Skin Manifestations

Erythema nodosum (EN) and pyoderma gangrenosum (PG) are the most frequent cutaneous manifestations among skin lesions [44]. EN is the most frequent cause of inflammatory nodules in the lower extremities and is associated with IBD in 11% of

Ibd Skin Manifestation

cases. It occurs more often in UC than in CD, and it is three to six times more frequent in women than in men, with a peak incidence at the age of 20-30 years. There are several conditions associated with EN.

EN develops in parallel with the colitis whereas PG may be concomitant or subsequent, even developing years after colectomy [45]. EN is characterised by sudden onset of multiple, bilateral, symmetrical, painful, red and warm nodules arising mainly on the extensor surfaces of the arms and legs. These nodules are often associated with systemic symptoms, such as fever, malaise and joint pain. The typical course of the disease lasts 3-6 weeks, but the residual bruiselike lesions may last for months. As for the presence of different EIM in the same patient (i.e. EN, anky-losing spondylitis and uveitis), there are numerous hypotheses to explain overlapping syndromes, one of which is based on the assumption of a common antigen, an isoform of tropomyosin, in the eyes, skin and joints. The likely aetiology is a hypersensitive response due to deposition of immune complex in and around venules in the septa of connective tissue in subcutaneous fat. Treatment for EN usually focuses on the underlying disease since EN usually regresses when the bowel disease is brought under control and recurs when it flares up. Corticosteroids, 5-aminosalicylates (5-ASA), azathioprine, cyclosporine and other immunosuppressants are the main types of medication used. Topical hydrocortisone can also be used symptomatically. Supportive treatment includes leg elevation, support stockings and bed rest [46].

PG is a rare, destructive skin lesion characterised by nodules and pustules, which can lead to formation of ulcers with necrotic bases (Fig. 2). PG is seen in 1-10% of UC patients and 0.5-20% of CD patients. It occurs equally in men and women, with a peak incidence between 25 and 54 years of age. From 50% to 78% of patients with PG have underlying disease, such as IBD, myeloproliferative or rheumatic disease. PG has been described in four variants: ulcerative, pustular, bullous and vegetative. Ulcerative and pustular PG are associated with IBD [47]. The pathogenesis of PG has not been clearly explained as yet but is probably due to a vasculitis caused by precipitation of immunocomplexes. PG is sometimes quite difficult to treat, depending on severity of the skin lesions and degree of bowel inflammation. In UC, appropriate treatment for the colonic inflammation is important, but neither medical nor surgical treatment can guarantee results in terms of healing the skin lesions [48]. It is now well established that topical treatment is usually insufficient, even in association with systemic treatment, so supportive treatment has to be combined with systemic therapy. Although measures to clean the lesions and prevent bacterial overgrowth are important, in-depth debridement is not encouraged because it can cause new lesions. Topical 5-ASA is not effective, and systemic 5-ASA has limited effect in treating the associated intestinal disease. Steroids are the most effective, first-line treatment for acute PG. High intravenous doses are used for refractory lesions. Initial doses range from 1 mg to 2 mg/kg per day. Among the immunosuppressants, cyclosporine and tacrolimus are effective in the treatment of PG. A retrospective study reported that 11 steroid-refractory cases of IBD with associated PG rapidly healed within 4-5 days of administering cyclosporine therapy, irrespective of intestinal disease activity; the authors suggested using 6-mercaptopurine and aza-thioprine as maintenance therapy and that long-term azathioprine is useful in PG for its steroid-sparing effect [49]. We reported on a case of PG refractory to cyclosporine that rapidly responded to oral therapy with tacrolimus (0.1 mg/kg per day), and the patient remained in remission with azathioprine therapy alone after discontinuing tacrolimus [50]. The effectiveness of infliximab has been reported in many studies. A recent randomised placebo-controlled study showed that it was superior to placebo in the treatment of PG. Patients randomised to receive infliximab were given a dose of 5 mg/kg weekly, and by the second week, 46% had improved as opposed to only 6% in the placebo group. There was no difference in outcome between PG patients with and without associated IBD. Other retrospective studies demonstrated the efficacy of infliximab in healing PG skin lesions but found that patients often require repeated courses of and had to be maintained on infliximab [51-53]. A recent case report described the efficacy of leukocyte apheresis (an extracorporeal leukocyte removal therapy) in a UC patient with PG who achieved a rapid and sustained remission of skin lesions [54].

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