Published online Jul 28, 2016. doi: 10.3748/wjg.v22.i28.6444
Peer-review started: March 23, 2016
First decision: May 12, 2016
Revised: May 25, 2016
Accepted: June 15, 2016
Article in press: June 15, 2016
Published online: July 28, 2016
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The systemic therapies available for the management of Psoriasis (PsO) patients who cannot be treated with more conservative options, such as topical agents and/or phototherapy, with the exception of acitretin, can worsen or reactivate a chronic infection. Therefore, before administering immunosuppressive therapies with either conventional disease-modifying drugs (cDMARDs) or biological ones (bDMARDs) it is mandatory to screen patients for some infections, including hepatitis B virus (HBV) and hepatitis C virus (HCV). In particular, the patients eligible to receive an immunosuppressive drug must be screened for the following markers: antibody to hepatitis B core, antibody to hepatitis B surface antigen (anti-HBsAg), HBsAg, and antibody to HCV (anti-HCV). In case HBV or HCV infection is diagnosed, a close collaboration with a consultant hepatologist is needed before and during an immunosuppressive therapy. Concerning therapy with immunosuppressive drugs in PsO patients with HBV or HCV infection, data exist mainly for cyclosporine a (CyA) or bDMARDs (etanercept, adalimumab, infliximab, ustekinumab). The natural history of HBV and HCV infection differs significantly as well as the effect of immunosuppression on the aforementioned infectious diseases. As a rule, in the case of active HBV infection, systemic immunosuppressive antipsoriatic therapies must be deferred until the infection is controlled with an adequate antiviral treatment. Inactive carriers need to receive antiviral prophylaxis 2-4 wk before starting immunosuppressive therapy, to be continued after 6-12 mo from its suspension. Due to the risk of HBV reactivation, these patients should be monitored monthly for the first 3 mo and then every 3 mo for HBV DNA load together with transaminases levels. Concerning the patients who are occult HBV carriers, the risk of HBV reactivation is very low. Therefore, these patients generally do not need antiviral prophylaxis and the sera HBsAg and transaminases dosing can be monitored every 3 mo. Concerning PsO patients with chronic HCV infection their management with immunosuppressive drugs is less problematic as compared to those infected by HBV. In fact, HCV reactivation is an extremely rare event after administration of drugs such as CyA or tumor necrosis factor-α inhibitors. As a rule, these patients can be monitored measuring HCV RNA load, and ALT, aspartate transaminase, gamma-glutamyl-transferase, bilirubin, alkaline phosphatase, albumin and platelet every 3-6 mo. The present article provides an updated overview based on more recently reported data on monitoring and managing PsO patients who need systemic antipsoriatic treatment and have HBV or HCV infection as comorbidity.
Core tip: At present, no guidelines give clear indications regarding the management of psoriasis patients with concomitant hepatitis B or hepatitis C virus infection who need a systemic treatment. On the basis of the available literature data, this paper provides an overview in this field from a practical point of view. A particular emphasis is given, with regard to the use of biological drugs, in the aforementioned patients.
- Citation: Bonifati C, Lora V, Graceffa D, Nosotti L. Management of psoriasis patients with hepatitis B or hepatitis C virus infection. World J Gastroenterol 2016; 22(28): 6444-6455
- URL: https://www.wjgnet.com/1007-9327/full/v22/i28/6444.htm
- DOI: https://dx.doi.org/10.3748/wjg.v22.i28.6444
Psoriasis (PsO) is a frequent inflammatory immunomediated disease affecting approximately 2% of the population[1]. Various clinical types of psoriasis exist. The plaque-type, also known as psoriasis vulgaris (PV), is the most common form (80%-90% of the cases)[2]. Typical lesions of PV are represented by monomorphic, sharply demarcated erythematous plaques covered by silvery lamellar scales. From 70% to 80% of patients are affected by limited forms of PsO and need to be treated only with topical and or photo-therapy[2]. Patients with more extensive PsO (> 10% of the body surface area) or psoriatic arthritis (PsA) are in greater need of treatment. For these patients prolonged systemic therapies are often necessary[2-4].
The therapeutic armamentarium available for the cure of PsO encompasses the conventional disease-modifying drugs (cDMARDs) and biological DMARDs (bDMARDs) (Table 1).
Recommended doses for adult patients | |
Conventional DMARDs | |
Acitretine | 0.25-1 mg/kg per day |
Cyclosporin a | 2-5 mg/kg per day |
Methotrxate | 10 mg to 25 mg per week |
Biologic DMARDs | |
Infliximab | 5 mg/kg at 0, 2 and 6 wk followed by a maintenance regimen of 5 mg/kg every 8 wk |
Adalimumab | 80 mg initially, 40 mg on day 8, and 40 mg every other week thereafter |
Etanercept | 50 mg subcutaneously 2 times a week for 3 mo; (starting doses of 50 mg once a week have been shown to be effective); maintenance: 50 mg subcutaneously once a week |
Golimumab12 | 50 mg once a month |
Certolizumab pegol12 | 400 mg at 0, 2 and 4 wk followed by a maintenance regimen of 200 mg every other week |
Ustekinumab3 | 45 mg initially, 45 mg at 4 wk, followed by a maintenance regimen of 45 mg every 12 wk3 |
Secukinumab2 | 300 mg at 0, 1, 2, 3, and 4 wk followed by a maintenance regimen of 300 mg every 4 wk. For some patients, a dose of 150 mg may be acceptable |
cDMARDS represent the first line of therapies in high-need psoriatic patients, while bDMARDs are for those subjects in whom cDMARDs have either failed, were not tolerated, or were contraindicated[5-8].
The choice of a systemic treatment depends upon several variables linked to both the characteristics of a given patient and those of the drug administered.
Regarding the systemic treatments currently available for PsO, with the exception of acitretin, all the other drugs listed in Table 1 are immunosuppressive[9-11]. Therefore, the guidelines presently available, although with some differences among them, recommend screening PsO patients for some common infectious diseases [human immunodeficiency virus, latent tuberculosis, hepatitis B virus (HBV) and hepatitis C virus (HCV)] before starting an immunosuppressive treatment[12-18].
In particular, for HBV and HCV infection, screening for the following serologic markers should be evaluated: antibody to hepatitis B core (anti-HBc), antibody to hepatitis B surface antigen (anti-HBsAg), hepatitis B surface antigen (HBsAg) and antibody to HCV (anti-HCV)[12,15,18,19]. In case of detection of one or more markers of HBV infection the patients must be evaluated for the presence of HBV DNA in the sera[20]. If anti-HCV serum is detected, HCV RNA should be searched for by a sensitive method[20]. The existence of either HBV or HCV infection or both in PsO patients eligible for a systemic therapy poses a series of challenging problems. In particular, the administration of an immunosuppressive drug can alter the relationship between the host and the virus and worsen a coexisting chronic infection. Moreover, cDMARDs have different degrees of hepatic toxicity[9,11] therefore increasing the risk of worsening an already compromised liver as a consequence of the HBV or HCV infection.
PsO patients with infectious diseases such as HBV or HCV are excluded by the randomized controlled clinical trial. Therefore, data available on PsO patients with HBV or HCV infection, treated with systemic drugs, rely mainly on the reports of single cases or analyses of small groups of patients.
The aim of the present article is to describe how to manage and monitor PsO patients with HBV or HCV infection who need systemic antipsoriatic drugs.
The first aspect to consider in patients with severe PsO and concomitant HBV infection, is to define the phase of the latter disease[18-20] and the degree of possible liver damage. To do so, a close collaboration between dermatologist and hepatologist is needed[18-20].
As a rule, during the active phases of HBV infection, systemic anti-psoriatic therapies should be deferred. After an adequate control of infection, by means of anti HBV drugs is obtained[18-21], therapies should be started. Active HBV infection includes different phases[22-24] not necessarily sequential, such as: (1) acute infection (defined as new-onset HBV infection that may or may not be icteric or symptomatic); and (2) chronic (defined as the persistence of HBsAg for six months or more) and encompassing different phases (immune-tolerant, HbeAg-positive immune-active, HBeAg-negative immune reactivation).
