Endocrine Abstracts

Adult Growth Hormone Deficiency (GHD) is a condition characterized by low grade chronic inflammation; increased levels of free light chains of immunoglobulins have been described; moreover, it shares some features with metabolic syndrome (MetS), including insulin resistance and oxidative stress, but with a different pattern of antioxidant response. Finally, it is known that GH, directly or via IGF-1 activity, influences many aspects of immune response; both humoral and cellular branches are modulated, but no data are available about complement function.

CH50 is a screening assay for the activation of the classical complement pathway and it is sensitive to the reduction, absence and/or inactivity of any component of the pathway. The CH50 tests the functional capability of serum complement components of the classical pathway to lyse sheep red blood cells (SRBC) pre-coated with rabbit anti-sheep red blood cell antibody (haemolysin). The subclasses of IgG can also depict a scenario of immune response, knowing the different functions of specific subclasses. No data are reported on CH50 and IgG subclasses in GHD.

Therefore, we performed a case-control study in a group of adult GHD patients evaluating CH50 levels and IgG subclasses to further explore the pattern of inflammatory markers in this condition.

We includedpatients with total GHD (GH peak after stimulation with GHRH+arginine <9 ng/ml with BMI < 30 or <4 ng/ml with BMI ≥ 30 kg/m²; n = 15) or partial GHD (peak between 9 and 16 ng/ml with BMI < 30 kg/m² n = 12) with mean ± SEM BMI 27.7 ± 2.6 kg/m² and mean ± SEM age 51.3 ± 2.5 ys. We also included a control group (n = 29) of patients matched by age (mean ± SEM 49.4 ± 1.7 ys).

An opposite pattern of the parameters studied was observed, with a significant increase of CH50 in GHD vs controls (Mean ± SEM 51.2 ± 2.5 and 30.5 ± 1.7 U/l respectively, P < 0.05), while a significant decrease of IgG4 was present in the same groups (0.23 ± 0.05 and 0.62 ± 0.11 g/l respectively, P < 0.05).

These datasubstantiate the hypothesis of chronic low-grade inflammation in GHD even if a causal relationship cannot be established and a vicious circle could ensue, with increase in inflammatory molecules in turn influencing GH secretion. However, these data cannot be conclusive and further studies are needed to establish the role of such molecules as biological markers and their usefulness in prognostic and personalized treatment of such condition.