastric ulceration and the presence of radiopaque lead pellets in the pyloric region of the stomach. Histopathological examination confirmed extensive gastric mucosal damage. Treatment included the elimination of lead, fluid therapy and administration of proton pump inhibitors, antibiotics and mucosal protectants. Incorporating psyllium husk into the diet helped to enhance lead excretion. Follow-up imaging after two weeks showed absence of lead pellets and normal gastric mucosa. This case underscores the importance of comprehensive diagnostic and therapeutic approaches for chronic gastric ulcers in dogs, emphasising the role of multimodal imaging and targeted treatment strategies. [ABSTRACT FROM AUTHOR]

Schmidt's syndrome, or autoimmune polyendocrine syndrome type 2 (APS-2), is an uncommon disorder characterized by the co-occurrence of autoimmune thyroiditis and adrenalitis. APS-2 is defined as a combination of Addison's disease, autoimmune thyroid disease, and/or type 1 diabetes mellitus. It is an autosomal dominantly inherited polygenic disorder with incomplete penetrance; the candidate genes include but are not limited to HLA-DR3, HLA-DR4, CTLA-4, PTPN22, and CD25-IL-2. Autoimmune thyroiditis, often Hashimoto's disease, results in hypothyroidism. Primary adrenal failure results in enhanced secretion of adrenocorticotrophic hormone melanocyte and co-secretion of melanocyte-stimulating hormone, contributing to hyperpigmentation. Mineralocorticoid deficiency results in salt wasting, fatigue and cramps, postural hypotension, and hyperkalemia. Cortisol, an insulin counter-regulatory hormone, plays a pivotal role in maintaining euglycemia; deficiency predisposes to the development of hypoglycemia. We here report a rare presentation of Schmidt's syndrome as hypoinsulinemic hypoglycemia in a middle-aged male patient. Management includes treatment of acute hypoglycemic episodes with glucose or glucagon, long-term glucocorticoids and mineralocorticoids for adrenal insufficiency, and thyroid hormone supplements for hypothyroidism. This case report and brief overview aim to contribute to the scientific understanding of Schmidt's syndrome/APS-2. Additionally, here we briefly outline the diagnostic challenges in hypoglycemia evaluation, including the utilization of Whipple's triad and the gold standard supervised 72-hour fast and evaluation for primary adrenal and thyroid insufficiencies.

Petrified ear (PE), an exceptional entity, stands for the calcification ± ossification of auricular cartilage (CAC/OAC); its pathogenic traits are still an open matter. Endocrine panel represents one of the most important; yet, no standard protocol of assessments is available. Our objective was to highlight most recent PE data and associated endocrine (versus non-endocrine) ailments in terms of presentation, imagery tools, hormonal assessments, biopsy, outcome, pathogenic features. This was a comprehensive review via PubMed search (January 2000–March 2024). A total of 75 PE subjects included: 46 case reports/series (N = 49) and two imagery-based retrospective studies (N = 26) with CAC/OAC prevalence of 7–23% (N = 251) amid routine head/temporal bone CT scans. Endocrine PE (EPE): N = 23, male/female ratio = 10.5; average age = 56.78, ranges: 22–79; non-EPE cohort: N = 26; male/female ratio = 1.88, mean age = 49.44; ranges: 18–75 (+a single pediatric case).The longest post-diagnosis follow-up was of 6–7 years. The diagnosis of PE and endocrine anomalies was synchronous or not (time gap of 10–20 years). A novel case in point (calcified EPE amid autoimmune poly-endocrine syndrome type 2 with a 10-year post-diagnosis documented follow-up) was introduced. We re-analyzed EPE and re-classified another five subjects as such. Hence, the final EPE cohort (N = 50) showed: adrenal insufficiency was the most frequent endocrine condition (36%) followed by hypopituitarism (22%) and hypothyroidism (18%); 39% of the patients with adrenal failure had Addison's disease; primary type represented 72% of all cases with hypothyroidism; an endocrine autoimmune (any type) component was diagnosed in 18%. We propose the term of "endocrine petrified ear" and a workflow algorithm to assess the potential hormonal/metabolic background in PE. [ABSTRACT FROM AUTHOR]

The BVNA Congress 2024 is a veterinary conference that will be held at the Telford International Centre from October 11-13. The conference program offers a wide range of sessions on topics such as referral nursing, emergency and critical care, equine care, and exotics, zoo, and wildlife. The schedule is subject to change, so it is recommended to check the BVNA website for the most up-to-date information. In addition to the educational sessions, there will also be an exhibition and a Blue Light Party & Awards event. [Extracted from the article]