Acitretin is the only drug that could be administered during the active phases of HBV infection. However, the administration of said drug should be reserved only for selected cases without a severe impairment of liver function.
In daily clinical practice the more frequent scenarios that can be encountered are represented by patients with serological markers indicative of a previous exposure to HBV, with low or undetectable viral load. In particular, these subjects can be in one of the following infectious phases: (1) inactive HBV infection [serum HBV DNA < 2000 IU/mL, normal alanin aminotransferase (ALT) levels, HBsAg present, antibody to hepatitis B envelope antigen (anti-HBeAg)] present, minimal liver necroinflammation but variable fibrosis); (2) occult HBV infection (serum HBV DNA < 200 IU/mL or undetectable, HbsAg negative, anti-HBc positive, anti-HBs negative); and (3) resolved HBV infection [(rHBV); anti-HBs positive ± anti-HBc]. Some confusion exists regarding the terms “occult carrier” and “rHBV”. In fact, some Authors define as “occult carriers” (or “potential occult carriers”) those patients who are indicated by other authors as rHBV and vice versa[22-27]. In this paper, the terms will be used following the above reported classification. The patients, whether inactive or occult carriers or with rHBV, can be at risk of HBV reactivation (defined as the sudden increase in HBV replication) after starting an immunosuppressive therapy[28]. As expected, the risk is significantly greater in the inactive carriers as compared to occult ones. Even more rare is the case of viral reactivation in rHBV[29]. The possible occurrence of one of the three previously mentioned infectious phases in a given PsO patient, raises some problems regarding their therapeutic management. In particular: (1) which drug can be safely administered? (2) which patients need anti HBV prophylaxis to prevent HBV reactivation? And (3) which serological markers should be monitored after an antipsoriatic therapy is started?
To answer these questions the cDMARDs and bDMARDs must be analyzed separately.
Acitretin: Acitretin administration is considered, due to its potential hepatotoxicity, a relative contraindication in hepatitis resulting from viral infections[18]. However, acitretin (preferably in association with ultraviolet B therapy) can be a possible option in those subjects without significant signs of liver damage as revealed by serological [ALT, aspartate transaminase (AST), gamma-glutamyl-transferase (GGT), bilirubin, alkaline phosphatase] and instrumental (ultrasonography, fibroscan) methods. Unfortunately, the effectiveness of acitretin as monotherapy and its side-effects (teratogenicity, mucosal dryness, hypertriglyceridemia) other than the potential hepatic toxicity[30] limits its use in many patients.
Cyclosporin a: The current dermatologic guidelines on the management of psoriatic disease do not give clear indications regarding the use of cyclosporin a (CyA) in patients with PsO and concomitant HBV infection[18]. The only reports of HBV reactivation concern severe immunosuppressed subjects such as renal transplant recipients and hematological patients[31,32].
In a cohort of patients with rheumatoid arthritis (RA) who were anti-HBc positive and/or anti-HBs positive (defined by the Authors as resolved HBV infection) treated with either cDMARDs and or bDMARDs, CyA did not result associated with an activation of HBV infection[33]. However, the potential risks of HBV reactivation should not be underestimated also using the relatively low doses of CyA as those usually given to PsO patients. Lacking clear indications, and on the basis of our personal experience, we believe that CyA could be administered to patients who are HBV occult carriers or with rHBV if adequately monitored (see below).
Methotrexate: Data available on the use of methotrexate (MTX) in patients with HBV infection were gathered from patients with rheumatologic or inflammatory bowel disease[34,35]. Whether or not MTX can be safely administered to patients with a history of HBV infection is not clear[34,36].
Basically, in the dermatological field, the different guidelines agree on avoiding MTX therapy in all patients whose seromarkers indicate an exposition to HBV[12,18,37].
TNF inhibitors: There is evidence from experimental models that TNF plays a critical role in HBV clearance from infected hepatocytes[38]. Therefore, a detrimental effect is expected in terms of worsening or reactivation of HBV infection in subjects treated with TNF inhibitors (TNFis).
Over the past years several cases of HBV reactivation have been reported with either infliximab (IFX), adalimumab (ADA) or etanercept (ETA) therapy, mainly in patients with rheumatologic inflammatory diseases or inflammatory bowel disease[21,39,40].
Whether or not different TNFis carry a different risk of HBV reactivation is currently not clear[41]. Some studies suggest a major risk of HBV reactivation for IFX as compared to other TNFis[21].
Presently, literature data regarding the administration of TNFis in PsO or PsA subjects with concomitant HBV infection is available for 200 patients[42-56]. The majority of subjects reported are inactive or occult carriers, or with rHBV.
On the whole, patients were treated for a period ranging from 24 wk[43] to 6 years[52]. The TNFi more frequently administered was ETA, followed by ADA and finally IFX.
In Table 2 are summarized the cases of PsO and/or PsA grouped in: (1) inactive carriers; and (2) occult carriers or rHBv. The cases shown in Table 2, are limited to those for whom there was sufficient information in each report to permit their inclusion in one of the two above cited groups.
Ref. | Diagnosis, n | Inactive carriers (HBsAg+), n | Occult carriers or resolved HBV (anti-HBc+, anti-HBs- or anti-HBs ± anti-HBc), n | Prophylaxis2, n | Reactivation, n |
Charpin et al[42] | PsA, 5 | 0 | 5 | 0 | 0 |
Prestinari et al[43] | PsO, 1 | 0 | 1 | 0 | 0 |
Nosotti et al[44] | PsO, 4; PsA, 3 | 1 | 6 | 1 (Lamivudine) | 0 |
Caporali et al[45] | PsA, 4 | 0 | 4 | 0 | 0 |
Kim et al[46] | PsA, 2 | 0 | 2 | 0 | 0 |
Fotadiou et al[47] | PsO, 7 | 7 | 0 | 7 (Lamivudine) | 0 |
Prignano et al[48] | PsO, 12 | 0 | 12 | 0 | 0 |
Cassano et al[49] | PsO, 28; PsA, 34 | 0 | 62 | 0 | 0 |
Cho et al[50] | PsA, 2 | 2 | 0 | 0 | 1 |
Navarro et al[51] | PsO, 13 | 0 | 13 | 0 | 0 |
Laurenti et al[52] | PsA, 8 | 1 | 7 | 1 (Lamivudine) | 0 |
Navarro et al[53] | PsO, 4 | 4 | 0 | 3 (Lamivudine); 1 (adefovir2 entecavir) | 0 |
1Sanz-Bueno et al[54] | PsO, 20 | 0 | 20 | 0 | 0 |
As shown in Table 2, none of the patients who were occult carriers or with rHBV experienced an HBV reactivation during TNFis therapy. None of the above cited subjects received antiviral prophylaxis.
Concerning patients who were inactive carriers, none of those who received antiviral prophylaxis experienced an HBV reactivation. On the contrary, HBV reactivation has been reported only in one case of an inactive carrier who did not receive antiviral prophylaxis (Table 2). In addition, two other patients of the same series with chronic HBV, who did not take prophylaxis, had viral reactivation[50].
Regarding the use of TNFis in PsO with active HBV infection only one case has been reported so far[57]. Said subject received lamivudine therapy one month before starting IFX. This therapy was continued during treatment with TNFi for 6 mo with a significant improvement of PsO and a decrease of both viral load and transaminases. Thereafter, to obtain a better control of viral replication, lamivudine was substituted with enetecavir and at the 9th month a further decrease of viral load was recorded, transaminases levels being within normal range and PsO under control.
Ustekinumab: Ustekinumab (UTK) is a fully human immunoglobulin G1k monoclonal antibody, anti-IL12p40, which binds to the shared p40 subunit of IL-12 and IL-23 with high affinity and specificity[8]. Because IL-12 plays a key role in triggering an effective cellular immune response directed towards the elimination of intracellular pathogens[58,59] its inhibition can contribute to HBV reactivation.
