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. 2025 Mar 21;14(7):2145.
doi: 10.3390/jcm14072145.

Endotyping Insulin-Glucose Homeostasis in Hidradenitis Suppurativa: The Impact of Diabetes Mellitus and Inflammation

Nessr Abu Rached  1   2 , Johannes W Dietrich  3   4   5   6 , Lennart Ocker  1   2 , Eggert Stockfleth  1   2 , Yannik Haven  1   2 , Daniel Myszkowski  1   2 , Falk G Bechara  1   2
Affiliations

Endotyping Insulin-Glucose Homeostasis in Hidradenitis Suppurativa: The Impact of Diabetes Mellitus and Inflammation

Nessr Abu Rached et al. J Clin Med. .

Abstract

Background: Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease often associated with metabolic disorders such as diabetes mellitus. Recent research suggests a link between systemic inflammation and insulin-glucose dysregulation in HS. This study investigates the relationship between insulin-glucose homeostasis, diabetes mellitus and the haptoglobin concentration in HS patients. Methods: We assessed 95 HS patients and 49 controls using validated fasting-based function tests, including the Structural Parameter Inference Approach (SPINA), Homeostasis Model Assessment (HOMA) and Quantitative Insulin Sensitivity Check Index (QUICKI). Results: The HS patients had a significantly higher fasting insulin concentration (97.2 vs. 69.0 pmol/L, p = 0.035), increased insulin resistance (HOMA-IR: 3.47 vs. 2.57, p = 0.016) and impaired insulin sensitivity (SPINA-GR: 1.34 vs. 1.76 mol/s, p = 0.017). In diabetes, the insulin sensitivity was more strongly reduced (SPINA-GR: 0.61 vs. 1.41 mol/s, p = 0.0057) and the insulin resistance increased (HOMA-IR: 7.3 vs. 3.2, p = 0.017). Higher haptoglobin concentrations were accompanied by worse glycaemic control, demonstrating a significantly elevated fasting glucose (5.77 vs. 5.11 mmol/L, p = 0.043) concentration and HbA1c (5.7% vs. 5.4%, p = 0.0081) fraction. Conclusions: Our findings suggest that chronic inflammation in HS contributes to metabolic dysregulation, worsening insulin resistance and glycaemic control, particularly in those with elevated haptoglobin or diabetes.

Keywords: HOMA-IR; HS; dermato-endocrinology; hidradenitis suppurativa; insulin resistance; insulin–glucose homeostasis.

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Conflict of interest statement

N.A. received funding, travel support, and/or personal honoraria for lectures from Novartis Pharma, Recordati Rare Diseases Germany GmbH, Janssen-Cilag GmbH and Johnson & Johnson that were independent of the work submitted. T.G. has received speaker and/or advisory board honoraria from BMS, Sanofi-Genzyme, MSD, Novartis Pharma, Roche, Abbvie, Almirall, Janssen, Lilly, Pfizer, Pierre Fabre, and Merck-Serono outside the submitted work. F.G.B. has received honoraria for participation in advisory boards, in clinical trials, and/or as a speaker from AbbVie Inc., AbbVie Deutschland GmbH & Co. KG, Acelyrin, Beiersdorf, Boehringer Ingelheim Pharma GmbH & Co. KG, Celltrion, Dr. Wolff, Incyte Corporation, Janssen-Cilag GmbH, Johnson & Johnson, Merck, Mölnlycke, MoonLake, Novartis Pharma GmbH, Sanofi, Sitala and UCB Pharma. E.S. has received lecture fees from Almirall, Leo, Pierre Favre and Philips. L.O. has received honoraria as a speaker and/or travel support from Novartis Pharma GmbH, Incyte Biosciences Corporation and Janssen. J.W.D. received funding and personal fees from Novo Nordisk, VitalAire, Abbott, Medtronic, Oviva, myhomecare, Aidhere, Ascensia Diabetes Care, Sanofi-Henning, Hexal AG, Bristol-Myers Squibb, Egetis Therapeutics and Pfizer and is the co-owner of the intellectual property rights for the patent “System and Method for Deriving Parameters for Homeostatic Feedback Control of an Individual” (Singapore Institute for Clinical Sciences, Biomedical Sciences Institutes, Application Number 201208940-5, WIPO number WO/2014/088516). All the other authors (D.M. and Y.H.) declare no conflicts of interest.

Figures

Figure 1
Figure 1
Compared to normal controls, insulin sensitivity is more heterogeneous but, on average, lower in patients with HS and partly compensated for by increased pancreatic beta-cell function: calculated biomarkers for insulin sensitivity (SPINA-GR, (a)), pancreatic beta-cell function (SPINA-GBeta, (b)) and loop gain (disposition index, SPINA-DI, (c)). Shaded areas denote the reference ranges for the respective parameters in a healthy population with a normal BMI; * significant result.
Figure 2
Figure 2
In patients with HS and diabetes, insulin sensitivity is reduced (a) without dynamic compensation via pancreatic beta-cell function (b), resulting in a reduced loop gain of the feedback control system (c). See the legend of Figure 1 for additional explanations; **, p < 0.01; ****, p < 0.001.
Figure 3
Figure 3
In persons with HS and a high haptoglobin concentration, insulin sensitivity and beta-cell function are similar but combine to provide a reduced disposition index. See the legend of Figure 1 for additional explanations.
Figure 4
Figure 4
The majority of patients with HS and diabetes are faced with rather low insulin sensitivity and a lack of dynamic compensation via pancreatic beta-cell function, resulting in a reduced disposition index. Plot of SPINA-GBeta versus SPINA-GR in patients with HS and controls.
See this image and copyright information in PMC

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