Adrenocortical reserve and morphology in tuberculosis.
Ninety seven patients (63 males, mean age 31.8 years, SD 2.3) with various forms of tuberculosis were studied. All of them were HIV negative. Thirty normal control subjects (16 males, mean age 36.4 years, SD 1.8) were also studied. Fifty-eight of the 97 patients (59.8%) were malnourished (BMI < 18 kg/m2). The mean basal serum cortisol was lower in the TB group (n = 91) (351 nmol/1; SD 150) as compared to the normal control group (n = 8) (402 nmol/1; SD 93) but this difference did not attain statistical significance. Following administration of synthetic ACTH (cosyntropin), the 30 and 60 minutes mean serum cortisol values in the TB group were significantly lower as compared to the normal control group (p < 0.05). Forty five of the 91 patients (49.5%) who underwent the ACTH stimulation test had compromised adrenal reserve. Fourteen of the 86 patients (16.3%) in whom adrenal morphology was studied revealed adrenal gland enlargement on abdominal CT scan. ACTH stimulation was done in 12 of these 14 patients and eight of them had compromised adrenal reserve. Repeat ACTH stimulation done six months to one year after treatment in 13 patients revealed significantly increased 30 minutes (p < 0.05) and 60 minutes (p < 0.05) serum cortisol values. While nine of these 13 patients were negative responders before treatment, only three of them had evidence of compromised adrenal reserve after one year of antituberculosis treatment, (p < 0.05). Serum cortisol values in patients with drug-sensitive and drug-resistant tuberculosis did not differ significantly. Patients with drug-resistant tuberculosis had a higher prevalence of adrenal gland enlargement (7 of the 30) as compared to those with drug-sensitive tuberculosis (7 of the 56) (p = NS). Subclinical adrenal insufficiency is prevalent in a significant number of patients with both drug-sensitive and drug-resistant tuberculosis, and in some of these it is associated with adrenal gland enlargement. The compromised adrenal reserve and enlargement seem to reverse with therapy.
Prasad
G A
GA
Department of Medicine, All India Institute of Medical Sciences, New Delhi.
Sharma
S K
SK
Mohan
A
A
Gupta
N
N
Bajaj
S
S
Saha
P K
PK
Misra
N K
NK
Kochupillai
N P
NP
Pande
J N
JN
D000305:Adrenal Cortex Hormones / Q000097:blood / Q000378:metabolism; D000311:Adrenal Glands / Q000000981:diagnostic imaging / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000328:Adult; D000995:Antitubercular Agents / Q000494:pharmacology; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood* / Q000378:metabolism*; D007538:Isoniazid / Q000494:pharmacology; D008297:Male; D012293:Rifampin / Q000494:pharmacology; D014057:Tomography, X-Ray Computed; D014376:Tuberculosis / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D018088:Tuberculosis, Multidrug-Resistant / Q000097:blood / Q000503:physiopathology
D000305:Adrenal Cortex Hormones; D000995:Antitubercular Agents; D000324:Adrenocorticotropic Hormone; D007538:Isoniazid; D012293:Rifampin; D006854:Hydrocortisone