From 2013, 28 cases of PsO with concomitant HBV infection have been treated with UTK[53,54,60-62]. The duration of treatments ranged from 4 mo[60] to 3 years[63].
In Table 3, 22 out of the 28 above cited patients are shown, since 6 subjects belong to the case series reported by Sanz-Bueno et al[54] and included in Table 2.
Ref. | Diagnosis, n | Inactive carriers (HBsAg+), n | Occult carriers or resolved HBV (anti-HBc+, anti-HBs- or anti-HBs ± anti-HBc), n | Prophylaxis1, n | Reactivation, n |
Navarro et al[53] | PsO 1 | 1 | 0 | 1 (Entecavir) | 0 |
Chiu et al[60] | PsO 14 | 112 | 3 | 4 (Entecavir) | 2 |
Hayashi et al[61] | PsO 5 | 0 | 5 | 0 | 0 |
Koskinas et al[62] | PsO 1 | 0 | 1 | 0 | 1 |
Steglich et al[63] | PsO 1 | 0 | 1 | 1 (Lamivudine) | 0 |
At present the lack of data does not permit us to draw any conclusions about the safety of UTK in patients with HBV infection.
However, as shown in Table 3, 2 of the 11 inactive carriers and one patient with rHBV experienced a reactivation of HBV infection after 4 mo, 7 mo and 16 wk, respectively[60,62]. Antiviral prophylaxis was not administered to said subjects.
On the basis of the above reported data, it is clear that HBV infection does not represent a barrier to the administration of an immunosuppressive therapy in patients with severe PsO. However, when a patient is eligible to a long-lasting immunosuppressive therapy such as bDMARDs, the risk of HBV reactivation must be taken into account.
It is widely accepted that all subjects who are inactive carriers need an antiviral prophylaxis[10,38-40]. The latter should be started 2-4 wk before a bDMARD is given and continued for 6-12 mo after its suspension[10,38-40]. Concerning the type of antiviral drug to be administered, the American Gastroenterology Association (AGA) suggests a third generation nucleos(t)ide (entecavir or tenofovir) due to their high resistance to lamivudine[64].
Whether or not patients who are occult carriers or with rHBV infection should receive antiviral prophylaxis is a debatable issue[10,38-40,64]. The recent AGA guidelines suggest administering antiviral prophylaxis also in patients who are HbsAg-negative/anti-HBc positive (whether or not anti-HBs positive) treated with either TNFis or UTK[64]. However, in the context of PsO treatment with bDMARDs patients do not seem to carry a concrete risk of HBV reactivation. Therefore, in the above mentioned category of patients prophylaxis against HBV reactivation is probably not necessary[10,44].
Regarding patients who are inactive carriers, considering the risk of HBV reactivation during therapy with a bDMARD, HBV DNA, ALT and AST, serum levels should be monitored monthly for the first 3 mo, then quarterly and continued after 6-12 mo of discontinuation of the aforementioned treatment[10,44]. More controversial is whether or not to measure HBV DNA serum levels in those PsO or PsA patients who are occult carriers or with rHBV treated withimmunosuppressive drugs (CyA or bDMARDs)[10,40,44]. As already stated above, said patients do not seem to run a concrete risk of HBV reactivation. Moreover, the measurement of viral load is an expensive test. Therefore, occult carriers as well as patients with rHBV, can be monitored every 3 mo, checking for the presence in the serum of HBsAg in conjunction with the measurement of ALT and AST levels[10,44]. Monitoring should be continued with the same above cited timing after 6-12 mo from the discontinuation of the immunosuppressive therapy.
After acute HCV infection occurs, from 15% to 25% of subjects spontaneously clear viremia while 75% to 85% of individuals develop chronic HCV infection[65].The diagnosis of this last condition is based on the detection of both HCV antibodies and HCV RNA in the presence of signs of chronic hepatitis, either by elevated aminotransferases or by histology[66]. For the majority of patients the course of chronic HCV infections is benign. However, from 10% to 20% of subjects develop cirrhosis, generally in a time gap from 20 to 30 years[65]. It has been estimated that each year 1% to 4% of patients with HCV related cirrhosis will develop hepatocellular carcinoma (HCC), and 20% will further progress to decompensated cirrhosis[65].
In contrast to HVB, HCV reactivation is not very common[67]. However, when HCV reactivation occurs, its morbidity and mortality rates are similar to those of HBV reactivation[20].
Concerning the treatment of PsO patients with concomitant HCV infection, a relatively limited number of data are available.
Among cDMARDs, acitretin and CyA could be two possible options while MTX is in general contraindicated for its substantial risk of hepatic toxicity[9,12,17,18]. Among bDMARDs, TNFis seems to be a relatively safe option (see below).
Very few data are at present available concerning the management with UTK of HCV infected patients since this biologic was introduced on the market several years after TNFis. Moreover, the use of UTK is presently approved only for PsO and PsA patients.
In the past, CyA has been considered by some Authors as third line as compared to TNFis in PsO subjects with HCV infection[67].
However, several data indicate that both CyA and TNFis do not seem to cause different risks in worsening the chronic course of HCV infection[68-72].
CyA and bDMARDs are probably the more frequently administered drugs for high-need PsO patients with concomitant HCV infection.
No data are currently available concerning the concomitant administration of systemic therapies for PsO and the new direct-acting antiviral medications approved for the treatment of chronic HCV infection.
In the following paragraphs treatment with CyA or bDMARDs of PsO patients with HCV infection are described.
CyA: Due to immunosuppresive activity, a detrimental effect of CyA in individuals with a chronic infection such as HCV, could be expected. However, experimental and clinical data indicate that CyA, in addition to its anti-inflammatory activity, can inhibit HCV viral replication[73]. In particular, this last effect has been found in patients carrying genotype 1 or 4 HCV[71,72]. However, also in patients carrying genotype 2, which is scarcely sensitive to antiviral effect of CyA, no worsening of HCV infection has been observed in spite of a favourable clinical course of their immunomediated diseases[72]. Said data clearly indicate that immunosuppressive and antiviral activity of CyA follow different pathways[73].
Current available literature data on PsO patients with concomitant HCV infection treated with low dose of CyA include 11 patients, 7 of whom affected by PsA[69-72,74]. These patients received CyA for a period ranging from 16 to 38 mo and none experienced a worsening of their HCV infection. In some patients a lowering of HCV RNA serum levels has been reported[69].
TNFis: Data available concerning the management with TNFis of PsO patients with HCV infection are increasing.
TNF-α is a key cytokine in stimulating immunomediated response to infections, especially against intracellular pathogens. Therefore, after inhibition of TNF-α, a worsening of a viral infection such as HCV could be expected. However, experimental and clinical data suggest that increased levels of TNF-α can have a detrimental effect on HCV infection[75-77]. In particular, the aforementioned cytokine seems to reduce cell capabilityto respond to interferon (IFN) signalling and, consequently, impair viral clearance[76]. Moreover, a direct correlation between elevated levels of TNF-α and those of ALT has been reported, with increased TNF-α levels having more severe histological activity[75,77]. A further indication that decreasing TNF-α concentrations can play a favourable effect on HCV infection comes from a study in which etanercept was administered as adjuvant to IFN and ribavirin in a group of HCV infected patients[78]. These subjects showed a higher decline of viral load and ALT as compared to the placebo group.
In addition to the data above reported, further observations indicate that TNFis can be safely administered to patients with different immune-mediated diseases and concomitant HCV infection[39,40,79]. In particular, in most of said patients viral load remained stable or decreased[39,40,79]. Serum HCV RNA increase > 1 log above baseline was rarely recorded and could not be confidently attributed to TNFis.
