International Journal of Clinical Case Reports 2017, Vol.7, No.11, 45-48
47
Physical examination may find cutaneous and mucosal pigmentation, weight loss and hypotension.
Routine laboratory findings include hyponatremia, hyperkalemia, azotemia, hypoglycemia and hypercalcemia.
Specific biochemical tests include low basal levels of cortisol and elevated ACTH level. Rapid ACTH stimulation
test is also usually used to establish the diagnosis of adrenal insufficiency (Dorin et al., 2003).
Imaging studies done at an early stage, frequently demonstrates enlargement of the adrenals with a
pseudo-tumoral aspect on CT scan. At a later stage, the enlarged tuberculous adrenals decreased in size because of
fibrosis and calcification.
In Guo’s study, 75% of cases had mass-like adrenal enlargement when the duration of the disease was less than
one year, whereas in longstanding disease beyond three years adrenal glands are usually smaller (Guo et al.,
2007).
Peripheral rim enhancement with low attenuation in the center of the adrenals is an appealing feature of adrenal
tuberculosis. This feature represents the pathologic findings of central caseous necrosis surrounded by fibrous
tissue and granulomatous inflammatory tissue. This feature is however, not specific to tuberculosis and it may be
seen in adrenal tumors with central necrosis (Yang et al., 2006). The peripheral rim enhancement decreases with
time.
Adrenal calcification is a common sign of tuberculosis, but it is not specific, as it can also be seen in adrenal
tumors in about 10%. It can be present in all stages of the disease. The overall prevalence of calcification in the
study of Vita was 53% at the time of diagnosis and indicated long-standing tuberculosis (Vita et al., 1985). Wang
described small calcification on CT scan in 22% patients with active tuberculosis (Wang et al., 1998).
Pathologic studies of the adrenals glands infected by tuberculous mycobacterium revealed caseous necrosis area
and tuberculous granuloma at an early stage which causes destruction of the adrenal cortex leading to fibrosis and
calcification (Efremidis et al., 1996).
3 Conclusion
Although tuberculosis is less frequent than before, it remains a classic cause of adrenal insufficiency, notably in
developing countries. Therefore, it needs to be considered in the differential diagnosis of adrenal insufficiency or
bilateral adrenal masses.
Conflicts of interests
The authors declare that no competing interests exist.
References
Arlt W., and Allolio B., 2003, Adrenal insufficiency, Lancet, 361: 1881-1893
Dorin R.I., Qualls C.R., and Crapo L.M., 2003, Diagnosis of adrenal insufficiency, Ann Intern Med., 139: 194-204
PMid:12899587
Efremidis S.C., Harsoulis F., Douma S., Zafiriadou E., Zamboulis C., and Kouri A., 1996, Adrenal insufficiency with enlarged adrenals, Abdom Imag, 21:
168-171
PMid:8661767
Guo Y.K., Yang Z.G., Li Y., Ma E.S., Deng Y.P., Min P.Q., Yin L.L., and Chen T.W., 2007, Addison’s disease due to adrenal tuberculosis: contrast-enhanced CT
features and clinical duration correlation, Eur J Radiol, 62: 126-131
PMid:17182208
Kelestimur F., 2004, The endocrinology of adrenal tuberculosis: The effects of tuberculosis on the hypothalamo-pituitary-adrenocortical function, J Endocrinol
Invest, 27(4): 380-386
