Case Report of a 14-Year-Old Girl with Addison\'s Disease Under Initial Presumptive Diagnosis of Anorexia Nervosa: Confusingly Similar and Yet so Different? Abstract: Objective: Primary adrenal insufficiency (Addison\'s disease) is a rare differential diagnosis of anorexia nervosa. This case report presents important differential diagnostic aspects. Methods: We prepared a case report of a 14-year-old female patient according to the CARE guidelines, taking the patient\'s and the child\'s parents\' view into consideration. Results: The diagnosis of primary adrenocortical insufficiency was reached using specific laboratory diagnostics approximately 9 months after the onset of symptoms, including sudden body weight loss. Significant differential diagnostic aspects were the absence of a body schema disorder and skin hyperpigmentation prominent in the physical examination. The patient experienced a high psychosocial burden because of the unclear diagnosis over 9 months. The diagnosis and substitution therapy with hydrocortisone led to a rapid improvement of the physical and psychological symptoms. Conclusions: This case report emphasizes the importance of a thorough somatic differential diagnosis in the context of a suspected anorexia nervosa.
Zusammenfassung: Zielsetzung: Die primäre Nebennierenrindeninsuffizienz (Morbus Addison) stellt eine seltene Differenzialdiagnose der Anorexia nervosa dar. Der hier vorgestellte Case Report verfolgt die Zielsetzung, wichtige differenzialdiagnostische Aspekte darzulegen. Methoden: Ein Case Report über eine 14-jährige Patientin wurde gemäß der CARE-Guidelines erarbeitet. Patientinnensicht sowie Sicht der Kindseltern wurden berücksichtigt. Ergebnisse: Durch eine gezielte Labordiagnostik konnte die Diagnose einer primären Nebennierenrindeninsuffizienz ca. 9 Monate nach Beginn der Symptomatik mit plötzlichem Gewichtsverlust gestellt werden. Hilfreiche differenzialdiagnostische Aspekte waren das Nichtvorhandensein einer Körperschemastörung bei der Patientin sowie dermale Hyperpigmentierungen, die in der körperlichen Untersuchung auffielen. Es bestand eine hohe psychosoziale Belastung durch die unklare Diagnosestellung über 9 Monate. Diagnosestellung und sofortige Substitutionstherapie mit Hydrocortison konnten eine rapide Besserung der körperlichen und psychischen Symptome bewirken. Schlussfolgerung: Die Kasuistik unterstreicht die Bedeutung einer gründlichen somatischen Differenzialdiagnostik im Rahmen der Abklärung eines Verdachts auf Anorexia nervosa.

Primary adrenal insufficiency (PAI) is a rare disease which represents the end stage of a destructive process involving the adrenal cortex. Occasionally it may be caused by bilateral adrenal hemorrhagic infarction in patients with antiphospholipid syndrome (APS). We herein report the challenging case of a 30-year-old female patient with systemic lupus erythematosus (SLE) and secondary APS who was admitted to the emergency department (ED) due to fever, lethargy, and syncopal episodes. Hyponatremia, hyperkalemia, hyperpigmentation, shock, altered mental status, and clinical response to glucocorticoid administration were features highly suggestive of an acute adrenal crisis. The patient\'s clinical status required admission to the intensive care unit (ICU), where steroid replacement, anticoagulation, and supportive therapy were provided, with a good outcome. Imaging demonstrated bilateral adrenal enlargement attributed to recent adrenal hemorrhage. This case highlights the fact that bilateral adrenal vein thrombosis and subsequent hemorrhage can be part of the thromboembolic complications seen in both primary and secondary APS and which, if misdiagnosed, may lead to a life-threatening adrenal crisis. High clinical suspicion is required for its prompt diagnosis and management. A literature search of past clinical cases with adrenal insufficiency (AI) in the setting of APS and SLE was conducted using major electronic databases. Our aim was to retrieve information about the pathophysiology, diagnosis, and management of similar conditions.