At present, 45 PsO and 33 PsA patients with concomitant HCV infection have been treated with TNFis[48,53,80-106]. Diagnosis, ALT and viral load outcomes at the last follow-up of the mentioned subjects are shown in Table 4. Of all the patients reported, 66 received a single TNFi (56 ETA, 9 ADA, 1 IFX). Six patients were treated sequentially with 2 TNFIs (1 with IFX and then ADA, 4 with ETA and then ADA and 1 with ETA and then IFX). One patient was treated sequentially with 3 TNFis (ETA followed by IFXand then ADA).
Ref. | Diagnosis, n | Concomitant HCV therapy, n | ALT outcomes at last follow-up compared to baseline, n | HCV viral load outcome at last follow-up compared to baseline, n |
Khanna et al[80] | PsA, 1 | 1 (N/A) | 1 (N/A) | 1 (N/A) |
Magliocco et al[81] | PsA, 3 | 0 | 3 (=) | 2 (↓); 1(N/A) |
Cecchi et al[82] | PsO, 1 | 0 | 1 (=) | 1 (=) |
De Simone et al[83] | PsO, 2 | 0 | 2 (=) | 2 (↓) |
Asladinis et al[84] | PsA, 1 | 0 | 1 (=) | 1 (↓) |
Rokshar et al[85] | PsO, 1 | 0 | 1 (N/A) | 1 (=) |
Pitarch et al[86] | PsA, 1 | 1 (N/A) | 1 (=) | 1 (N/A) |
Linadarki et al[87] | PsA, 1 | 0 | 1 (=) | 1 (=) |
Alcaide et al[88] | PsO, 1 | 0 | 1 (=) | 1 (=) |
Piccolo et al[89] | PsO, 1 | 0 | 1 (↑) | 1 (↓) |
Collazzo et al[90] | PsO, 1 | 0 | 1 (=) | 1 (N/A) |
Cassano et al[91] | PsO, 1 | 0 | 1 (=) | 1 (=) |
Cavazzana et al[92] | PsA, 1 | 0 | 1 (=) | 1 (=) |
Behnam et al[93] | PsO, 1 | 1 (IFN + Rib) | 1 (↓) | 1 (↓) |
Ventura et al[94] | PsO, 1; PsA, 1 | 0 | 2 (↓) | 1 (↑); 1 (↓) |
Paradisi et al[95] | PsA, 2 | 0 | 2 (=) | 2 (=) |
Prignano et al[96] | PsO, 1 | 0 | 1 (N/A) | 1 (=) |
Richetta et al[97] | PsO, 11 | 0 | 1 (N/A) | 1 (N/A) |
Garavaglia et al[98] | PsO, 3; PsA, 2 | 1 (IFN + Rib) | 1 (=); 4 (↓) | 3 (=); 1 (↓) |
Gandhi et al[99] | PsO, 1 | 0 | 1 (↓) | 1 (↓) |
Di Lernia et al[100] | PsO, 13 | 0 | 1 (=) | 1 (=) |
Zanni et al[101] | PsA, 3 | 0 | 3 (=)4 | 3 (=) |
Prignano et al[48] | PsO, 6 | 0 | 6 (=) | 6 (=) |
Mederacke et al[102] | PsA, 1 | 1 (IFN + Rib) | 1 (N/A) | 1 (↓) |
Navarro et al[53] | PsO, 202 | 3 (IFN + Rib) | See references | See references |
Bartalesi et al[103] | PsO, 1 | 1 (IFN + Rib) | 1 (↓) | 1 (↓) |
Costa L et al[104] | PsA, 15 | 0 | 13 (=); 2 (↓) | 14 (=); 1 (↓) |
Di Nuzzo et al[105] | PsA, 2 | 1 (IFN + Rib) | 1 (=); 1 (↓) | 2 (↓) |
Salvi et al[106] | PsO, 1 | 0 | 1 (↑) | 1 (=) |
The duration of TNFis was highly variable ranging from 1 to 48 mo[97,105].
At baseline, liver biopsy specimens were available from 16 patients which revealed various grades of fibrosis ranging from F0 to F4[81-85,87,95,96,99,101-103]. Of said subjects only 2 underwent a second liver biopsy control which showed no significant histological changes compared to pretreatment findings[95].
As shown in Table 4, in the majority of the patients described, ALT and HCV RNA viral load remained unchanged or declined during TNFis therapy.
On the whole, the safety profile of TNFis appears to be reasonably good inPsO patients with concomitant HCV infection even if 4 cases of hepatocelluar carcinoma (HCC) were recorded[53,105]. However, 3 out of 4 said patients were affected by cirrhosis and it is impossible to draw any conclusion regarding a possible role of TNF inhibition in the appearance of the above cited HCC.
UTK: Concerning IL 12 and IL 23, both targeted by UTK, little is known about their activity in HCV infection. Presently available data suggest that IL-12 can have a relevant role against HCV in either acute or chronic phases of infection[57,107,108].
At present, seven patients with PsO and HCV infection have been treated with UTK. Abuchar et al[109] in 2013, described the case of one patient with erythrodermic PsO and HCV infection who, after 2 mo of UTK therapy, experienced a very good response regarding his PsO without worsening of HCV infection.
Chiu et al[60] reported their experience on 4 PsO patients with HCV infection who received UTK for a period ranging from 5 to 11 mo. During the follow-up period, HCV viral copy numbers increased in 3 cases with only one subject meeting the criterion of HCV reactivation, recorded after 1 mo of UTK therapy. This last patient, who at baseline had a diagnosis of cirrhosis and previous HCC experienced a recurrence of HCC after 4 mo of UTK treatment.
Navarro et al[53], in a study published in 2013, reported that two PsO patients with concomitant HCV infection received UTK for 16 and 12 mo, respectively. The first patient, at the end of follow-up, showed a decrease of viral load and slight increase of both ALT and AST. In the second patient at the end of follow-up, viral load remained unchanged with a slight decrease of both ALT and AST serum levels.
More data are needed to better define whether or not UTK can have a role in the treatment of PsO patients with HCV infection.
No guidelines are currently available on how to monitor PsO patients with HCV infection during treatment with CyA or bDMARDs.
Monitoring liver function tests (ALT, AST, alkaline phosphatase, bilirubin, albumin and platelet) and HCV-RNA load every 3-6 mo could be a valuable option for the majority of the patients.
However, it is important to point out that an optimal follow-up of the above-cited patients requires a strict collaboration with a consultant hepatologist. This latter will decide the timing of instrumental examinations, whether or not to perform a liver biopsy and whether or not to offer a prophylactic anti-viral treatment.
HBV and HCV are the pathogens which more frequently cause chronic hepatitis[110].
Only few studies have evaluated the prevalence of the above-cited infectious disease in the PsO population. In 2011, Yang et al[111] reported an increased prevalence of HBV and HCV in PsO Taiwanese patients. In 2010, Cohen et al[112] in their study performed in Israel found an increased prevalence of HBC but not of HBV in PsO compared to control. The different frequency of HBV and HCV infection, as well as of PsO worldwide, can account for the discrepancies among the data published so far.
The chance to encounter in clinical practice PsO patients in high need of treatment who are HBV or HCV infected, should not be underestimated. Concerning said issue all current guidelines recommend screening PsO patients eligible for an immunosuppressive therapy due to the presence of HBV and HCV infection. However, no guidelines presently available give indications on how to manage and monitor these patients. Notwithstanding the above-cited limitations, immunosuppressive therapies should not be an insurmountable barrier for subjects with severe PsO and concomitant chronic HBV or HCV infection.
As already stated in this paper, it is essential that the aforementioned patients be referred to a hepatologist for expert clinical management.
