Search Results

You are looking at 1 - 1 of 1 items for

  • Author: Jesper Eugen-Olsen x
Clear All Modify Search
Charlotte Höybye Patient Area Endocrinology and Nephrology, Infection and Inflammation Theme, Karolinska University Hospital, Stockholm, Sweden
Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden

Search for other papers by Charlotte Höybye in
Google Scholar
PubMed
Close
,
Laia Faseh Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden

Search for other papers by Laia Faseh in
Google Scholar
PubMed
Close
,
Christos Himonakos Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden
Department of Medicine, Karlstad Hospital, Karlstad, Sweden

Search for other papers by Christos Himonakos in
Google Scholar
PubMed
Close
,
Tomasz Pielak NUTOPI Sp. z o. o., Poznan, Poland

Search for other papers by Tomasz Pielak in
Google Scholar
PubMed
Close
, and
Jesper Eugen-Olsen Clinical Research Centre, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark

Search for other papers by Jesper Eugen-Olsen in
Google Scholar
PubMed
Close

Growth hormone deficiency (GHD) syndrome is associated with adverse levels of several risk factors for cardiovascular diseases (CVD), including metabolic inflammation. However, the impact of GHD and GH treatment on low-grade inflammation is unknown. The aim of the study was to establish the level of the low-grade inflammation biomarker soluble urokinase plasminogen activator receptor (suPAR) in adults with GHD and the response to long-term GH treatment. Measurements of suPAR and CRP were performed in bio-bank serum samples from 72 adults, 34 males and 38 females, with GHD before and during at least 5 years of GH treatment. Mean age was 52.5 ± 15.5 years, BMI 27.3 ± 5 kg/m2. Clinical evaluations and blood sampling were performed at routine visits. Data on demography, anthropometry, lab results and clinical events were retrieved from post-marketing surveillance study databases and medical records. suPAR and high-sensitive (hs) CRP were analysed using ELISA and immunochemistry, respectively. At baseline blood pressure, lipid profile and fasting glucose were within the normal reference range. Baseline geometric mean and 95% CI of suPAR was 2.9 (2.7–3.3) ng/mL and of CRP 2.3 (0.6–4.0) mg/L. Mean follow-up was 8 ± 2 years. The suPAR levels remained stable during follow-up, although individual increases were seen on occurrence or presence of co-morbidities. In contrast, levels of CRP decreased. In conclusion, the decrease in CRP and indirectly the absence of an expected increase in suPAR over time indicates a favourable effect of GH on low-grade inflammation.

Open access