Addison\'s disease which is due to dysfunction of the adrenal gland, with abnormal secretion of glucocorticoids and mineralocorticoids, is rare. By inducing inflammation and disorders of water and electrolyte metabolism, Addison\'s disease may accelerate progression of co-existed cardiovascular diseases. Addison\'s disease combined with cardiovascular disease is infrequent, only 10 cases in the literature.
We reported a 51-year-old male patient with unstable angina pectoris and hypotension. Changes on coronary angiography within 2 years suggested rapid progression of coronary artery disease in a patient with low cardiovascular risk. An additional clue of skin hyperpigmentation, fatigue and further examination confirmed the diagnosis of Addison\'s disease caused by adrenal tuberculosis. After hormone replacement treatment, the frequency and severity of the angina pectoris were alleviated significantly, as were hypotension, hyperpigmentation and fatigue.
The combination of Addison\'s disease and coronary artery disease in one patient is rare. Addison\'s disease can induce inflammation and disorders of water and electrolyte metabolism, which may further accelerate the course of coronary artery disease. Meanwhile, the hypotension in Addison\'s disease may affect the coronary blood flow, which may result in an increased susceptibility to unstable angina in the presence of coronary stenosis. So, we should analyze comprehensively if the coronary artery disease progress rapidly.

An 8-year-old intact male pointer presented with lethargy and hypoalbuminemia. On abdominal ultrasonography, both adrenal glands were reduced in thickness. Based on the ACTH stimulation test results and the absence of electrolyte abnormalities, the dog was diagnosed with atypical hypoadrenocorticism. After treatment with low-dose prednisolone, his general condition improved, and blood tests normalized. The dog died 818 days later, and a complete autopsy was performed. Histologically, the architecture of the zonae fasciculata and reticularis was disrupted in both adrenal glands; however, the zona glomerulosa remained relatively normal. In summary, in this study, we detailed the pathological presentation of atypical hypoadrenocorticism without electrolyte abnormalities.

BACKGROUND: Pituitary-dependent hypercortisolism (PDH) is one of the most common endocrine disorders in veterinary medicine. However, there are few reports on pituitary tumor apoplexy (PTA) in dogs and no reports on its surgical intervention in veterinary medicine. Accordingly, the appropriate treatment is unknown. Herein, a case of PDH and PTA in a dog treated surgically is described.
METHODS: A mongrel female dog (spayed; age, 8 years and 8 months; weight, 6.1 kg) with persistently elevated alkaline phosphatase underwent adrenocorticotropic hormone (ACTH) stimulation testing (post-stimulation cortisol: 20.5 μg/dL), abdominal ultrasonography (adrenal gland thickness: left, 5.7 mm; right, 8.1 mm), and brain magnetic resonance imaging (MRI) (pituitary-to-brain ratio [PBR], 0.61) at the referral hospital, resulting in a diagnosis of PDH (day 0). On day 9, the dog visited XXXX for the preparation of pituitary surgery to treat PDH. However, on days 10-15, the dog developed a loss of energy and appetite, bloody diarrhea, vomiting, and a decreased level of consciousness. However, on day 16, the dog\'s condition recovered. A preoperative MRI scan performed on day 52 (the day of surgery) showed apoplexy in the dorsal pituitary region (PBR, 0.68). Based on the PTA findings, the risks of surgery were described to the owner, and approval was obtained. At the time of trans-sphenoidal surgery, a partial pituitary resection was performed with preservation of the PTA area due to adhesions between the PTA area of the right side of the pituitary and surrounding tissues. The resected pituitary tissue was diagnosed as an ACTH-producing adenoma, with necrotic and hemorrhagic findings. As of day 290, endogenous ACTH and cortisol levels did not exceed the reference range.
CONCLUSIONS: The acute signs that occurred on days 10-15 were most likely caused by PTA. Therefore, when signs similar to those detected in acute hypoadrenocorticism are observed in dogs with PDH, it is necessary to include PTA as a differential diagnosis. Trans-sphenoidal surgery may be effective in PDH-affected dogs that develop PTA, but careful attention should be paid to tissue adhesions secondary to hemorrhage that may occur after PTA.