Manuscript Source: Invited manuscript
Specialty Type: Gastroenterology and Hepatology
Country of Origin: Italy
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P- Reviewer: Gonzalez-Reimers E, Harmanci O S- Editor: Ma YJ L- Editor: A E- Editor: Ma S
1. | Christophers E. Psoriasis--epidemiology and clinical spectrum. Clin Exp Dermatol. 2001;26:314-320. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 577] [Cited by in F6Publishing: 555] [Article Influence: 24.1] [Reference Citation Analysis (0)] |
2. | Boehncke WH, Schön MP. Psoriasis. Lancet. 2015;386:983-994. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 1395] [Cited by in F6Publishing: 1626] [Article Influence: 180.7] [Reference Citation Analysis (0)] |
3. | Finlay AY. Current severe psoriasis and the rule of tens. Br J Dermatol. 2005;152:861-867. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 243] [Cited by in F6Publishing: 253] [Article Influence: 13.3] [Reference Citation Analysis (0)] |
4. | Mrowietz U, Kragballe K, Reich K, Spuls P, Griffiths CE, Nast A, Franke J, Antoniou C, Arenberger P, Balieva F. Definition of treatment goals for moderate to severe psoriasis: a European consensus. Arch Dermatol Res. 2011;303:1-10. [PubMed] [Cited in This Article: ] |
5. | European Medicines Agency. Find medicine - Humira [Humira: EPAR - Product Information]. 2014; Available from: http://www.ema.europa.eu/docs/en_GB/document_library/EPAR_-Product_Information/human/000481/WC500050870.pdf. [Cited in This Article: ] |
6. | European Medicines Agency. Find medicine - Enbrel [Enbrel: EPAR - Product Information]. 2015; Available from: http://www.ema.europa.eu/docs/en_GB/document_library/EPAR__Product_Information/human/000262/WC500027361.pdf. [Cited in This Article: ] |
7. | European Medicines Agency. Find medicine - Remicade [Remicade: EPAR - Product Information]. 2014; Available from: http://www.ema.europa.eu/docs/en_GB/document_library/EPAR_-_Product_Information/human/000240/WC500050888.pdf. [Cited in This Article: ] |
8. | European Medicines Agency. Find medicine - Stelara [Stelara: EPAR - Product Information]. 2014; Available from: http://www.ema.europa.eu/docs/en_GB/document_library/EPAR_- _Product_Information/human/000958/WC500058513.pdf. [Cited in This Article: ] |
9. | Czarnecka-Operacz M, Sadowska-Przytocka A. The possibilities and principles of methotrexate treatment of psoriasis - the updated knowledge. Postepy Dermatol Alergol. 2014;31:392-400. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 44] [Cited by in F6Publishing: 46] [Article Influence: 4.6] [Reference Citation Analysis (0)] |
10. | Koutsianas C, Thomas K, Vassilopoulos D. Prevention of HBV reactivation in patients treated with biologic agents. Expert Rev Clin Pharmacol. 2016; Epub ahead of print. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 7] [Cited by in F6Publishing: 8] [Article Influence: 1.0] [Reference Citation Analysis (0)] |
11. | Booij MT, Van De Kerkhof PC. Acitretin revisited in the era of biologics. J Dermatolog Treat. 2011;22:86-89. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 28] [Cited by in F6Publishing: 28] [Article Influence: 2.0] [Reference Citation Analysis (0)] |
12. | Hsu S, Papp KA, Lebwohl MG, Bagel J, Blauvelt A, Duffin KC, Crowley J, Eichenfield LF, Feldman SR, Fiorentino DF. Consensus guidelines for the management of plaque psoriasis. Arch Dermatol. 2012;148:95-102. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 121] [Cited by in F6Publishing: 128] [Article Influence: 10.7] [Reference Citation Analysis (0)] |
13. | Nast A, Boehncke WH, Mrowietz U, Ockenfels HM, Philipp S, Reich K, Rosenbach T, Sammain A, Schlaeger M, Sebastian M. S3 - Guidelines on the treatment of psoriasis vulgaris (English version). Update. J Dtsch Dermatol Ges. 2012;10 Suppl 2:S1-95. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 198] [Cited by in F6Publishing: 210] [Article Influence: 17.5] [Reference Citation Analysis (0)] |
14. | Smith CH, Anstey AV, Barker JN, Burden AD, Chalmers RJ, Chandler DA, Finlay AY, Griffiths CE, Jackson K, McHugh NJ. British Association of Dermatologists’ guidelines for biologic interventions for psoriasis 2009. Br J Dermatol. 2009;161:987-1019. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 324] [Cited by in F6Publishing: 347] [Article Influence: 24.8] [Reference Citation Analysis (0)] |
15. | Motaparthi K, Stanisic V, Van Voorhees AS, Lebwohl MG, Hsu S. From the Medical Board of the National Psoriasis Foundation: Recommendations for screening for hepatitis B infection prior to initiating anti-tumor necrosis factor-alfa inhibitors or other immunosuppressive agents in patients with psoriasis. J Am Acad Dermatol. 2014;70:178-186. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 48] [Cited by in F6Publishing: 51] [Article Influence: 4.6] [Reference Citation Analysis (0)] |
16. | Abramson A, Menter A, Perrillo R. Psoriasis, hepatitis B, and the tumor necrosis factor-alpha inhibitory agents: a review and recommendations for management. J Am Acad Dermatol. 2012;67:1349-1361. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 33] [Cited by in F6Publishing: 37] [Article Influence: 3.1] [Reference Citation Analysis (0)] |
17. | Menter A, Gottlieb A, Feldman SR, Van Voorhees AS, Leonardi CL, Gordon KB, Lebwohl M, Koo JY, Elmets CA, Korman NJ. Guidelines of care for the management of psoriasis and psoriatic arthritis: Section 1. Overview of psoriasis and guidelines of care for the treatment of psoriasis with biologics. J Am Acad Dermatol. 2008;58:826-850. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 869] [Cited by in F6Publishing: 907] [Article Influence: 56.7] [Reference Citation Analysis (0)] |
18. | Nast A, Gisondi P, Ormerod AD, Saiag P, Smith C, Spuls PI, Arenberger P, Bachelez H, Barker J, Dauden E. European S3-Guidelines on the systemic treatment of psoriasis vulgaris--Update 2015--Short version--EDF in cooperation with EADV and IPC. J Eur Acad Dermatol Venereol. 2015;29:2277-2294. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 299] [Cited by in F6Publishing: 304] [Article Influence: 33.8] [Reference Citation Analysis (0)] |
19. | Ahn CS, Dothard EH, Garner ML, Feldman SR, Huang WW. To test or not to test? An updated evidence-based assessment of the value of screening and monitoring tests when using systemic biologic agents to treat psoriasis and psoriatic arthritis. J Am Acad Dermatol. 2015;73:420-428.e1. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 27] [Cited by in F6Publishing: 28] [Article Influence: 3.1] [Reference Citation Analysis (0)] |
20. | Bojito-Marrero L, Pyrsopoulos N. Hepatitis B and Hepatitis C Reactivation in the Biologic Era. J Clin Transl Hepatol. 2014;2:240-246. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 2] [Cited by in F6Publishing: 6] [Article Influence: 0.6] [Reference Citation Analysis (0)] |
21. | Pérez-Alvarez R, Díaz-Lagares C, García-Hernández F, Lopez-Roses L, Brito-Zerón P, Pérez-de-Lis M, Retamozo S, Bové A, Bosch X, Sanchez-Tapias JM. Hepatitis B virus (HBV) reactivation in patients receiving tumor necrosis factor (TNF)-targeted therapy: analysis of 257 cases. Medicine (Baltimore). 2011;90:359-371. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 219] [Cited by in F6Publishing: 199] [Article Influence: 15.3] [Reference Citation Analysis (0)] |
22. | WHO. Guidelines for the prevention, care and treatment of persons with chronic hepatitis B infection. Geneva Switzerland: World Health Organization 2015; . [Cited in This Article: ] |
