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Abstract
BackgroundCaused by Mycobacterium leprae (ML), leprosy presents a strong immune-inflammatory component, whose status dictates both the clinical form of the disease and the occurrence of reactional episodes. Evidence has shown that, during the immune-inflammatory response to infection, the growth hormone/insulin-like growth factor-I (GH/IGF-I) plays a prominent regulatory role. However, in leprosy, little, if anything, is known about the interaction between the immune and neuroendocrine systems.MethodsIn the present retrospective study, we measured the serum levels of IGF-I and IGBP-3, its major binding protein. These measurements were taken at diagnosis in nonreactional borderline tuberculoid (NR BT), borderline lepromatous (NR BL), and lepromatous (NR LL) leprosy patients in addition to healthy controls (HC). LL and BL patients who developed reaction during the course of the disease were also included in the study. The serum levels of IGF-I, IGFBP-3 and tumor necrosis factor-alpha (TNF-α) were evaluated at diagnosis and during development of reversal (RR) or erythema nodosum leprosum (ENL) reaction by the solid phase, enzyme-labeled, chemiluminescent-immunometric method.ResultsThe circulating IGF-I/IGFBP-3 levels showed significant differences according to disease status and occurrence of reactional episodes. At the time of leprosy diagnosis, significantly lower levels of circulating IGF-I/IGFBP-3 were found in NR BL and NR LL patients in contrast to NR BT patients and HCs. However, after treatment, serum IGF-I levels in BL/LL patients returned to normal. Notably, the levels of circulating IGF-I at diagnosis were low in 75% of patients who did not undergo ENL during treatment (NR LL patients) in opposition to the normal levels observed in those who suffered ENL during treatment (R LL patients). Nonetheless, during ENL episodes, the levels observed in RLL sera tended to decrease, attaining similar levels to those found in NR LL patients. Interestingly, IGF-I behaved contrary to what was observed during RR episodes in R BL patients.ConclusionsOur data revealed important alterations in the IGF system in relation to the status of the host immune-inflammatory response to ML while at the same time pointing to the circulating IGF-I/IGFBP-3 levels as possible predictive biomarkers for ENL in LL patients at diagnosis.
Highlights
Caused by Mycobacterium leprae (ML), leprosy presents a strong immune-inflammatory component, whose status dictates both the clinical form of the disease and the occurrence of reactional episodes
Since the spectral clinical forms of leprosy occur as a result of the capacity of the host to mount anywhere from low- (LL)-to-high (TT) cell-mediated immunity (CMI) responses against ML, the serum levels of Insulinlike growth factor-I (IGF-I) and Insulin-like growth factor binding protein-3 (IGFBP-3) were compared among patients having the different clinical forms at the pre-multidrug therapy (MDT) stage
Those who did not undergo reactional episodes during the course of the disease were included in this analysis, and the levels found in leprosy patients were compared with those of the healthy controls (HC)
Summary
Caused by Mycobacterium leprae (ML), leprosy presents a strong immune-inflammatory component, whose status dictates both the clinical form of the disease and the occurrence of reactional episodes. Lepromatous leprosy (LL) is a progressively disseminating disease characterized by extensive bacterial multiplication within host cells and low cell-mediated immunity (CMI) to the pathogen Between these two poles are the borderline forms (characterized by their intermediate clinical and immunological patterns), commonly referred to as borderline tuberculoid (BT), borderline borderline (BB), and borderline lepromatous (BL) in accordance with their proximity to either one of the spectral extremes. Nerve damage occurs in all clinical forms of the disease and may progress during multidrug therapy (MDT) itself and even subsequent to patient release, due, for the most part, to the occurrence of acute immuneinflammatory episodes known as leprosy reactions. Our understanding of the physiopathology of reaction remains limited so that further research is urgently needed to more clearly define laboratory biomarkers capable of accurately identifying the leprosy patients most at risk of developing reaction
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