Purpose: The simultaneous occurrence of primary ovarian insufficiency (POI) and autoimmune diseases has been noted and debated in some epidemiological research. This bidirectional two-sample Mendelian randomization (MR) study aimed to investigate the causal relationships between autoimmune diseases and POI. Methods: We obtained summary-level data for ten autoimmune diseases and POI from published large-scale genome-wide association studies and the FinnGen consortium of European ancestry. A series of filtering steps was performed to discern independent genetic variants. Causal estimates were mainly calculated by the inverse variance weighting method and verified through multiple sensitivity analyses. Results: Of the ten autoimmune diseases, genetically predicted Addison's disease (odds ratio [OR] = 1.26, 95% confidence interval [CI]: 1.09–1.47, P = 0.003) and systemic lupus erythematosus (OR = 1.12, 95% CI 1.02–1.24, P = 0.021) were associated with an increased risk of POI, and sensitivity analyses confirmed the robustness of the results. In addition, there were weak associations between liability to POI and elevated risks of type 1 diabetes (OR = 1.05, 95% CI 1.00–1.10, P = 0.046) and autoimmune thyroid disease (OR = 1.03, 95% CI 1.01–1.05, P = 0.015). Conclusion: This study revealed that Addison's disease and systemic lupus erythematosus are potential risk factors for POI, underscoring the necessity to consider the impact of autoimmune factors in the diagnosis and treatment of POI. [ABSTRACT FROM AUTHOR]

The skin–brain axis has been suggested to play a role in several pathophysiological conditions, including opioid addiction, Parkinson's disease and many others. Recent evidence suggests that pathways regulating skin pigmentation may directly and indirectly regulate behaviour. Conversely, CNS-driven neural and hormonal responses have been demonstrated to regulate pigmentation, e.g., under stress. Additionally, due to the shared neuroectodermal origins of the melanocytes and neurons in the CNS, certain CNS diseases may be linked to pigmentation-related changes due to common regulators, e.g., MC1R variations. Furthermore, the HPA analogue of the skin connects skin pigmentation to the endocrine system, thereby allowing the skin to index possible hormonal abnormalities visibly. In this review, insight is provided into skin pigment production and neuromelanin synthesis in the brain and recent findings are summarised on how signalling pathways in the skin, with a particular focus on pigmentation, are interconnected with the central nervous system. Thus, this review may supply a better understanding of the mechanism of several skin–brain associations in health and disease. [ABSTRACT FROM AUTHOR]

Key Clinical Message: Autoimmune polyglandular syndrome type 1 (APS‐1) is a rare disorder defined by the presence of at least two of the following conditions: chronic mucocutaneous candidiasis (CMC), chronic hypoparathyroidism, and Addison's syndrome. Despite the lack of CMC and autoimmune history, APS‐1 can be diagnosed using genetic testing. We present the case of a 28‐year‐old female patient with a history of hypocalcemia due to hypoparathyroidism since the age of 2 years. She presented to the endocrine clinic with hypogonadism, primary amenorrhea, and primary ovarian insufficiency. Addison's disease was eventually diagnosed, despite a negative Synacthen test. The adrenal crisis required intravenous hydrocortisone therapy. No CMC was documented, and there was no family history of such conditions. The diagnosis of APS‐1 was confirmed by genetic testing, revealing homozygous pathogenic variants of the autoimmune regulator gene. Management included oral calcium and calcitriol and oral hydrocortisone and fludrocortisone for Addison's disease. Hormonal induction of secondary sexual characteristics was initiated. The patient received combined oral estrogen and progesterone pills. This case highlights the critical significance of early recognition, thorough evaluation, and tailored treatment for patients with APS‐1 to enhance their quality of life and mitigate potentially life‐threatening complications. This underscores the importance of screening for associated minor autoimmune diseases as part of a holistic approach to care. [ABSTRACT FROM AUTHOR]

This article, titled "Engaging With Purpose: What Motivational Interviewing Has Taught Me About Creating Behaviour Change," is the first part of a two-part series that explores the author's personal journey of being diagnosed with type 1 diabetes (T1D) and the insights gained from her experience as a clinical psychologist and trainer in Motivational Interviewing (MI). The author emphasizes the importance of therapeutic engagement, acknowledging ambivalence about change, and incorporating MI techniques in diabetes education to empower individuals to actively manage their health. The article highlights the complexity of behavior change in diabetes education and the need for empathetic and meaningful conversations to support individuals with diabetes. [Extracted from the article]

