Glucose Metabolism in Patients With Psoriasis

N.U. Friis; N. Hoffmann; M. Gyldenløve; L. Skov; T. Vilsbøll; F.K. Knop; H. Storgaard


The British Journal of Dermatology. 2019;180(2):264-271. 

In This Article

Abstract and Introduction


Background: Epidemiological studies strongly suggest that psoriasis predisposes to type 2 diabetes. Several theories have been proposed to explain how these disease entities might be pathophysiologically connected.

Objectives: Our primary objective was to elucidate whether clinical data support the notion of common pathophysiological denominators in patients with psoriasis and type 2 diabetes, and thus to delineate the association between the two conditions that has arisen on the basis of epidemiological studies.

Methods: We reviewed clinical studies investigating parameters of glucose metabolism in patients with psoriasis. The PubMed and Embase databases were searched for studies investigating glucose metabolism in adult patients with psoriasis as a primary or secondary end point. Studies had to include a relevant control group.

Results: Twenty-six clinical studies reporting on insulin resistance, glucose tolerance or insulin secretion were eligible for review. The results were widely conflicting, with less than half of the studies showing results suggestive of defective glucose metabolism in patients with psoriasis. In general, the studies suffered from a lack of information regarding possible confounders and patient characteristics. Furthermore, the research methods varied, and in all but one study they might not have been appropriate to detect early and subtle defects in glucose metabolism.

Conclusions: The available literature does not unequivocally support common pathophysiological denominators in psoriasis and type 2 diabetes. Well-designed clinical studies are needed to expose potential diabetogenic defects in the glucose metabolism in patients with psoriasis.


Psoriasis is a multifactorial immune-mediated chronic inflammatory skin disease associated with an extensive range of comorbidities including cardiovascular disease, metabolic syndrome, depression and type 2 diabetes (T2D).[1] Like psoriasis, T2D is a complex disease with a multifactorial aetiology. According to the World Health Organization, the worldwide prevalence of diabetes has doubled since 1980 and shows no signs of regressing.[2]

T2D is characterized by insulin resistance in skeletal muscle and adipose tissue (collectively named peripheral insulin resistance) and in the liver (central or hepatic insulin resistance), as well as impaired insulin secretion from pancreatic beta cells.[3] In the progression from normal glucose tolerance through prediabetes to overt T2D there is initially a phase of normal fasting and postprandial glucose levels maintained by compensatorily increased insulin secretion from pancreatic beta cells.[4] Prediabetes and T2D develop when the beta cells are not capable of secreting enough insulin to keep up with the insulin resistance, resulting in relative insulin deficiency and increasing plasma glucose levels (Figure 1). Insulin resistance, dysfunction of the insulin-secreting beta cells and impaired glucose tolerance are thus early signs of disturbances in glucose metabolism appearing prior to the development of overt T2D.[4]

Figure 1.

The development of type 2 diabetes. This figure was created using Servier Medical Art, licensed under the Creative Commons Attribution 3_0 Unported License:

Epidemiological studies strongly support an association between psoriasis and T2D,[5–10] and several lines of evidence point to a dose–response effect, with more severe psoriasis associated with a higher risk of T2D.[5,6,9,10] Thus, epidemiological data firmly suggest that psoriasis predisposes to T2D, but the pathophysiological link between psoriasis and T2D is, as yet, poorly understood.

With the epidemiological evidence uniformly pointing to an association between psoriasis and the risk of developing T2D, we set out to provide a critical review of clinical studies examining glucose metabolism in patients with psoriasis. The aim was to investigate whether patients with psoriasis display the well-known early signs of disturbances in glucose metabolism seen in the progression to T2D.