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6) Disseminated Infections: In the immunocompromized in the form of oesophagitis, pneumonia.
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The Skin and Viral Liver DiseaseMastrolonardo M.1[1] Department of Dermatology, University of Foggia, Foggia, Italy1. Cutaneous lichen planus (LP): flat, polygonal, lilac red-coloured pruritic papules (Courtesy of Professor M. Mucous LP: papular, hyperkeratotic variant (‘lace network’ pattern) (Courtesy of Professor M. Mucous LP: papular, hyperkeratotic variant (‘sprinkle of lime’ pattern) (Courtesy of Professor E. Mucous LP: mixed type, with a combination of erosive and hyperkeratotic lesions (Courtesy of Professor M. Ranking of therapeutic options for treatment of moderate-to-severe psoriasis in chronic carriers of HBV.
IntroductionIt is undisputable that a multifaceted biological interplay exists between the skin and the liver. Mixed cryoglobulinemic vasculitisCryoglobulins are a family of anomalous proteins which tend to precipitate at low temperatures (<37°C), such as those currently found in the extremities (namely hands, feet, ear and nose).
The integument can firstly be viewed as a ‘gate’ through which hepatotropic viruses may access the blood stream. The prototype of cryoglobulinaemic diseases in HCV infected patients is ‘mixed cryoglobulinemia’ (MC). In this respect, one may think of the huge number of B and C virus hepatites that must have been acquired in a more or less distant past due to either intravenous drug consumption, use of contaminated equipment in beauty and health care-related procedures, or even dermal tattooing. Of note, up to more than a half of HCV-infected patients show circulating cryoglobulins, and rates of 30 to 100% of HCV positive serologies have been reported in carriers of circulating cryoglobulins, with an unexplained predominance in the Mediterranean basin. Moreover, one may consider that some cases of herpes simplex virus hepatitis have been reported in the literature which are not unlikely ascribable to systemic dissemination from primary muco-cutaneous lesional foci.Yet, the skin may also be viewed as a ‘mirror’ capable of projecting on the body surface more or less specific echoes of disease conditions involving the liver. In MC tissue damage results from deposition of immune complexes containing rheumatoid factor, polyclonal IgG, complement and HCV RNA on endothelial surfaces of small- to medium-sized vessels, which in turn leads to vascular inflammation. A recent review of the issue by Hazin and coworkers [1] is introduced by the following simple but just as brilliant statement: “Dysfunction in the body’s second largest organ, the liver, often yields changes in the body’s largest organ, the skin”.
The prevalent histological pattern of MC is neutrophilic ‘leukocytoclastic’ vasculitis; however, ‘necrotizing’ vasculitis, with intimal fibrinoid necrosis and infiltration of the entire vessel wall and perivascular space, may also be observed [27]. The most trivial paradigm sustaining such an obvious assumption is jaundice when it is sustained by primary failure of hepatocytes to perform one of their main functions, that is to conjugate bilirubin into a secretable form.
The skin is one of the most commonly affected organs, along with kidneys and peripheral nerves.
However, further and less obvious paradigms, such as cutaneous manifestations of mixed cryoglobulinemia in HCV infected patients, will also be discussed. Thus, the dermatologist may play a helpful role in early detection of previously unrecognized HCV infections.
Since the issue that will be specifically reviewed in this chapter is all the many possible links between skin and virus-induced liver disease, this introductory framework is to be completed by mentioning the not unusual circumstances in which neither the skin nor the liver disease in itself, but treatments undertaken to cure a disease of one of the two organs may have undesired consequences on the other one. In fact, the appearance of cutaneous lesions on extremities, particularly in cooler weather, must always raise clinical suspicion. This seems obviously true thinking of some double-edged risky circumstances in which either worsening of psoriasis in patients undergoing interferon plus ribavirin therapy, or reactivation of latent viral infections under immunosuppressive treatment of the skin disease, is observed.2.