BACKGROUND: Since the onset of the coronavirus disease (COVID-19) pandemic, a variety of long–COVID-19 symptoms and autoimmune complications have been recognized. CASES: We report three cases of autoimmune premature poor ovarian response in patients aged 30–37 years after mild to asymptomatic COVID-19 before vaccination, with nucleotide antibody confirmation. Two patients failed to respond to maximum-dose gonadotropins for more than 4 weeks, despite a recent history of response before having COVID-19. After a month of prednisone 30 mg, these two patients had normal follicle-stimulating hormone (FSH) levels, high oocyte yield, and blastocyst formation in successful in vitro fertilization cycles. All three patients have above-average anti-müllerian hormone levels that persisted throughout their clinical ovarian insufficiency. Two patients had elevated FSH levels, perhaps resulting from FSH receptor blockade. One patient, with a history of high response to gonadotropins 75 international units per day and below-normal FSH levels, had no ovarian response to more than a month of gonadotropins (525 international units daily), suggesting autoimmune block of the FSH glycoprotein and possible FSH receptor blockade. CONCLUSION: Auto-antibody production in response to COVID-19 before vaccination may be a rare cause of autoimmune poor ovarian response. Although vaccination is likely protective, further study will be required to evaluate the effect of vaccination and duration of autoimmune FSH or FSH receptor blockade. [ABSTRACT FROM AUTHOR]

This review examines respiratory complications in autoimmune rheumatic diseases within intensive care units (ICUs). The respiratory system, primarily affected in diseases like rheumatoid arthritis, systemic lupus erythematosus, and scleroderma, often leads to respiratory failure. Common manifestations include alveolar hemorrhage, interstitial fibrosis, and acute respiratory distress syndrome. Early recognition and treatment of non-malignant conditions are crucial to prevent rapid disease progression, with ICU mortality rates ranging from 30% to 60%. Delayed immunosuppressive or antimicrobial therapy may result in organ system failure. Collaboration with rheumatic specialists is vital for accurate diagnosis and immediate intervention. Mortality rates for rheumatic diseases in the ICU surpass those of other conditions, underscoring the need for specialized care and proactive management. The review emphasizes comprehensive assessments, distinguishing disease-related complications from underlying issues, and the importance of vigilant monitoring to enhance patient outcomes. [ABSTRACT FROM AUTHOR]

Background: Immune checkpoint inhibitors (ICPis) induce autoimmune diseases, including autoimmune polyendocrine syndrome type 2 (APS-2), which is defined as a combination of at least two of the following endocrinopathies: autoimmune thyroid disease, type 1 diabetes, and Addison's disease. Cases with the full triad are rare. We present a case of an elderly woman who developed APS-2 with the complete triad shortly after starting antiprogrammed cell death 1 (anti-PD1) treatment and review the related literature. Case: A 60-year-old woman, without any personal or family history of autoimmune and endocrine diseases, started the immunotherapy of anti-PD1 (camrelizumab) for squamous cell carcinoma of the urethral meatus. She developed primary hypothyroidism with elevated antibodies to thyroid peroxidase and thyroglobulin after 25 weeks of treatment, and developed primary adrenal insufficiency with adrenal crisis and fulminant type 1 diabetes with ketoacidosis after 45 weeks. Therefore, this patient met the diagnosis of APS-2 and was given multiple hormone replacement including glucocorticoid, levothyroxine and insulin therapy. Continuous improvement was achieved through regular monitoring and titration of the dosage. Conclusions: Different components of APS-2 may appear at different time points after anti-PD1 administration, and can be acute and life-threatening. A good prognosis can be obtained by appropriate replacement with multiple hormones. Insights: With the clinical application of ICPis to APS-2, the complexity of its treatment should be paid enough attention. [ABSTRACT FROM AUTHOR]

Purpose: Patients receiving long-term glucocorticoid (GC) treatment are at risk of osteoporosis, while bone effects of substitution doses in Addison's disease (AD) remain equivocal. The project was aimed to evaluate serum bone turnover markers (BTMs): osteocalcin, type I procollagen N-terminal propeptide (PINP), collagen C-terminal telopeptide (CTX), sclerostin, DKK-1 protein, and alkaline phosphatase (ALP) in relation to bone mineral density (BMD) during GC replacement. Methods: Serum BTMs and hormones were assessed in 80 patients with AD (22 males, 25 pre- and 33 postmenopausal females) on hydrocortisone (HC) substitution for ≥3 years. Densitometry with dual-energy X-ray absorptiometry covered the lumbar spine (LS) and femoral neck (FN). Results: Among BTMs, only PINP levels were altered in AD. BMD Z-scores remained negative except for FN in males. Considering T-scores, osteopenia was found in LS in 45.5% males, 24% young and 42.4% postmenopausal females, while osteoporosis in 9.0%, 4.0% and 21.1%, respectively. Lumbar BMD correlated positively with body mass (p = 0.0001) and serum DHEA-S (p = 9.899 × 10−6). Negative correlation was detected with HC dose/day/kg (p = 0.0320), cumulative HC dose (p = 0.0030), patient's age (p = 1.038 × 10−5), disease duration (p = 0.0004), ALP activity (p = 0.0041) and CTX level (p = 0.0105). However, only age, body mass, ALP, serum CTX, and sclerostin remained independent predictors of LS BMD. Conclusion: Standard HC substitution does not considerably accelerate BMD loss in AD patients and their serum BTMs: CTX, osteocalcin, sclerostin, DKK-1, and ALP activity remain within the reference ranges. Independent predictors of low lumbar spine BMD, especially ALP activity, serum CTX and sclerostin, might be monitored during GC substitution. [ABSTRACT FROM AUTHOR]

