Adrenal function in tuberculosis

Ellis, M E; Tayoub, F.

doi:10.1016/0007-0971(86)90003-3

Cited by 39 publications

(16 citation statements)

References 3 publications

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“…Additionally, DHEA seems to synergize with the GC anti-inflammatory effects, since this adrenal androgen is also a potent antiphlogistic hormone [56] . Recent studies in newly diagnosed pulmonary TB patients revealed augmented serum concentrations of IFN-␥ , IL-10, IL-6, and cortisol, with markedly reduced DHEA levels [57] , in line with other reports showing decreased DHEA levels in fluids of TB patients [58][59][60][61] .…”

Section: Hormonal and Cytokine Changes During Infectionssupporting

confidence: 87%

The Impact of Infectious Diseases upon Neuroendocrine Circuits

Pérez

Bottasso

Savino

2009

Neuroimmunomodulation

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During infectious diseases, neuroendocrine and immune networks act in concert, facilitating host response. It is known that infections cause profound immune changes, but the impact upon immunoendocrine circuits has been less studied. Disorders in the hypothalamic-pituitary-adrenal (HPA) axis were frequently observed associated with infections, and these changes often occur in parallel to alterations in the systemic cytokine network. Explanations for the infection-associated immunoendocrine disturbances include several and not mutually exclusive possibilities. Changes in cytokine levels can enhance or suppress the HPA axis, by acting at the hypothalamus-pituitary unit and/or at the adrenal glands. In situ inflammatory reactions or structural changes like vascular alterations or an enhanced extracellular matrix deposition in the endocrine microenvironment may also lead to a transient HPA dysfunction. Lastly, a microbe-related effect by means of pathogen infiltration or exploitation of the host’s hormonal microenvironment may be involved as well. A better understanding of the relevance of immunoendocrine communication during infectious diseases, and how disturbances in the flux of information lead to neuroendocrine immune-related disorders will provide important insights into mechanisms underlying the disease pathology.

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Section: Hormonal and Cytokine Changes During Infectionssupporting

confidence: 87%

The Impact of Infectious Diseases upon Neuroendocrine Circuits

Pérez

Bottasso

Savino

2009

Neuroimmunomodulation

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“…In parallel with increased cortisol concentrations, DHEA levels were decreased in the TB patients that we studied as well as in other groups of TB patients [85,86] . As commented, increased levels of GCs during acute conditions exert anti-inflammatory effects and favor an immune response that seems to be inefficient to eliminate intracellular pathogens [69][70][71] .…”

Section: Clinical and Immunological Implications Of Systemic Immunoenmentioning

confidence: 55%

Immunoendocrine Alterations during Human Tuberculosis as an Integrated View of Disease Pathology

Bay

Besedovsky²,

Rey³

2009

Neuroimmunomodulation

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Tuberculosis (TB) is a chronic infectious disease accompanied by excessive and/or prolonged cytokine production, which might affect the immunoendocrine communication and favor the establishment of an adverse state with important alterations in essential biological functions. Studies in blood from TB patients showed increased levels of interferon γ (IFN-γ), interleukin 10 (IL-10), and IL-6, accompanied by a modest increase in the levels of cortisol, prolactin, and thyroid hormones and markedly augmented concentrations of growth hormone. Conversely, testosterone and dehydroepiandrosterone (DHEA) levels were profoundly decreased, resulting in an increased cortisol/DHEA ratio. The finding that culture supernatants from Mycobacterium-tuberculosis-stimulated peripheral blood mononuclear cells (PBMCs) of TB patients inhibit DHEA secretion by a human adrenal cell line indicates that immune cells from these patients can directly affect the synthesis of this hormone. Supporting the existence of bidirectional interactions, in vitro treatment of PBMCs from TB patients with physiological concentrations of cortisol inhibited mycobacterial antigen-driven lymphoproliferation and IFN-γ production, whereas DHEA suppressed transforming growth factor β production from cases with progressive disease. Further analysis showed that plasma DHEA levels correlated positively with the in vitroproduction of IFN-γ by mycobacterial-stimulated PBMCs, and the cortisol/DHEA ratio was inversely correlated with IFN-γ production. Lastly, it was also shown that the immunoendocrine imbalance in TB patients was associated with weight loss, which in turn correlated with the impairment on their specific in vitro cellular immune responses. These immunoendocrine interactions may play a detrimental role during TB, in terms of the development of protective immune responses, control of tissue damage and metabolic disorders, being implicated in disease aggravation and the ‘classic’ TB consumption.

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“…5 A large study from South Africa published in 1986, before HIV became a serious clinical problem, found suboptimal responses to ACTH stimulation in 55% of patients with pulmonary TB. 6 Standard TB therapy includes the antibiotic rifampicin, which is a potent hepatic enzyme inducer that might contribute to adrenal insufficiency by accelerating the catabolism of cortisol. 7 The objective of this prospective study was to assess whether adrenocortical function was compromised in patients with active pulmonary TB during the initial period of therapy with two different antituberculosis regimens, one of which contained rifampicin and the other ciprofloxacin.…”

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confidence: 99%