Endocrine Abstracts

Addison’s disease (AD) occurs when 90% of the cortex of Adrenal Glands is affected. Most common causes of AD are autoimmune destruction, tuberculosis, hemorrhage due to meningococcal meningitis, metastatic cancers and adrenoleukodystrophy. AD is associated with other autoimmune disorders e.g., vitiligo, type-1 diabetes or hypothyroidism. Due to non-responsiveness of adrenals to Adrenocorticotrophic hormone (ACTH), α-melanocyte stimulating hormone levels increases and its pro-hormone peptide pro-opiomelanocortin production is strongly increased causing bronze pigmentation of exposed parts of the body. Other features include fatigue, lethargy unintentional weight loss, depression, irritability, vomiting, and loss of libido.

Case presentation: A 35 year old female house wife presented in the Endocrinology department with complaints of nausea, vertigo with tiredness, lethargy with mood swings from severe depression to irritability with yelling and beating her kids at times, hallucinations at night that she will die soon and whose going to take care of her children having unintentional weight loss and darkening of knuckles, palmar creases, lips and oral mucosa and tongue for the past 3 yrs. Treated with different antiemetics and antipsychotics. Different health care providers were unable to diagnose though features were suggestive of the disease and confirmed by labs. ACTH >1250 pg/ml (10-60). Serum cortisol 8 am 4.2 (5-23). Sodium 128 mEq/l (136-146). TSH :7.5 ulU/ml (0.4-4.2). FT4:0.4 ng/dl (0.8-2.37). FBS :80 mg/dl (<100). HB: 8.8 gm/dl (12-15). TPO antibodies positive. Hypothyroidism also cause depression. It co-presents with AD, a condition known as Schmidt syndrome (part of Autoimmune polyglandular syndrome). Depressive symptoms were the initial and devastating presentation of patient initially being misdiagnosed, as it did in this case. Neuropsychiatric symptoms were due to pigmentation of her face and hands and was desperate to remove them by creams or lotions because her brother was getting married, so was depressed and reluctant to face the guests with darkened patches. Neuropsychiatric symptoms that occur in AD were related to normal to mildly low glucose levels and hyponatremia which may cause brain damage. Decreased glucocorticoids also effect brain and cognitive function. Resulting in an increase in neural excitability, leading to an enhanced ability to detect sensory input, and precipitate hallucinations as well as lower the threshold for psychosis.

Conclusion: AD should always be kept in mind by physicians while treating a psychiatric patient (especially in cases of depression and psychosis) who have no past or family history of psychiatric illness or who fail medical therapy for depression.