This article reviews the dermatological manifestations that frequently arise in endocrine disorders, encompassing conditions such as diabetes mellitus, acromegaly, polycystic ovary syndrome, hypothyroidism, Addison's disease, among others. It explores the interactions between the endocrine system and the skin, highlighting how hormonal imbalances can result in a variety of skin symptoms. With a comprehensive approach, it offers important clinical insights for dermatologists and endocrinologists, aiming at a better understanding and an accurate diagnosis of these conditions. [ABSTRACT FROM AUTHOR]

Adrenal insufficiency is an uncommon disorder and presents with non‐specific symptoms. Identifying adrenal insufficiency in patients with chronic kidney disease requiring dialysis is increasingly difficult as there is a significant overlap of the signs and symptoms of adrenal insufficiency with those seen in chronic kidney failure. We highlight this diagnostic uncertainty in a case series of three patients with chronic kidney disease requiring hemodialysis as renal replacement therapy from a single center identified as hypoadrenal. Steroid replacement improved symptoms and hemodynamic parameters. Increased vigilance for adrenal insufficiency in dialysis patients is necessary. It is likely under recognized in hemodialysis patients given their multi‐morbidity. [ABSTRACT FROM AUTHOR]

Autoimmune nodopathies are inflammatory diseases of the peripheral nervous system with clinical and neurophysiological peculiar characteristics. In this nosological category, we find patients with autoantibodies against Neurofascin 140/186 and 155, Contactin1, and Caspr1 directed precisely towards nodal and paranodal structures. These antibodies are extremely rare and cause severe clinical symptoms. We describe the clinical case of a patient with autoimmune nodopathy caused by the coexistence of anti-neurofascin (NF) 186/140 and 155, characterized by progressive weakness in all limbs leading to tetraplegia, involving cranial nerves, and respiratory insufficiency. Response to first-line treatments was good followed by rapid dramatic clinical relapse. There are few reported cases of anti-pan NF neuropathy in the literature, and they present a clinical phenotype similar to our patient. In these cases, early recognition of clinical red flags of nodopathies and serial neurophysiological studies can facilitate the diagnosis. However, the severe clinical relapse suggests a possible early use of immunosuppressive therapies for this rare category of patients. [ABSTRACT FROM AUTHOR]

Autoimmunity seems to be present in a large proportion of women with spontaneous premature ovarian insufficiency (POI). Whether these women are at increased risk for autoimmune disease has not been determined to date. Therefore, the aim of this study was to investigate a large series of antibodies in order to shed more light into the autoimmune risk of POI women. In a prospective case–control study, blood samples from 66 patients with spontaneous POI and 66 healthy controls were analyzed for a series of autoimmune antibodies. POI women revealed significantly increased thyroglobulin antibodies (TGAb) (p = 0.045) and thyroid peroxidase antibodies (TPOAb) (p = 0.002). At least one abnormal autoimmune parameter was present in 37.9% of POI women, compared to 18.2% in healthy controls (p = 0.045). A strong association between POI and increased TGAb (adjusted odds ratio 3.586, p = 0.028), increased TPOAb (adjusted odds ratio 7.496, p = 0.003) and any increased autoimmune parameter (adjusted odds ratio 3.189, p = 0.008) could be demonstrated in a binary logistic regression model. A high prevalence of autoimmunity in POI women compared to a healthy young collective could be demonstrated. Thyroid antibodies were significantly increased in POI women. Our data highlight the increased risk for autoimmune diseases, especially for thyroid disorders. [ABSTRACT FROM AUTHOR]

Background: Routine clinical coding of clinical outcomes in outpatient consultations still lags behind the coding of episodes of inpatient care. Systematized Nomenclature of Medicine Clinical Terms (SNOMED CT) offers an opportunity for standardised coding of key clinical information. Identifying the most commonly required SNOMED terms and grouping these into a reference set will aid future adoption in routine clinical care. Objective: To create a common endocrinology reference set to standardise the coding for outcomes of outpatient endocrine consultations, using a semi‐automated extraction of information from existing clinical correspondence. Methods: Retrospective review of data from an adult tertiary outpatient endocrine clinic between 2018 and 2019. A total of 1870 patients from postcodes within two regional areas of NHS Grampian (Aberdeen City and Aberdeenshire) attended the clinic. Following consultation, an automated script extracted each problem statement which was manually coded using the 'disorder' concepts from SNOMED CT (UK edition). Results: The review identified 298 relevant endocrine diagnoses, 99 findings and 142 procedures. There were a total of 88 (29.5%) commonly seen endocrine conditions (e.g., Graves' disease, anterior hypopituitarism and Addison's disease) and 210 (70.5%) less commonly seen endocrine conditions. Subsequently, consultant endocrinologists completed a survey regarding the common endocrine conditions; 28 conditions have 100% agreement, 25 have 90%–99% agreement, 31 have 50%–89% agreement and 4 have less than 59% agreement (which were excluded). Conclusion: Automated text parsing of structured endocrine correspondence allowed the creation of a SNOMED CT reference set for common endocrine disorders. This will facilitate funding and planning of service provision in endocrinology by allowing more accurate characterisation of the patient cohorts needing specialist endocrine care. [ABSTRACT FROM AUTHOR]