The spectrum of skin involvement in MC ranges widely from ‘palpable purpura’ (which is the absolutely prevalent clinical scenario) [9] to urticarial vasculitis, necrotizing vasculitis, isolated necrotic ulcers, acral ischemias, acrocyanosis, and livedo reticularis (Figure 7 and 8). Of note, even in cases characterized by the highest clinical severity, the skin behaves very often like a sort of ‘emuntory system’, with poor or absent signs of internal organ involvement. Tatooing as risk factor for viral liver diseaseTatooing has been practiced for many centuries worldwide, and is a well-established risk factor for transfusion-transmitted diseases, including HBV and HCV [2]. Systemic vasculitis, involving the kidneys, the heart, the central nervous system and other viscera, is in fact unusual. Rare forms of viral hepatitis caused by agents which usually involve only the skinAfter primary infection, in the absence of any severe immune deficiency condition, herpesviruses like Herpes Simplex Viruses (HSV) type 1 or 2, and Varicella-Zoster virus (VZV) establish latency by remaining dormant in the dorsal root nerve ganglia. In patients who are intolerant to antivirals, or those with severe systemic disease, or those who have failed to reach SVR after antiviral therapy, symptomatic treatment with plasmapheresis, steroids or rituximab should be considered [27]. Porphyria cutanea tardaPorphyria cutanea tarda (PCT) is related to a deficient activity of the heme synthetic enzyme uroporphyrinogen decarboxylase (UROD), which may in turn be sustained by either UROD gene mutations or acquired liver insufficiency [28].
4, 5 and 6), herpetic lesions tend to heal within few weeks, with no or only minor scarring and dyschromic sequelae. As for VZV, post-herpetic neuralgia develops quite rarely, and is the worst occurrence reported after skin manifestations have faded. HCV prevalence in PCT sufferers is significantly higher than that reported in the general population.
In otherwise healthy subjects, disseminated herpes simplex virus hepatitis have been reported very exceptionally. Prevalence rates range from 17 to 65%, the latter having been reported in Southern Europe [29, 30]. In one case described by Miyazaki and coworkers in 1991 [4], the possibility that patient’s mucosal herpetic lesions might have behaved as a ‘gate’ for a large virus inoculum leading to visceral involvement either directly or after having overwhelmed local immune defenses has been considered.By contrast, HSV and VZV hepatitis are possible in patients whose cell-mediated immunity is severely impaired, for instance in malignancy or organ transplanted patients [5]. However, HCV alone is not likely to cause the disease, but it is thought to be a strong trigger for the development of deranged porphyrin metabolism in subjects with other known predisposing factors (such as, alcohol abuse or iron overload) [31].
In these cases, the skin rash may either be absent, coincide with, or supervene after visceral involvement. Laboratory diagnosis is based on detection of increased levels of uro-carboxyl porphyrins and heptacarboxyporphyrins in the urine, and on the presence of isocoproporphyrin in the feces. When cutaneous lesions are present, severity of skin involvement is often significantly increased compared to standard clinical pictures both in terms of number of lesions, diffusion over the body surface, and severity of tissue impairment.

Due to its porphyrin content, the urine of PCT patients is discoloured (chiefly after air and light exposure), while all ‘iron tests’ are negative. Notably, in a recent review of 74 cases of herpes simplex hepatitis [6], Sharma and Mosunjac highlighted that proper diagnosis was delayed in more than two-third of cases, despite a herpetic muco-cutaneous involvement was present in at least 70% of patients. Conversely, the occurrence of an unexplained impairment of liver function tests in an immunocompromised patient exhibiting skin herpetic lesions should always arouse a high degree of suspicion of visceral dissemination [7]. Fulminating herpetic hepatitis is a life-threatening occurrence, but it can be treated effectively if therapy is started early.