23. | Terrault NA, Bzowej NH, Chang KM, Hwang JP, Jonas MM, Murad MH. AASLD guidelines for treatment of chronic hepatitis B. Hepatology. 2016;63:261-283. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 1532] [Cited by in F6Publishing: 1486] [Article Influence: 185.8] [Reference Citation Analysis (2)] |
24. | European Association For The Study Of The Liver. EASL clinical practice guidelines: Management of chronic hepatitis B virus infection. J Hepatol. 2012;57:167-185. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 2323] [Cited by in F6Publishing: 2352] [Article Influence: 196.0] [Reference Citation Analysis (0)] |
25. | Marzano A, Angelucci E, Andreone P, Brunetto M, Bruno R, Burra P, Caraceni P, Daniele B, Di Marco V, Fabrizi F. Prophylaxis and treatment of hepatitis B in immunocompromised patients. Dig Liver Dis. 2007;39:397-408. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 160] [Cited by in F6Publishing: 155] [Article Influence: 9.1] [Reference Citation Analysis (0)] |
26. | López-Serrano P, Pérez-Calle JL, Sánchez-Tembleque MD. Hepatitis B and inflammatory bowel disease: role of antiviral prophylaxis. World J Gastroenterol. 2013;19:1342-1348. [PubMed] [DOI] [Cited in This Article: ] [Cited by in CrossRef: 23] [Cited by in F6Publishing: 22] [Article Influence: 2.0] [Reference Citation Analysis (0)] |
27. | López-Serrano P, de la Fuente Briongos E, Alonso EC, Pérez-Calle JL, Rodríguez CF. Hepatitis B and immunosuppressive therapies for chronic inflammatory diseases: When and how to apply prophylaxis, with a special focus on corticosteroid therapy. World J Hepatol. 2015;7:539-547. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 12] [Cited by in F6Publishing: 11] [Article Influence: 1.2] [Reference Citation Analysis (0)] |
28. | Hoofnagle JH. Reactivation of hepatitis B. Hepatology. 2009;49:S156-S165. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 412] [Cited by in F6Publishing: 405] [Article Influence: 27.0] [Reference Citation Analysis (0)] |
29. | Cantini F, Boccia S, Goletti D, Iannone F, Leoncini E, Panic N, Prignano F, Gaeta GB. HBV Reactivation in Patients Treated with Antitumor Necrosis Factor-Alpha (TNF-α) Agents for Rheumatic and Dermatologic Conditions: A Systematic Review and Meta-Analysis. Int J Rheumatol. 2014;2014:926836. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 46] [Cited by in F6Publishing: 52] [Article Influence: 5.2] [Reference Citation Analysis (0)] |
30. | Ormerod AD, Campalani E, Goodfield MJ. British Association of Dermatologists guidelines on the efficacy and use of acitretin in dermatology. Br J Dermatol. 2010;162:952-963. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 85] [Cited by in F6Publishing: 90] [Article Influence: 6.4] [Reference Citation Analysis (0)] |
31. | Sandrini S, Callea F, Cristinelli L, Savoldi S, Setti G, Scaini P, Scolari F, Scalzini A, Pizzoccolo G, Maiorca R. Viral hepatitis in HBsAg-positive renal transplant patients treated with cyclosporin and steroids. Nephrol Dial Transplant. 1990;5:525-530. [PubMed] [Cited in This Article: ] |
32. | Dai MS, Kao WY, Shyu RY, Chao TY. Restoration of immunity and reactivation of hepatitis B virus after immunosuppressive therapy in a patient with severe aplastic anaemia. J Viral Hepat. 2004;11:283-285. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 14] [Cited by in F6Publishing: 16] [Article Influence: 0.8] [Reference Citation Analysis (0)] |
33. | Urata Y, Uesato R, Tanaka D, Kowatari K, Nitobe T, Nakamura Y, Motomura S. Prevalence of reactivation of hepatitis B virus replication in rheumatoid arthritis patients. Mod Rheumatol. 2011;21:16-23. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 34] [Cited by in F6Publishing: 63] [Article Influence: 4.5] [Reference Citation Analysis (0)] |
34. | Oshima Y, Tsukamoto H, Tojo A. Association of hepatitis B with antirheumatic drugs: a case-control study. Mod Rheumatol. 2013;23:694-704. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 4] [Cited by in F6Publishing: 12] [Article Influence: 1.0] [Reference Citation Analysis (0)] |
35. | Alfadhli AA, McDonald JW, Feagan BG. Methotrexate for induction of remission in refractory Crohn’s disease. Cochrane Database Syst Rev. 2005;CD003459. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 34] [Cited by in F6Publishing: 57] [Article Influence: 3.0] [Reference Citation Analysis (0)] |
36. | Laohapand C, Arromdee E, Tanwandee T. Long-term use of methotrexate does not result in hepatitis B reactivation in rheumatologic patients. Hepatol Int. 2015;9:202-208. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 28] [Cited by in F6Publishing: 30] [Article Influence: 3.3] [Reference Citation Analysis (0)] |
37. | Kalb RE, Strober B, Weinstein G, Lebwohl M. Methotrexate and psoriasis: 2009 National Psoriasis Foundation Consensus Conference. J Am Acad Dermatol. 2009;60:824-837. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 221] [Cited by in F6Publishing: 199] [Article Influence: 13.3] [Reference Citation Analysis (0)] |
38. | Calabrese LH, Zein NN, Vassilopoulos D. Hepatitis B virus (HBV) reactivation with immunosuppressive therapy in rheumatic diseases: assessment and preventive strategies. Ann Rheum Dis. 2006;65:983-989. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 159] [Cited by in F6Publishing: 171] [Article Influence: 9.5] [Reference Citation Analysis (0)] |
39. | Sansone S, Guarino M, Castiglione F, Rispo A, Auriemma F, Loperto I, Rea M, Caporaso N, Morisco F. Hepatitis B and C virus reactivation in immunosuppressed patients with inflammatory bowel disease. World J Gastroenterol. 2014;20:3516-3524. [PubMed] [DOI] [Cited in This Article: ] [Cited by in CrossRef: 29] [Cited by in F6Publishing: 26] [Article Influence: 2.6] [Reference Citation Analysis (0)] |
40. | Viganò M, Degasperi E, Aghemo A, Lampertico P, Colombo M. Anti-TNF drugs in patients with hepatitis B or C virus infection: safety and clinical management. Expert Opin Biol Ther. 2012;12:193-207. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 69] [Cited by in F6Publishing: 76] [Article Influence: 5.8] [Reference Citation Analysis (0)] |
41. | Lee YH, Bae SC, Song GG. Hepatitis B virus reactivation in HBsAg-positive patients with rheumatic diseases undergoing anti-tumor necrosis factor therapy or DMARDs. Int J Rheum Dis. 2013;16:527-531. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 77] [Cited by in F6Publishing: 77] [Article Influence: 7.7] [Reference Citation Analysis (0)] |
42. | Charpin C, Guis S, Colson P, Borentain P, Mattéi JP, Alcaraz P, Balandraud N, Thomachot B, Roudier J, Gérolami R. Safety of TNF-blocking agents in rheumatic patients with serology suggesting past hepatitis B state: results from a cohort of 21 patients. Arthritis Res Ther. 2009;11:R179. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 73] [Cited by in F6Publishing: 79] [Article Influence: 5.3] [Reference Citation Analysis (0)] |
43. | Prestinari F, Ferguglia G, Laria G. Etanercept in a patient with severe psoriasis and latent viral hepatic disease and latent tuberculosis. Am J Clin Dermatol. 2010;11 Suppl 1:57-58. [PubMed] [DOI] [Cited in This Article: ] [Cited by in F6Publishing: 1] [Reference Citation Analysis (0)] |