Autoimmune Addison's disease (AAD) is a rare but life-threatening endocrine disorder caused by an autoimmune destruction of the adrenal cortex. A previous genome-wide association study (GWAS) has shown that common variants near immune-related genes, which mostly encode proteins participating in the immune response, affect the risk of developing this condition. However, little is known about the contribution of copy number variations (CNVs) to AAD susceptibility. We used the genome-wide genotyping data from Norwegian and Swedish individuals (1,182 cases and 3,810 controls) to investigate the putative role of CNVs in the AAD aetiology. Although the frequency of rare CNVs was similar between cases and controls, we observed that larger deletions (>1,000 kb) were more common among patients (OR = 4.23, 95% CI 1.85-9.66, p = 0.0002). Despite this, none of the large case-deletions were conclusively pathogenic, and the clinical presentation and an AAD-polygenic risk score were similar between cases with and without the large CNVs. Among deletions exclusive to individuals with AAD, we highlight two ultra-rare deletions in the genes LRBA and BCL2L11, which we speculate might have contributed to the polygenic risk in these carriers. In conclusion, rare CNVs do not appear to be a major cause of AAD but further studies are needed to ascertain the potential contribution of rare deletions to the polygenic load of AAD susceptibility. [ABSTRACT FROM AUTHOR]

Primary adrenal tuberculosis is an extremely rare benign lesion that typically presents with no clinical symptoms in its early stages, making it prone to clinical misdiagnosis. We report a case of a middle-aged man initially thought to have adrenal nodules, which further examination revealed to be adrenal tuberculosis accompanied by Addison's disease. This report discusses the diagnostic approach, progressive features, and treatment options for this rare disease.

BackgroundDogs with hypoadrenocorticism (HA) have clinical signs and clinicopathologic abnormalities that can be mistaken as other diseases. In dogs with a differential diagnosis of HA, a machine learning model (MLM) has been validated to discriminate between HA and other diseases. This MLM has not been evaluated as a screening tool for a broader group of dogs.HypothesisAn MLM can accurately screen dogs for HA.AnimalsDogs (n = 1025) examined at a veterinary hospital.MethodsDogs that presented to a tertiary referral hospital that had a CBC and serum chemistry panel were enrolled. A trained MLM was applied to clinicopathologic data and in dogs that were MLM positive for HA, diagnosis was confirmed by measurement of serum cortisol.ResultsTwelve dogs were MLM positive for HA and had further cortisol testing. Five had HA confirmed (true positive), 4 of which were treated for mineralocorticoid and glucocorticoid deficiency, and 1 was treated for glucocorticoid deficiency alone. Three MLM positive dogs had baseline cortisol ≤2 μg/dL but were euthanized or administered glucocorticoid treatment without confirming the diagnosis with an ACTH-stimulation test (classified as "undetermined"), and in 4, HA was ruled out (false positives). The positive likelihood ratio of the MLM was 145 to 254. All dogs diagnosed with HA by attending clinicians tested positive by the MLM.Conclusions and clinical importanceThis MLM can robustly predict HA status when indiscriminately screening all dogs with blood work. In this group of dogs with a low prevalence of HA, the false positive rates were clinically acceptable.

BackgroundClinical findings of glucocorticoid-deficient hypoadrenocorticism (GDH) can overlap with other diseases, presenting a diagnostic challenge.ObjectivesDescribe clinicopathologic and ultrasonographic features of dogs with GDH and those suspected of having GDH that had the disease ruled out.AnimalsSix hundred twenty-three dogs.MethodsRecords from dogs with suspected GDH between 2003 and 2018 were reviewed. Dogs with hyperkalemia or hyponatremia were excluded. Dogs were categorized as controls when the resting serum cortisol or post-ACTH cortisol concentration were > 2 μg/dL. Clinicopathologic and ultrasonographic features were compared between groups. The optimal cut-point, area under the receiver operating characteristic curve (AUC), sensitivity, and specificity were calculated for individual features used to detect GDH.ResultsDogs were categorized as GDH (n = 29) or controls (n = 594). Lymphocyte count (>1750 cells/L; sensitivity, 96.6%; 95% confidence interval [CI], 82.8%-99.8%; specificity, 60.3%; 95% CI, 56.3%-64.1%; AUC, 0.828; 95% CI, 0.762-0.894) and albumin/globulin ratio (

