Role Of Cortisol In Pathogenesis Research Articles

Serum Cortisol Levels in Lichen Planus: A Systematic Review with Meta-Analysis.

Lichen planus (LP) is an autoimmune, mucocutaneous, T-cell mediated chronic inflammatory disease that involves the oral mucosa. The prevalence of LP is 0.04–2% in general population with a female predilection. Patients with skin lesions also manifest oral lesions predominantly and about 25% present with only oral lesions. The aim of the systematic review is to analyze the serum cortisol levels in LP patients to elucidate the role of cortisol in pathogenesis of the lesion. A comprehensive search was done using electronic data bases such as PUBMED, EMBASE, SCIENCE DIRECT, COCHRANE, GOOGLE, manual search, and back references of the articles were extracted. A total of seven relevant articles were reviewed and analyzed. Electronic database and manual search identified 55 articles. Out of which, 33 were excluded after reading titles and removing duplication and 23 studies were evaluated in detail after reading the abstract and full text. A final of seven studies were included based on the inclusion criteria to meet the research question. All the studies analyzed the serum cortisol levels in LP patients and also in healthy subjects. Within the limitations of this review, it can be inferred that Cortisol is an established stress hormone and Serum cortisol estimation could be an important indicator in identifying susceptible oral lichen planus patients.

Relationship between type 2 diabetes mellitus and hypothalamic-pituitary-adrenal axis

Hypercortisolism often leads to impaired glucose tolerance or type 2 diabetes mellitus. On the other hand, changes in the regulation of hypothalamic-pituitary-adrenal axis become a matter of debate in patients with type 2 diabetes mellitus/metabolic syndrome. Authors assessed the hypothalamic-pituitary-adrenal axis activity and subclinical Cushing's syndrome occurrence in 50 patients with type 2 diabetes mellitus in comparison to 25 sex-, age-, and BMI-matched control nondiabetic subjects. 1 mg dexamethasone suppression test with NIH recommended cut-off level for adrenal incidentaloma (serum cortisol after suppression > 138 nmol/l) was used to postulate the diagnosis of subclinical hypercortisolism. There were no significant differences in serum ACTH, DHEA-S, baseline serum cortisol as well as serum cortisol after suppression of 1 mg dexamethasone/subclinical Cushing's syndrome prevalence in both diabetic and control groups (18 vs. 24% respectively, p = 0.54) and there was no relation to the type of treatment (OAD vs. insulin) in group of diabetics. When divided according to age, diabetics older than 60 years suppressed their serum cortisol significantly worse than their age-related controls (99.3 vs. 85.5 nmol/l, p = 0.0001). Furthermore, diabetics did not show an age-related decrease in DHEA-S levels, whereas controls did (r = -0.302, p = 0.033; r = -0.596, p = 0.0017 respectively). Within the group of diabetics, a positive correlation between C-peptide levels and baseline serum cortisol/DHEA-S levels was detected as well (r = 0.445, p = 0.001 and r = 0.339, p = 0.017 respectively). Our data show relatively high but comparable lack of cortisol suppression in both diabetic and control groups; however, we consider the subclinical Cushing's syndrome diagnose to be criteria dependent. There is no dependence of type of diabetes treatment (OAD vs. insulin) on HPA axis activity. Our results might indicate the possible role of cortisol in pathogenesis of type 2 diabetes mellitus in patients with metabolic syndrome as well as possible protective role of DHEA-S within the frame of secondary contraregulatory mechanisms aimed to improve insulin sensitivity and reduce the hyperinsulinemia.