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| __NOTOC__ | | __NOTOC__ |
| '''For patient information, click [[Adrenal atrophy (patient information)|here]]'''
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| {{Adrenal_atrophy}} | | {{Adrenal_atrophy}} |
| {{CMG}} | | {{CMG}}; {{AE}} {{MHP}} |
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| '''Associate Editor-In-Chief:'''
| | {{SK}} [[Adrenal atrophy]]; [[Adrenal insufficiency]]; [[Adrenal crisis]] |
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| ==Treatment== | | ==Treatment== |
| [[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]] |
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| Adrenal atrophy is the irreversible damage to the adrenal tissue, due to direct trauma or the secondary causes. As a result, treatment of the adrenal atrophy is a conservative treatment.
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| For adrenal crisis:
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| *Intravenous fluids
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| *Intravenous steroids
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| The cortisol deficiency is treated by supplementing with cortisol, prednisolone, prednisone, methylprednisolone, and dexamethasone.
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| The mineralocorticoid insufficiency is also cured by the fludrocortisone.
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| ===Primary Prevention===
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| Primary prevention of the adrenal atrophy consists of avoiding overuse of exogenous corticosteroid drugs.
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| ===Secondary Prevention===
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| 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.<ref name="pmid19500761">{{cite journal |vauthors=Hahner S, Allolio B |title=Therapeutic management of adrenal insufficiency |journal=Best Pract Res Clin Endocrinol Metab |volume=23 |issue=2 |pages=167–79 |date=April 2009 |pmid=19500761 |doi=10.1016/j.beem.2008.09.009 |url=}}</ref><ref name="pmid7170268">{{cite journal |vauthors=Barnett AH, Espiner EA, Donald RA |title=Patients presenting with Addison's disease need not be pigmented |journal=Postgrad Med J |volume=58 |issue=685 |pages=690–2 |date=November 1982 |pmid=7170268 |pmc=2426562 |doi=10.1136/pgmj.58.685.690 |url=}}</ref>
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| ==Case Studies== | | ==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.
| | [[Adrenal atrophy case study one|Case #1]] |
| 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.
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| 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.
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| 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.<ref name="pmid25165474">{{cite journal| author=Upadhyay J, Sudhindra P, Abraham G, Trivedi N| title=Tuberculosis of the adrenal gland: a case report and review of the literature of infections of the adrenal gland. | journal=Int J Endocrinol | year= 2014 | volume= 2014 | issue= | pages= 876037 | pmid=25165474 | doi=10.1155/2014/876037 | pmc=4138934 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25165474 }} </ref>
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