Addison's disease, also known as primary adrenal insufficiency (PAI), is a rare endocrine disorder characterized by a decrease in all three adrenal hormones. This case report describes a 32-year-old female who presented with generalized weakness, fatigue, weight loss, and hyperpigmentation. Based on her symptoms and laboratory findings, a diagnosis of Addison's disease was made. She was started on hormone replacement therapy, and her symptoms improved significantly.

Abstract Case Description An 18‐month‐old spayed female domestic short haired cat was presented for poor appetite, lethargy, exaggerated swallowing, and regurgitation 2 weeks after endoscopic retrieval of gastric foreign material. Clinical Findings The cat was quiet with tacky mucous membranes on physical examination. Point‐of‐care blood testing identified mild azotemia, moderate hypercalcemia, and a sodium‐to‐potassium ratio of 26. An ultrasound examination the next day identified moderate to marked bilateral adrenomegaly. Cytology of a fine needle aspirate of the adrenal glands was consistent with necrosis and associated inflammation. Hypoadrenocorticism was diagnosed by a confirmatory adrenocorticotropic hormone stimulation test. Treatment and Outcome The cat normalized both clinically and biochemically after treatment with prednisolone and desoxycorticosterone pivalate. Clinical Relevance Acute adrenal necrosis has been well documented in human medicine after anesthetic events. To our knowledge, hypoadrenocorticism caused by cytologically confirmed acute adrenal necrosis has not been previously reported in dogs and cats.

Abstract Background Dogs with eunatremic, eukalemic hypoadrenocorticism (EEH) typically show signs of chronic gastrointestinal disease (CGD). Previous glucocorticoid administration (PGA) can give false‐positive results on the ACTH stimulation test (ACTHst). Hypothesis/Objectives To determine the prevalence of EEH in dogs with signs of CGD, and to identify clinical and clinicopathological features for EEH and PGA. Animals One hundred twelve dogs with CGD (101 non‐PGA and 11 PGA), 20 dogs with EEH. Methods Multicenter prospective cohort study. Basal serum cortisol (BSC) concentration was measured in dogs with signs of CGD. When BSC was 1250 pg/mL) than in non‐PGA dogs (13.5, 7.3‐46.6 pg/mL). Cortisol‐to‐ACTH ratio was lower (P

Skin colour usually depends upon melanin, haemoglobin, and carotenoids. Pigmentary disorders indicate an increased amount of melanin, leading to a darker colour of the skin, called hypermelanosis. Addison’s disease is a rare endocrinal disorder with severe oral and systemic manifestations. Any form of diffuse skin hyper-pigmentation which is more pronounced on sun-exposed areas mimics Addison’s disease and is called Addisonian pigmentation. Pigmentation often precedes other manifestations by months to years and hence can lead to early diagnosis and can prevent life-threatening adrenal crisis. The most common cause of adrenal insufficiency in developing countries is tuberculosis. A similar pattern of pigmentation has been reported in Cushing’s syndrome, ectopic ACTH-producing tumours, vitamin B12 deficiency, and thyrotoxicosis. Addisonian pigmentation can be a manifestation of multiple systemic diseases; hence, an inter-disciplinary approach is needed with extensive clinical and laboratory evaluation. It is not merely a cosmetic concern. Not much data are available in the literature regarding this entity. This brief review serves as an important source for clinicians to stay up-to-date regarding the history, clinical presentation, differential diagnosis, and management of this entity.

Background. Cytokine storm syndromes (CSS) are life-threatening systemic inflammatory disorders caused by immune system dysregulation. They can lead to organ failure and are triggered by various factors, including infections, malignancy, inborn errors of immunity, and autoimmune conditions. Trisomy 21 (TS21), also known as Down syndrome, is a genetic disorder associated with immune dysfunction, increased infection susceptibility, and inflammation. While TS21 has been linked to infectious-triggered hyperinflammation, its role as a primary cause of CSS has not been confirmed. Case Presentation. We present a case of a 16-year-old male with TS21 with fever, rash, joint pain, and abdominal symptoms. Extensive investigations ruled out infections, autoimmune conditions, malignancies, and inborn errors of immunity as triggers for a CSS. The patient's symptoms improved with treatment using IL-1 inhibition and corticosteroids. Conclusions. This case reinforces that TS21 is an immune dysregulation disorder and highlights the importance of considering CSS in TS21 patients, even when triggers are unclear. The positive response to IL-1 inhibition in this patient suggests that dysregulation of the IL-1 superfamily and the NLRP3 inflammasome may contribute to CSS in TS21. This finding raises the possibility of using IL-1 inhibition as a treatment approach for CSS in TS21 patients. [ABSTRACT FROM AUTHOR]

