• DOI:10.1111/bjd.16696
• Corpus ID: 52114086

Liver–skin axis: a new view or viewed already?

@article{Nobili2018LiverskinAA,
  title={Liver–skin axis: a new view or viewed already?},
  author={Valerio Nobili},
  journal={British Journal of Dermatology},
  year={2018},
  volume={179}
}

• V. Nobili
• Published 1 July 2018
• Medicine
• British Journal of Dermatology

In October 1987, I. Sarkany published the article ‘The skin– liver connection’ in the journal Clinical and Experimental Dermatology. The scientist pointed out: ‘everything has been thought of before, but the difficulty is to think of it once more’. That said, it seems that much of the recent scientific discovery in the area of the liver–skin axis, in the broadest sense, has been thought of before. The difference, of course, is the degree of scientific sophistication nowadays with which we can see an indisputable link between these two major organ systems. Moreover, there are plenty of good reasons for studying the interplay between the skin and the liver, in addition to the ascertained appreciation of morphological changes. So starting with liver diseases, regardless of whether they affect the synthetic, excretory, conjugation or regulatory mechanisms, they may induce jaundice, itching and pigmentary disorders, as well as nail and hair abnormalities. In this issue of the BJD, Prussick and Miele have explored the link between psoriasis and nonalcoholic fatty liver disease (NAFLD). Briefly, for both NAFLD and psoriasis, the pathogenesis is not completely clear; however, genetic, immunological and environmental factors are thought to be involved. It would particularly seem that the two diseases share the following common factors: (i) a contribution of genetic factors to the pathogenesis; (ii) a deregulated cytokine network leading to the release of multiple pro-inflammatory mediators; and (iii) a number of environmental factors that have also been identified as possible triggers. Moreover, these mechanisms are multifactorial and they often overlap with metabolic abnormalities, which frequently coexist in patients with psoriasis. When reading the review by Prussick and Miele, we can imagine the liver–skin axis as a bidirectional pathway. In fact, as reported by Mantovani et al., it is easy to speculate that several pro-inflammatory cytokines [e.g. interleukin (IL)-6, IL-17, tumour necrosis factor] are overproduced by lymphocytes and keratinocytes into the skin of patients with psoriasis, to take part, at least partly, in the pathogenesis of systemic insulin resistance and that it is patients with psoriasis with a greater insulin resistance are those who sustain NAFLD. On the other hand, it sounds conceivable that the release of pro-inflammatory, pro-oxidant and pro-atherogenic mediators from the steatotic and inflamed liver, the so-called NASH liver (nonalcoholic steatohepatitis), may adversely influence the severity of psoriasis by both an increased keratinocyte proliferation and an increased inflammation. This, in turn, leads to a magnification of the phenomenon. In fact, recent studies have shown that NAFLD is highly prevalent in patients with psoriasis and that psoriasis is considered to be an independent risk factor for NAFLD. In view of what is written above, there is reason to believe that dermatologists need to recognize the link between psoriasis and NAFLD. In doing so, this should allow for a proper evaluation of psoriasis, together with an informed decisionmaking process, about which pharmacological treatments to prescribe and whether a consultation with a hepatologist is justified, as some conventional drugs for psoriasis could potentially be hepatotoxic. Additional studies assessing the biological mechanisms linking NAFLD with psoriasis are also needed. However, given the current feeling that NAFLD is highly prevalent in patients with psoriasis, an increasing clinical awareness for underlying NAFLD in this population may be warranted.