However, the persisting lack of aim-oriented studies based on standardized methods and criteria results in some uncertainty [33]. Clinically, cutaneous LP is characterized by flat, polygonal, lilac red papules which may remain isolated, or merge into larger plaques (Figure 9 and 10). Skin manifestations related to HCVCutaneous manifestations of acute infection are sporadic and show no substantial specificity, ranging from urticaria, erythema multiforme, leukocytoclastic vasculitis to erythema nodosum.
On the contrary, there exists a wide panel of skin conditions linked, to a varying degree, with chronic HCV infection [8, 9].
The occurrence of skin disorders of any type has been in fact reported in up to 17% of HCV patients (Table 1) [10]. The flexor aspects of the limbs, the upper back, and the lumbar region are frequently involved, but the disease can spread over the entire body surface. On the other hand, the clinical alliance between HCV and a broad list of other skin conditions has not yet received sufficient support [9, 11].
Mucous LP chiefly affects the mouth and, less frequently, genitalia, conjunctiva, and esophagus. In this context, anecdotal reports have mostly been made in the literature of associations with pityriasis rubra pilaris [12], sarcoidosis [13], vitiligo [8], cholestatic and non-cholestatic pruritus [14, 15], prurigo nodularis [16], cutaneous polyarteritis nodosa [17], pyoderma gangrenosum [18], subacute cutaneous lupus erythematosus [19], primary localized cutaneous amyloidosis [20], pigmented purpuric dermatosis [21], actinic porokeratosis [22], pityriasis lichenoide [23], generalized granuloma annulare [24], disseminated Kaposi’s sarcoma [25] and necrolytic acral erythema [26].
The mucosal lesions consist of erosive erythematous patches (Figure 11), or horny micro-papules arranged in a reticular pattern recalling a lace network (or a sprinkle of lime) (Figures 12 and 13), or a combination of both (Figure 14). Of note, in most of the above circumstances it seems quite difficult to sift consistently the direct contribution of HCV infection per se from that attributable to antiviral treatment. A data set which is therefore of the outmost relevance in this regard is that provided by an U.S. The prominence of certain HLA haplotypes (such as, HLA-DR1), or detection of cytokine gene polymorphisms in some case series [34], support a genetic predisposition to the disease. In this study, the aforementioned strong association with cryoglobulinemia, porphyria cutanea tarda and lichen planus found an authoritative confirmation. The basal epidermis injury observed in LP is attributed to cytotoxic T lymphocytes, which in fact predominate into the infiltrate along with minor subpopulations of macrophages and dendritic cells. However, a statistically significant link was also observed with vitiligo, but this finding did not receive further comparable support from the rest of the literature, and remains rather inexplicable.
In this context, a significant role of plasmacytoid dendritic cells has been also recognized.
In fact, these cellular effectors are viewed as the driving force to the end-stage T cell-mediated epidermal damage, in that they would be able to give rise to an inflammatory type I interferon signaling pathway which, in turn, would amplify and maintain cytotoxic T cell attack to keratinocytes [35]. Cross-reactivity between endogenous and environmental antigens is widely suspected, but the exact nature of the triggering antigen is still obscure.
Among the putative exogenous factors involved in LP, one of the most outstanding candidates appears to be HCV. An ample body of biological evidences supporting this view exists in the literature, and has been reviewed in recent years [36, 37]. These circumstances have recently led Baccaglini and coworkers [37] to launch somewhat provocatively the subversive hypothesis of a fake association via a ‘third factor’ consisting of a still unidentified confounder. However, at least on epidemiological grounds, the existence of a ‘two-way’ association between LP and HCV infection seems currently beyond question worldwide.
On the basis of these circumstances, screening for anti-HCV antibodies is substantially advisable in patients with LP, especially in countries with the highest seroprevalence rates.
In this regard, it has been suggested that routine HCV testing would be cost-effective in geographical districts in which HCV prevalence is 7% or more [40].
Yet, in the absence of standardized criteria and guidelines, individual case-by-case screening strategies are more suitably recommended [37].