Aplastic anemia (AA) and hypoplastic myelodysplastic syndrome are paradigms of autoimmune hematopoietic failure (AHF). Myelodysplastic syndrome and acute myeloid leukemia are unequivocal myeloid neoplasms (MNs). Currently, AA is also known to be a clonal hematological disease. Genetic aberrations typically observed in MNs are detected in approximately one-third of AA patients. In AA patients harboring MN-related genetic aberrations, a poor response to immunosuppressive therapy (IST) and an increased risk of transformation to MNs occurring either naturally or after IST are predicted. Approximately 10%-15% of patients with severe AA transform the disease phenotype to MNs following IST, and in some patients, leukemic transformation emerges during or shortly after IST. Phenotypic transformations between AHF and MNs can occur reciprocally. A fraction of advanced MN patients experience an aplastic crisis during which leukemic blasts are repressed. The switch that shapes the disease phenotype is a change in the strength of extramedullary inflammation. Both AHF andMNs have an immune-active bone marrow (BM) environment (BME). In AHF patients, an inflamed BME can be evoked by infiltrated immune cells targeting neoplastic molecules, which contributes to the BM-specific autoimmune impairment. Autoimmune responses in AHF may represent an antileukemic mechanism, and inflammatory stressors strengthen antileukemic immunity, at least in a significant proportion of patients who have MN-related genetic aberrations. During active inflammatory episodes, normal and leukemic hematopoieses are suppressed, which leads to the occurrence of aplastic cytopenia and leukemic cell regression. The successful treatment of underlying infections mitigates inflammatory stress-related antileukemic activities and promotes the penetration of leukemic hematopoiesis. The effect of IST is similar to that of treating underlying infections. Investigating inflammatory stress-powered antileukemic immunity is highly important in theoretical studies and clinical practice, especially given the wide application of immune-activating agents and immune checkpoint inhibitors in the treatment of hematological neoplasms. [ABSTRACT FROM AUTHOR]

This article, titled "Ranting in 2024: It's Not More of the Same," discusses various issues in the medical system as of 2024. The author highlights the challenges and inefficiencies of the preauthorization process, which can lead to delays in treatment and impact patient outcomes. They also address the high cost of certain medications, particularly glucagon-like-peptide-1 receptor agonists (GLP1-RAs), and the role of pharmacy benefit managers (PBMs) in driving up prices. The article further explores the politicization of public health, particularly during the COVID-19 pandemic, and the need for better care for older adults with type 1 diabetes (T1D). The author concludes by acknowledging that while many frustrations exist within the medical system, there are also individuals who accept and even enjoy these challenges. [Extracted from the article]

Immunological abnormalities, the resulting endocrinopathies, and their treatments may impact bone health and 25-hydroxyvitamin D (25-OHD) in patients with autoimmune polyglandular syndromes (APS). Several etiologies contribute to increased risk for low bone mineral density (BMD), including vitamin D deficiency. This study evaluated the vitamin D level and BMD of patients with APS. We performed a cross-sectional study on 44 patients with APS and 55 age and gender-matched control subjects. Among patients with APS, 14 were classified as APS-2 [Addison's disease (AD)+autoimmune thyroid disease (ATD) and/or type 1 diabetes(T1D)]. In contrast, the other 30 were APS-3 (ATD+T1D+other autoimmune diseases). Serum samples were analyzed for vitamin D levels. The lumbar spine and femoral neck BMD were measured by dual X-ray absorptiometry. Z-scores were obtained by comparison with age- and gender-matched average values (both patients and controls). The accepted normal levels were Z-score>–1 and 25-OHD>30 ng/ml. Patients with APS showed 25-OHD levels and BMD significantly lower than healthy controls (p<0.001 and p<0.05, respectively). The highest prevalence of abnormal BMD was observed in the APS-2 subgroup (13 out of 14 patients, 92.6%). Identifying and treating vitamin D deficiency and low BMD is critical in APS patients. The fact that the significant endocrine component of APS-2 is AD, and these patients receive chronic long-term glucocorticoid therapy can be shown as the reason for this result. However, more extensive prospective controlled studies are needed to confirm these findings. [ABSTRACT FROM AUTHOR]

