Adrenal atrophy: Difference between revisions
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[[Adrenal atrophy medical therapy|Medical Therapy]] | [[Adrenal atrophy interventions|Interventions]] | [[Adrenal atrophy surgery|Surgery]] | [[Adrenal atrophy primary prevention|Primary Prevention]] | [[Adrenal atrophy secondary prevention|Secondary Prevention]] | [[Adrenal atrophy cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Adrenal atrophy future or investigational therapies|Future or Investigational Therapies]] | [[Adrenal atrophy medical therapy|Medical Therapy]] | [[Adrenal atrophy interventions|Interventions]] | [[Adrenal atrophy surgery|Surgery]] | [[Adrenal atrophy primary prevention|Primary Prevention]] | [[Adrenal atrophy secondary prevention|Secondary Prevention]] | [[Adrenal atrophy cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Adrenal atrophy future or investigational therapies|Future or Investigational Therapies]] | ||
===Primary Prevention=== | ===Primary Prevention=== | ||
Revision as of 19:19, 24 January 2022
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Adrenal atrophy Microchapters |
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Diagnosis |
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Case Studies |
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Adrenal atrophy On the Web |
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American Roentgen Ray Society Images of Adrenal atrophy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor-In-Chief:
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Adrenal atrophy from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X Ray | CT | MRI | Ultrasound | Other Imaging Findings | Other Diagnostic Studies
Treatment
Medical Therapy | Interventions | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Primary Prevention
Primary prevention of the adrenal atrophy consists of avoiding overuse of exogenous corticosteroid drugs.
Secondary Prevention
The secondary prevention of the adrenal atrophy is also known as early diagnosis of any steroid or mineralocorticoid deficiency in the body, as discussed at the causes section, and its early appropriate treatments.[1][2]
Case Studies
A 46-year-old man presented to his physician with a 3-month history of generalized weakness and 15-pound unintentional weight loss. He denied sick contacts, specifically exposure to tuberculosis, smoking, alcohol consumption, or the use of illicit substances. Physical examination revealed abdominal distension and free fluid but was otherwise unremarkable. A diagnostic paracentesis revealed an exudative effusion with a positive Ziehl Neelsen stain for acid fast bacilli. The patient was started on treatment. One month after starting antitubercular therapy he presented to the hospital with worsening fatigue, salt craving, vomiting, loss of libido, and erectile dysfunction. On examination, he had low blood pressure and appeared cachectic. In addition, he had bitemporal muscle wasting and hyperpigmentation of skin, oral mucosa, and nails. Laboratory evaluation was significant for hyponatremia, hyperkalemia, and mild hypercalcemia. A random cortisol was 2.5 mcg/dL with an ACTH of 531.2 pcg/mL. The basal and cosyntropin stimulated serum cortisol were, respectively 1.8 mcg/dL and 2.0 mcg/dL, which was consistent with the diagnosis of primary adrenal insufficiency most likely due to tuberculosis. A computed tomography scan of the abdomen with intravenous contrast revealed bilaterally enlarged adrenal glands (4 cm × 3.3 cm on the right, 2.3 cm × 2.1 cm on the left). On review of his prior CT scan of the abdomen, the patient had bilaterally enlarged adrenal glands at the time of his initial presentation as well. A biopsy was obtained from the patient’s right adrenal gland and the findings were in consistent with granulomatosis with caseification necrosis, besides wide cellular disorganization and atrophy and compensatory hypertrophy. He was initially treated with intravenous hydrocortisone and was subsequently discharged on hydrocortisone and fludrocortisone. His symptoms have improved significantly. However, he is requiring slightly higher dose of hydrocortisone, which could be due to CYP 3A4 induction by rifampicin. He is likely to require lifelong treatment for adrenal atrophy, caused by tuberculosis infection.[3]
- ↑ Hahner S, Allolio B (April 2009). "Therapeutic management of adrenal insufficiency". Best Pract Res Clin Endocrinol Metab. 23 (2): 167–79. doi:10.1016/j.beem.2008.09.009. PMID 19500761.
- ↑ Barnett AH, Espiner EA, Donald RA (November 1982). "Patients presenting with Addison's disease need not be pigmented". Postgrad Med J. 58 (685): 690–2. doi:10.1136/pgmj.58.685.690. PMC 2426562. PMID 7170268.
- ↑ Upadhyay J, Sudhindra P, Abraham G, Trivedi N (2014). "Tuberculosis of the adrenal gland: a case report and review of the literature of infections of the adrenal gland". Int J Endocrinol. 2014: 876037. doi:10.1155/2014/876037. PMC 4138934. PMID 25165474.