This section is to be concluded by underscoring that true cases of idiopathic LP need sometimes to be differentiated from so-called lichenoid eruptions (LE), which somehow resemble LP on both clinical and histological grounds [41]. LE are often caused by (and develop at sites of) contact with dental restorative amalgams or stomatological devices, due to their content of methacrylic acid esthers, nickel, mercury, copper and gold [32]. However, LE may be also induced by a huge array of systemic drugs whose number is in steady increase [42], ranging from angiotensin-converting enzyme inhibitors to non-steroidal anti-inflammatory drugs, antimalarials and proton pump inhibitors.
The reader should be aware that the list includes the agents employed for treatment HCV infection, interferon and ribavirin [43]. Skin manifestations related To HBVBoth range and frequency of extrahepatic manifestations in patients with HBV infection are considerably lower compared with those observed in HCV infected subjects [44, 45].
A French multicenter, retrospective, cross-sectional study of 190 patients with chronic hepatitis B has rated the overall incidence of clinical and biologic extrahepatic manifestations to be 16% and 15%, respectively [46]. As more specifically regards the skin, vasculitis, psoriasis and pruritus were found to occur in only 1% of cases each. Of note, in striking contrast with HCV populations, in HBV patients cryoglobulinemia and related disease manifestations have been reported in only 2% of cases.
Many clinical and laboratory observations have long cast significant doubts on the actual biological relevance of this association. On this regard, literature yields rates up to 15% for cryoglobulin detection in HBV patients, although no signs or symptoms of related vasculitis are observed in the great majority of cases [47]. Alternatively, induction of local IC formation by viral antigens, interaction between tissue antigens and virus-induced autoantibodies, or direct tissue damage by viral replication have also been invoked. However, this issue remains highly controversial [45, 48, 49].Cutaneous manifestations of HBV infection (Table 2) are observed both in the incubation, prodromal phase and in chronic state of disease.

In the former, a clinical scenario in which intermingled signs of either a mild ‘flu-like’ or a more serious ‘serum sickness-like’ syndrome have been described. Gianotti-crosti syndromeGianotti-Crosti syndrome (GCS) [54], also termed ‘papular acrodermatitis of childhood’, is a peculiar, self-limited and largely asymptomatic skin eruption featuring almost monomorphous papular or papulovesicular lesions located mainly on the face and distal aspects of the four limbs (Figure 16).
Histology is noncontributory, with upper dermis perivascular round cellular infiltrates and endothelial swelling as the prevailing findings.
Children aged from a few months to 15 years (with a peak between 1 and 6 years) are mostly involved, but adults (of note, only females) may be also affected.
Originally described as in strict conjunction with sole HBV infection, GCS has been subsequently linked to an array of infectious agents, including other viruses (such as, HAV, CMV and EBV) and bacteria (such as, Borrelia burgdorferi and ?-hemolytic streptococci). Neither viral bodies nor viral antigens have ever been demonstrated in the context of skin lesions, and the pathogenesis of GCS remains largely unclear. Current views on the issue span from a role of immune complex deposition to occurrence of virus-related delayed hypersensitivity reactions. Furthermore, an association between immunization and GCS has long been outlined, with anti-HBV and anti-HAV vaccinations being included in the list of triggering factors [54-57]. Remarkably, it has been proposed that occurrence of GCS after the first vaccine administration does not contraindicate completion of the immunization protocol, as GCS does not recur after the subsequent boostering injections [55]. Finally, in addition to that with GCS, an association has also been reported between HBV infection and a much rarer, but equally peculiar skin eruption involving the extremities, i.e. Polyarteritis nodosa Recognition of a strong linkage between HBV and polyarteritis nodosa (PAN) dates back to the 1970s. Rates of prevalence of positive HBV serologies have been estimated up to 50% among PAN patients. However, these figures have decreased significantly over the last four decades, and are currently less than 5% [45]. A major role in this respect must have been played by improved blood transfusion safety measures, other general hygiene precautions and extensive vaccination campaigns.