44. | Nosotti L, Francesconi F, Izzi S, Berardesca E, Morrone A, Bonifati C. Safety of antitumour necrosis factor-α therapy in psoriatic patients with hepatitis B virus infection. Br J Dermatol. 2010;162:1408-1410. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 20] [Cited by in F6Publishing: 21] [Article Influence: 1.5] [Reference Citation Analysis (0)] |
45. | Caporali R, Bobbio-Pallavicini F, Atzeni F, Sakellariou G, Caprioli M, Montecucco C, Sarzi-Puttini P. Safety of tumor necrosis factor alpha blockers in hepatitis B virus occult carriers (hepatitis B surface antigen negative/anti-hepatitis B core antigen positive) with rheumatic diseases. Arthritis Care Res (Hoboken). 2010;62:749-754. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 87] [Cited by in F6Publishing: 93] [Article Influence: 6.6] [Reference Citation Analysis (0)] |
46. | Kim YJ, Bae SC, Sung YK, Kim TH, Jun JB, Yoo DH, Kim TY, Sohn JH, Lee HS. Possible reactivation of potential hepatitis B virus occult infection by tumor necrosis factor-alpha blocker in the treatment of rheumatic diseases. J Rheumatol. 2010;37:346-350. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 58] [Cited by in F6Publishing: 61] [Article Influence: 4.1] [Reference Citation Analysis (0)] |
47. | Fotiadou C, Lazaridou E, Ioannides D. Safety of anti-tumour necrosis factor-α agents in psoriasis patients who were chronic hepatitis B carriers: a retrospective report of seven patients and brief review of the literature. J Eur Acad Dermatol Venereol. 2011;25:471-474. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 32] [Cited by in F6Publishing: 35] [Article Influence: 2.7] [Reference Citation Analysis (0)] |
48. | Prignano F, Ricceri F, Pescitelli L, Zanieri F, Lotti T. Tumour necrosis factor-α antagonists in patients with concurrent psoriasis and hepatitis B or hepatitis C: a retrospective analysis of 17 patients. Br J Dermatol. 2011;164:645-647. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 11] [Cited by in F6Publishing: 21] [Article Influence: 1.6] [Reference Citation Analysis (0)] |
49. | Cassano N, Mastrandrea V, Principi M, Loconsole F, De Tullio N, Di Leo A, Vena GA. Anti-tumor necrosis factor treatment in occult hepatitis B virus infection: a retrospective analysis of 62 patients with psoriatic disease. J Biol Regul Homeost Agents. 2011;25:285-289. [PubMed] [Cited in This Article: ] |
50. | Cho YT, Chen CH, Chiu HY, Tsai TF. Use of anti-tumor necrosis factor-α therapy in hepatitis B virus carriers with psoriasis or psoriatic arthritis: a case series in Taiwan. J Dermatol. 2012;39:269-273. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 48] [Cited by in F6Publishing: 50] [Article Influence: 3.8] [Reference Citation Analysis (0)] |
51. | Navarro R, Concha-Garzón MJ, Castaño C, Casal C, Guiu A, Daudén E. Outcome of patients with serology suggestive of past hepatitis B virus infection during antitumor necrosis factor therapy for psoriasis. Int J Dermatol. 2014;53:909-911. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 12] [Cited by in F6Publishing: 13] [Article Influence: 1.3] [Reference Citation Analysis (0)] |
52. | Laurenti R, Giovannangeli F, Gubinelli E, Viviano MT, Errico A, Leoni L, Ballanti E, Migliore A. Long-term safety of anti-TNF adalimumab in HBc antibody-positive psoriatic arthritis patients: a retrospective case series of 8 patients. Clin Dev Immunol. 2013;2013:410521. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 11] [Cited by in F6Publishing: 14] [Article Influence: 1.3] [Reference Citation Analysis (0)] |
53. | Navarro R, Vilarrasa E, Herranz P, Puig L, Bordas X, Carrascosa JM, Taberner R, Ferrán M, García-Bustinduy M, Romero-Maté A. Safety and effectiveness of ustekinumab and antitumour necrosis factor therapy in patients with psoriasis and chronic viral hepatitis B or C: a retrospective, multicentre study in a clinical setting. Br J Dermatol. 2013;168:609-616. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 74] [Cited by in F6Publishing: 75] [Article Influence: 6.8] [Reference Citation Analysis (0)] |
54. | Sanz-Bueno J, Vanaclocha F, García-Doval I, Torrado R, Carretero G, Daudén E, Patricia Ruiz-Genao D, Alsina-Gibert MM, Pérez-Zafrilla B, Pérez-Rial G. Risk of Reactivation of Hepatitis B Virus Infection in Psoriasis Patients Treated With Biologics: A Retrospective Analysis of 20 Cases From the BIOBADADERM Database. Actas Dermosifiliogr. 2015;106:477-482. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 30] [Cited by in F6Publishing: 34] [Article Influence: 3.8] [Reference Citation Analysis (0)] |
55. | Giardina AR, Ferraro D, Ciccia F, Ferrante A, Di Stefano R, Craxì A, Triolo G. No detection of occult HBV-DNA in patients with various rheumatic diseases treated with anti-TNF agents: a two-year prospective study. Clin Exp Rheumatol. 2013;31:25-30. [PubMed] [Cited in This Article: ] |
56. | Vassilopoulos D, Apostolopoulou A, Hadziyannis E, Papatheodoridis GV, Manolakopoulos S, Koskinas J, Manesis EK, Archimandritis AI. Long-term safety of anti-TNF treatment in patients with rheumatic diseases and chronic or resolved hepatitis B virus infection. Ann Rheum Dis. 2010;69:1352-1355. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 109] [Cited by in F6Publishing: 113] [Article Influence: 8.1] [Reference Citation Analysis (0)] |
57. | Conde-Taboada A, Muñoz JP, Muñoz LC, López-Bran E. Infliximab treatment for severe psoriasis in a patient with active hepatitis B virus infection. J Am Acad Dermatol. 2009;60:1077-1080. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 15] [Cited by in F6Publishing: 18] [Article Influence: 1.2] [Reference Citation Analysis (0)] |
58. | Schurich A, Pallett LJ, Lubowiecki M, Singh HD, Gill US, Kennedy PT, Nastouli E, Tanwar S, Rosenberg W, Maini MK. The third signal cytokine IL-12 rescues the anti-viral function of exhausted HBV-specific CD8 T cells. PLoS Pathog. 2013;9:e1003208. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 145] [Cited by in F6Publishing: 151] [Article Influence: 13.7] [Reference Citation Analysis (0)] |
59. | Zeuzem S, Carreño V. Interleukin-12 in the treatment of chronic hepatitis B and C. Antiviral Res. 2001;52:181-188. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 28] [Cited by in F6Publishing: 30] [Article Influence: 1.3] [Reference Citation Analysis (0)] |
60. | Chiu HY, Chen CH, Wu MS, Cheng YP, Tsai TF. The safety profile of ustekinumab in the treatment of patients with psoriasis and concurrent hepatitis B or C. Br J Dermatol. 2013;169:1295-1303. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 106] [Cited by in F6Publishing: 106] [Article Influence: 10.6] [Reference Citation Analysis (0)] |
61. | Hayashi M, Umezawa Y, Fukuchi O, Ito T, Saeki H, Nakagawa H. Efficacy and safety of ustekinumab treatment in elderly patients with psoriasis. J Dermatol. 2014;41:974-980. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 56] [Cited by in F6Publishing: 57] [Article Influence: 7.1] [Reference Citation Analysis (0)] |
62. | Koskinas J, Tampaki M, Doumba PP, Rallis E. Hepatitis B virus reactivation during therapy with ustekinumab for psoriasis in a hepatitis B surface-antigen-negative anti-HBs-positive patient. Br J Dermatol. 2013;168:679-680. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 37] [Cited by in F6Publishing: 40] [Article Influence: 3.6] [Reference Citation Analysis (0)] |
63. | Steglich RB, Meneghello LP, Carvalho AV, Cheinquer H, Muller FM, Reginatto FP. The use of ustekinumab in a patient with severe psoriasis and positive HBV serology. An Bras Dermatol. 2014;89:652-654. [PubMed] [DOI] [Cited in This Article: ] [Cited by in F6Publishing: 1] [Reference Citation Analysis (0)] |