BACKGROUND: Addison\'s disease is primary adrenal dysfunction and is characterized by decrease of cortisol level and increase of adrenocorticotropic hormone (ACTH) level. It is known that infection is one of main causes of Addison\'s disease. Among various infections, tuberculous infection accounts for the majority of them. Recently the number of subjects with non-tuberculous mycobacterial infection has been increased, and the infection can also bring about Addison\'s disease. Mycobacterium avium complex (MAC) pulmonary disease accounts for the majority of non-tuberculous mycobacterial infection.
METHODS: An 83-year-old female was suspected of having adrenal failure in our outpatient care and hospitalized in our institution. There was pigmentation in her face, hands and legs, especially in auricle and nail beds in her hands and legs. In rapid ACTH load test (0.25 mg of 1-24 ACTH), cortisol level was not increased at all. An abdominal computed tomography (CT) showed swelling of both adrenal glands accompanied by calcification. QuantiFERON test was negative and mycobacterium tuberculosis complex was negative in PCR test using bronchial lung lavage fluid. These data ruled out the possibility of adrenal tuberculosis. It is known that MAC pulmonary disease accounts for the majority of non-tuberculous mycobacterial infection. In this subject, however, anti-MAC antibody was negative and MAC-related bacteria were not detected in PCR test using bronchial lung lavage fluid. These data ruled out the possibility of MAC pulmonary disease. Mycobacterium abscessus (Mab) was positive in bronchial lung lavage fluid culture. Based on these data, we diagnosed this subject with Addison\'s disease triggered by infection with mycobacterium abscessus, but not by adrenal tuberculous or MAC pulmonary disease. Decreased sodium level and increased eosinophil number were normalized and appetite loss was markedly mitigated after starting hydrocortisone therapy. A chest CT which was taken about 6 months later showed drastic reduction of consolidation in the upper lobe of the left lung although calcification in the adrenal gland was still observed.
CONCLUSIONS: We should bear in mind the possibility of Addison\'s disease triggered by another type of infection rather than adrenal tuberculosis or MAC pulmonary disease.

UNASSIGNED: to describe a clinical case of ocular sarcoidosis in a patient with Autoimmune Polyglandular Syndrome Type 2 (APS-2).
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: There may be an association between ocular sarcoidosis and APS or other autoimmune disorders.

Autoimmune polyendocrine syndrome type 2, also known as Schmidt\'s syndrome, is a rare autosomal dominant life-threatening syndrome. It is defined by the presence of Addison\'s disease in combination with at least one of the known autoimmune diseases: thyroid autoimmune disease, type 1 diabetes, and hypogonadism. It is more common in middle-aged females and is treatable if diagnosed early. However, in this case, we report Schmidt\'s syndrome in a young male without a family history. A 20-year-old male with a past medical history of hypothyroidism, adrenal insufficiency, and type 1 diabetes presented to the emergency department (ED) feeling lethargic, somnolent, and diaphoretic. Laboratory blood tests showed elevated thyroid-stimulating hormone, hyperkalemia of 6.4 mmol/L, and hyponatremia of 131 mmol/l indicating an Addisonian crisis. The patient had low blood glucose (at home: 60 mg/dL, and at ED: 85 mg/dL), hypotensive blood pressure of approximately 85/55 mmHg, and a peaked T-wave on EKG, which were consistent with the diagnosis of Schmidt\'s syndrome. Based on the laboratory findings and history, the patient was diagnosed with polyendocrine syndrome Type 2 (Schmidt\'s syndrome). The patient was treated for adrenal insufficiency first followed by thyroid insufficiency. Schmidt\'s syndrome is a rare disease and difficult to diagnose because the presentation depends on which gland is initially involved. A few cases have been reported in the literature of atypical presentations of Schmidt\'s syndrome. Therefore, this case report can contribute to the medical literature on Schmidt\'s syndrome, which can help in early diagnosis and improve patient outcomes.

COVID-19 (corona virus disease 2019), caused by the severe acute respiratory syndrome (SARS) coronavirus 2 (SARS-CoV-2), has spread throughout the globe and affected millions of people worldwide. Here, we report a patient with autoimmune polyglandular syndrome type 2 who presented with adrenal crisis, precipitated by COVID-19. We intend to highlight the importance of stress dosing in preventing adrenal crisis in patients with adrenal insufficiency (AI). A uniform structured education programme is needed to improve knowledge and practices in patients with AI in our country.

In 1877 Harriet Staunton died in Penge, Kent, and four members of her family were convicted of her murder by malicious starvation. The defence attempted to show that she had died from tuberculous meningitis, but reappraisal of the evidence leads to the conclusion that she died from tuberculous Addison\'s disease and that the defendants were wrongly convicted.