to describe a clinical case of ocular sarcoidosis in a patient with Autoimmune Polyglandular Syndrome Type 2 (APS-2). an 86-year-old female diagnosed with APS-2 was referred to our uveitis department with rapid visual loss in her left eye during a 3-month period. Her best-corrected visual acuity (BCVA) was counting fingers in her left eye (OS) and 20/40 in her right eye (OD). Slit-lamp biomicroscopy was unremarkable OD but revealed granulomatous keratic precipitates OS. Fundoscopy revealed bilateral optic disc oedema and +2 and 4+ vitritis (SUN classification) in her OD and OS, respectively. the patient underwent chest X-Ray which revealed bilateral hilar lymphadenopathy and fibrosis. On high-resolution computed tomography of the lungs, ground-glass opacities were visible, and a diagnosis of ocular sarcoidosis was presumed. After exclusion of infectious diseases, the patient was treated with methotrexate and oral corticosteroids and there was substantial improvement of the optic nerve oedema and vitritis. At the most recent visit, 2 years later, OS BCVA was 20/50. There may be an association between ocular sarcoidosis and APS or other autoimmune disorders. [ABSTRACT FROM AUTHOR]

Celiac disease (CD) is frequently associated with other autoimmune disorders. Different studies have explored the association between CD and single autoimmune endocrine disease (AED), especially autoimmune thyroiditis (AIT) and type-1 diabetes mellitus (T1DM). Data about CD as a component of autoimmune polyendocrine syndrome (APS) are scant. We analyzed a large dataset including prospectively collected data from 920 consecutive adult CD patients diagnosed in a third-level Italian institution in the 2013–2023 period, The prevalence of isolated autoimmune endocrine diseases and APS were collected. A total of 262 (28.5%) CD patients had at least one associated AED, with AIT (n = 223, 24.2%) and T1DM (n = 27, 2.9%) being the most frequent conditions. In most cases (n = 173, 66%), AEDs were diagnosed after CD. Thirteen patients (1.4%) had at least two of the requested three endocrinopathies, satisfying the diagnosis of APS. APS is a rare but not exceptional occurrence among Italian CD patients, underscoring the intricate and multifaceted nature of autoimmune disorders. Periodic evaluations of thyroid function and glycaemia should be recommended after the diagnosis of CD together with testing for autoantibodies that may be helpful in assessing disease risk before disease onset. Likewise, implementation of a systematic screening for CD amongst T1DM and other autoimmune endocrine diseases are paramount. [ABSTRACT FROM AUTHOR]

A 60-year-old male presented with extreme fatigue and weight loss 3 weeks after testing positive for coronavirus disease 2019. The course of coronavirus disease 2019 was mild, without pulmonary involvement. The patient showed symptoms and laboratory signs of new-onset diabetes without ketoacidosis and acute primary adrenal insufficiency, the latter of which was confirmed with an adrenocorticotrophic hormone stimulation test. Glutamic acid decarboxylase-65 antibody and antibodies to the adrenal cortex were positive in high titers. Previous medical records of the patient revealed no hyperglycemia or electrolyte abnormalities prior to current admission, but an earlier test result was compatible with primary hypothyroidism which was associated with autoimmune thyroiditis. He was therefore diagnosed with autoimmune polyglandular syndrome type II. Clinical and laboratory findings improved after starting appropriate hormone replacement therapies along with insulin. Coronavirus disease 2019 may induce a variety of autoimmune disorders in susceptible subjects. In our case, coronavirus disease 2019 might have simply precipitated type 1 diabetes and adrenal insufficiency in whom autoimmune thyroiditis may have been the first manifestation of an undiagnosed autoimmune polyglandular syndrome type II. Coronavirus disease 2019 might have triggered autoimmunity in the patient who was possibly predisposed to autoimmune disorders. Anyhow, more research is required to evaluate the possible link between coronavirus disease 2019 and autoimmune disorders. [ABSTRACT FROM AUTHOR]

Objective: The aim was to evaluate autonomic dysfunction by investigating exercise time, the chronotropic index (CI), and heart rate recovery (HRR) during an exercise stress test (EST) in patients with primary adrenal insufficiency, also called Addison's disease (AD). Methods: Twenty-two patients with adrenal insufficiency and 25 healthy controls were included in this study. The data from the patients who underwent an EST were collected, analyzed, and reported. Results: The mean ages and genders of the patients with AD and the controls were insignificant. The baseline systolic and diastolic blood pressures (SBP and DBP) were significantly lower in the patients with AD compared to the controls before the EST. According to exercise-induced data, the SBP, DBP, and CI were insignificant for females and males between the groups. The exercise time, HRR1, and HRR2 were significantly decreased in the patients with AD compared to the controls. When the patients and controls were evaluated by gender, other than the HRR1 of the females, there were no differences between both genders. Additionally, a multiple logistic regression analysis showed that exercise time was independent and negatively related to the CI, HRR1, and HRR2 in the patients with AD. Conclusion: Exercise time and cardiac autonomic dysfunction in patients with AD may be related to mortality and morbidity. However, further studies and detailed analyses are needed on this subject. [ABSTRACT FROM AUTHOR]