The pathogenesis has largely been attributed to deposition of immune complexes containing HBsAg.
Of note, unlike other forms of PAN, in HBV-related PAN serum antineutrophilic cytoplasmic antibodies (ANCA) are only exceptionally detected. Histologically, PAN is characterized by transmural, usually segmental, necrotizing infiltration of medium-to-small vessels resulting in ischaemia, infarcts and haemorrhage, which ultimately lead to end-organ damage. If untreated, the course of PAN is often protracted, and symptoms and signs of multi-organ involvement are generally observed. Cutaneous PAN has also been reported in 10 to 50% of cases, depending on the case series examined.
Livedo reticularis and painful subcutaneous nodules (usually along the arteries of the lower limbs) are commonly described.
Further anecdotal reports of skin disorders observed in conjunction with HBV infection include acanthosis nigricans [61] and generalized granuloma annulare [62].
Finally, the association with lichen planus (LP), which is now undisputed in HCV infection, is instead highly controversial in HBV carriers. A number of earlier studies have provided some support for this view, but such biological alliance has more recently received repeated confutations [63, 64] and is currently considered unfounded.
Skin unfavorable effects of HBV immunizationHepatitis B vaccination may also be hazardous for the skin. Skin manifestations related to HAVApart from the ‘paradigm’ of jaundice, HAV infection is very occasionally linked to significant cutaneous side-events. Bufo, Foggia, Italy)Figure 16.Gianotti-Crosti syndrome (‘papular acrodermatitis of childhood’) (Courtesy of Professor E. Skin adverse effects related to ‘standard of care’ treatment of chronic HCV infectionThe ‘fingerprint detector’ effectThe combination of pegylated interferon ? (PEG-INF) and ribavirin (RBV), which is the current ‘standard of care’ (SOC) in the management of chronic HCV infection, has significantly improved the treatment outcome. Moreover, vast rates of patients are unable to tolerate antiviral therapy, and account for nearly 10% of premature treatment discontinuations [74, 75]. More specifically regarding skin adverse events (AEs), in a recent large-scale prospective study of 2871 Japanese patients, dermatologic undesired manifestations were the third most common reason for therapy withdrawal [75]. INF alone may give raise to a wide variety of cutaneous AEs, the frequency of which has been estimated from 13 to 23%, and the association with RBV has led to an increased incidence of skin AEs compared to those observed during INF monotherapy era [75-80].
By contrast, not local or generalized manifestations have to be linked to both agents, considering that the modes of action of INF and RBV are rather intermingled and their individual contribution seem thus quite undistinguishable.
Some reports are almost anecdotal, while the triad pruritus, skin xerosis and eczematous lesions are the principal hallmark of ‘hepatitis C treatment-associated dermatitis’ according to an in-depth review recently carried out by Lubbe and coworkers [81]. Pruritus is also generalized, and is not rarely refractory to standard antihistamine agents.
Eczema, which mainly affects the extensor aspects of limbs and sites exposed to friction (Figure 18 and 19), has been reported to sometimes take the appearance of so-called ‘nummular’ (discoid) eczema (Figure 20 and 21 or prurigo nodularis (Figure 22). As regards ‘eczema’, an extensive discussion of the vast archipelago of disease conditions which are currently collected under such term in the dermatological literature [82] is beyond the scope of the present textbook. Accordingly, histological hallmarks vary from epidermal oedema (‘spongiosis’), thickening of spinous and horny layers (‘acanthosis’ and ‘hyperkeratosis’, respectively) and more or less dense round cell infiltrates in the dermis.
Exogenous forms (also referred to as ‘contact dermatitis’) result from direct exposure of the skin surface to toxic agents (‘irritant contact dermatitis’) or allergens (‘allergic contact dermatitis’). As a counterpart, in the endogenous forms all the other forms of eczema (ranging from atopic eczema to so-called discoid or nummular eczema) which are not attributable to any recognizable contact offender, and whose pathomechanisms still remain largely obscure are to be included.

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