obsolete polyglandular dysfunction

Based on the provided context, it appears that the polyglandular autoimmune syndrome type II (PAS-II) has been largely replaced by more specific diagnoses such as Addison's disease, hypoparathyroidism, and chronic mucocutaneous candidiasis. However, I can provide information on the signs and symptoms of these related conditions.

Signs and Symptoms:

• Muscle, joint, and abdominal pain: This is a common symptom reported by patients with adrenal insufficiency (8).
• Weakness, fatigue, anorexia, nausea, diarrhea, and postural hypotension: These symptoms are also associated with adrenal insufficiency (8).
• Hypoparathyroidism: This condition can cause muscle cramps, weakness, and tetany (7).
• Chronic mucocutaneous candidiasis: This condition presents in infancy or early childhood as the initial sign, followed by the onset of hypoparathyroidism between the ages of 5-15 years (9).

Other symptoms:

• Organomegaly: Enlargement of organs such as the liver and spleen can occur in PAS-II (2).
• Endocrinopathy: This condition can affect multiple endocrine glands, leading to a range of symptoms including hypothyroidism, type 1 diabetes mellitus, and hypogonadism (7).
• Characteristic skin changes: Patients with PAS-II may experience skin manifestations such as alopecia, vitiligo, and autoimmune gastritis (4).

Additional information:

• Pernicious anemia: This condition can occur in patients with PAS-II due to autoimmune gastritis (4).
• Autoimmune thyroid disease: Hypothyroidism is a common endocrine manifestation of PAS-II (7).
• Type 1 diabetes mellitus: This condition can be associated with PAS-II, particularly in children (5).

Please note that these conditions have been largely replaced by more specific diagnoses, and the signs and symptoms listed above may not be directly applicable to modern patients. However, they provide a historical context for understanding the manifestations of polyglandular autoimmune syndromes.

References:

(1) - (10) correspond to the search results provided in the context.

Based on the provided context, it appears that there are various diagnostic tests used to identify polyglandular deficiency syndromes (PDS). Here's a summary of the relevant information:

• Cosyntropin (Cortrosyn) test: This is the standard test for primary adrenal insufficiency, with 95% sensitivity and 97% specificity [14]. The test involves administering synthetic adrenocorticotropic hormone (ACTH) to assess cortisol production.
• Other diagnostic indicators: For adrenal insufficiency, normal or low cortisol levels, elevated ACTH levels, and inadequate cortisol response to synthetic ACTH are indicative of the condition [9].
• Polyglandular deficiency syndromes (PDS): These conditions involve deficiencies in the function of several endocrine glands, which may occur simultaneously or sequentially. The etiology is often autoimmune, and diagnosis involves detecting deficient hormone levels [12].

It's worth noting that the context also mentions other diagnostic tests and procedures for polyglandular deficiency syndromes, but these are not explicitly mentioned here.

References:

[9] O Lavie · 2023 [12] Polyglandular syndromes type I, II, III (PDS) [14] The standard test for primary adrenal insufficiency is the cosyntropin (Cortrosyn) test

Based on the provided context, it appears that there are various treatments for different types of polyglandular dysfunctions.

Treatment Options

• For autoimmune polyglandular syndrome type 1 (APS1), immune suppression and modulation using drugs like glucocorticoids, calcineurin inhibitors, Methotrexate, Mycophenolate mofetil, Rituximab, and others are recommended [12].
• In some cases, treatment with hormone replacement therapy is necessary [14].
• For patients with XPID syndrome, treatment is mainly focused on hormone replacement therapy [13].

Specific Treatments

• Carbimazole was discontinued after 6 months of therapy in one case, resulting in remission of hyperthyroidism maintained at 1 year off treatment [4].
• Treatment with Hydrocortisone, Fludrocortisone, and Thionamides resulted in significant improvement in symptoms for one patient [5].

General Considerations

• The interaction of different hormonal therapies and pharmacological agents needs to be considered when treating multiple deficiencies [8].
• Detecting autoantibodies to each affected glandular tissue can help differentiate polyglandular deficiency syndromes from other causes [10].

Note: The information provided is based on the context, which includes various medical articles and studies. However, it's essential to consult a healthcare professional for personalized advice and treatment.

References: [4] by M Dick · 2020 · Cited by 3 [5] by N Zavrashvili · 2023 [8] by D Namboodiri [10] (no specific reference, but mentioned in the context) [12] by C Högenauer · 2001 · Cited by 93 [14] (no specific reference, but mentioned in the context)

Based on the provided context, it appears that there are several conditions that can be considered as differential diagnoses for obsolete polyglandular dysfunction.

• Congenital rubella: This is a viral infection acquired before birth that can cause various endocrine and other systemic abnormalities. [1]
• Hemochromatosis: Also known as excess iron storage in the body, this condition can lead to endocrine dysfunction among other symptoms. [8]
• Kearns-Sayre syndrome: A neuromuscular disorder that can also affect the endocrine system. [7]
• Myotonic dystrophy: A progressive muscle wasting and weakness disorder that can have systemic effects including endocrine dysfunction. [9]

Additionally, there are other conditions such as tuberculous hypoadrenalism and non-autoimmune hypothyroidism that can also be considered in the differential diagnosis of obsolete polyglandular dysfunction. These conditions can cause various endocrine abnormalities and may present similarly to polyglandular deficiency syndromes.

It's worth noting that the diagnosis of these conditions is typically made through a combination of clinical evaluation, laboratory tests, and imaging studies. [10]

References: [1] - 15 [7] - 7 [8] - 8 [9] - 9 [10] - 12