64. | Reddy KR, Beavers KL, Hammond SP, Lim JK, Falck-Ytter YT; American Gastroenterological Association Institute. American Gastroenterological Association Institute guideline on the prevention and treatment of hepatitis B virus reactivation during immunosuppressive drug therapy. Gastroenterology. 2015;148:215-219; quiz 216-217. [PubMed] [Cited in This Article: ] |
65. | Lee J, Conniff J, Kraus C, Schrager S. A Brief Clinical Update on Hepatitis C--The Essentials. WMJ. 2015;114:263-269; quiz 270. [PubMed] [Cited in This Article: ] |
66. | European Association for Study of Liver. EASL Recommendations on Treatment of Hepatitis C 2015. J Hepatol. 2015;63:199-236. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 877] [Cited by in F6Publishing: 898] [Article Influence: 99.8] [Reference Citation Analysis (0)] |
67. | Frankel AJ, Van Voorhees AS, Hsu S, Korman NJ, Lebwohl MG, Bebo BF, Gottlieb AB. Treatment of psoriasis in patients with hepatitis C: from the Medical Board of the National Psoriasis Foundation. J Am Acad Dermatol. 2009;61:1044-1055. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 40] [Cited by in F6Publishing: 41] [Article Influence: 2.7] [Reference Citation Analysis (0)] |
68. | Di Lernia V, Albertini G. Treatment of psoriasis with cyclosporine in patients with hepatitis C infection: risk or opportunity? J Am Acad Dermatol. 2010;63:342-343. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 4] [Cited by in F6Publishing: 3] [Article Influence: 0.2] [Reference Citation Analysis (0)] |
69. | Miura H, Itoh Y, Matsumoto Y, Tani M, Tanabe N, Isonokami M, Kurachi K, Kozuka T. Long-term administration of cyclosporin A to HCV-antibody-positive patients with dermatologic diseases. Int J Dermatol. 1999;38:310-314. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 15] [Cited by in F6Publishing: 16] [Article Influence: 0.6] [Reference Citation Analysis (0)] |
70. | Galeazzi M, Bellisai F, Giannitti C, Manganelli S, Morozzi G, Sebastiani GD. Safety of cyclosporin A in HCV-infected patients: experience with cyclosporin A in patients affected by rheumatological disorders and concomitant HCV infection. Ann N Y Acad Sci. 2007;1110:544-549. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 22] [Cited by in F6Publishing: 22] [Article Influence: 1.3] [Reference Citation Analysis (0)] |
71. | Manna R, Verrecchia E, Fonnesu C, Giovinale M, De Socio G, Curigliano V, Cerquaglia C, Soriano A, Granata M, Migliore A. Cyclosporine A: good response for patients affected by autoimmune disorders and HCV infection? Eur Rev Med Pharmacol Sci. 2009;13 Suppl 1:63-69. [PubMed] [Cited in This Article: ] |
72. | Giovanna Brunasso AM, Michetti P, Fancelli L, Massone C. Cyclosporine as monotherapy for psoriasis in the setting of chronic HCV infection: a forgotten therapeutical option. Hepat Mon. 2012;12:349-352. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 2] [Cited by in F6Publishing: 2] [Article Influence: 0.2] [Reference Citation Analysis (0)] |
73. | Watashi K, Hijikata M, Hosaka M, Yamaji M, Shimotohno K. Cyclosporin A suppresses replication of hepatitis C virus genome in cultured hepatocytes. Hepatology. 2003;38:1282-1288. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 425] [Cited by in F6Publishing: 403] [Article Influence: 19.2] [Reference Citation Analysis (0)] |
74. | Imafuku S, Tashiro A, Furue M. Ciclosporin treatment of psoriasis in a patient with chronic hepatitis C. Br J Dermatol. 2007;156:1367-1369. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 12] [Cited by in F6Publishing: 12] [Article Influence: 0.7] [Reference Citation Analysis (0)] |
75. | Zylberberg H, Rimaniol AC, Pol S, Masson A, De Groote D, Berthelot P, Bach JF, Bréchot C, Zavala F. Soluble tumor necrosis factor receptors in chronic hepatitis C: a correlation with histological fibrosis and activity. J Hepatol. 1999;30:185-191. [PubMed] [DOI] [Cited in This Article: ] [Cited by in F6Publishing: 1] [Reference Citation Analysis (0)] |
76. | Dill MT, Duong FH, Vogt JE, Bibert S, Bochud PY, Terracciano L, Papassotiropoulos A, Roth V, Heim MH. Interferon-induced gene expression is a stronger predictor of treatment response than IL28B genotype in patients with hepatitis C. Gastroenterology. 2011;140:1021-1031. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 208] [Cited by in F6Publishing: 206] [Article Influence: 15.8] [Reference Citation Analysis (0)] |
77. | Nelson DR, Lim HL, Marousis CG, Fang JW, Davis GL, Shen L, Urdea MS, Kolberg JA, Lau JY. Activation of tumor necrosis factor-alpha system in chronic hepatitis C virus infection. Dig Dis Sci. 1997;42:2487-2494. [PubMed] [Cited in This Article: ] |
78. | Zein NN. Etanercept as an adjuvant to interferon and ribavirin in treatment-naive patients with chronic hepatitis C virus infection: a phase 2 randomized, double-blind, placebo-controlled study. J Hepatol. 2005;42:315-322. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 135] [Cited by in F6Publishing: 129] [Article Influence: 4.8] [Reference Citation Analysis (0)] |
79. | Pompili M, Biolato M, Miele L, Grieco A. Tumor necrosis factor-α inhibitors and chronic hepatitis C: a comprehensive literature review. World J Gastroenterol. 2013;19:7867-7873. [PubMed] [DOI] [Cited in This Article: ] [Cited by in CrossRef: 71] [Cited by in F6Publishing: 60] [Article Influence: 5.5] [Reference Citation Analysis (0)] |
80. | Khanna M, Shirodkar MA, Gottlieb AB. Etanercept therapy in patients with autoimmunity and hepatitis C. J Dermatolog Treat. 2003;14:229-232. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 30] [Cited by in F6Publishing: 28] [Article Influence: 1.4] [Reference Citation Analysis (0)] |
81. | Magliocco MA, Gottlieb AB. Etanercept therapy for patients with psoriatic arthritis and concurrent hepatitis C virus infection: report of 3 cases. J Am Acad Dermatol. 2004;51:580-584. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 83] [Cited by in F6Publishing: 92] [Article Influence: 4.8] [Reference Citation Analysis (0)] |
82. | Cecchi R, Bartoli L. Psoriasis and hepatitis C treated with anti-TNF alpha therapy (etanercept). Dermatol Online J. 2006;12:4. [PubMed] [Cited in This Article: ] |
83. | De Simone C, Paradisi A, Capizzi R, Carbone A, Siciliano M, Amerio PL. Etanercept therapy in two patients with psoriasis and concomitant hepatitis C. J Am Acad Dermatol. 2006;54:1102-1104. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 34] [Cited by in F6Publishing: 37] [Article Influence: 2.1] [Reference Citation Analysis (0)] |
84. | Aslanidis S, Vassiliadis T, Pyrpasopoulou A, Douloumpakas I, Zamboulis C. Inhibition of TNFalpha does not induce viral reactivation in patients with chronic hepatitis C infection: two cases. Clin Rheumatol. 2007;26:261-264. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 46] [Cited by in F6Publishing: 46] [Article Influence: 2.6] [Reference Citation Analysis (0)] |
85. | Rokhsar C, Rabhan N, Cohen SR. Etanercept monotherapy for a patient with psoriasis, psoriatic arthritis, and concomitant hepatitis C infection. J Am Acad Dermatol. 2006;54:361-362. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 33] [Cited by in F6Publishing: 37] [Article Influence: 2.1] [Reference Citation Analysis (0)] |
86. | Pitarch G, Sanchez-Carazo JL, Mahiques L, Perez-Ferriols MA, Fortea JM. Treatment of psoriasis with adalimumab. Clin Exp Dermatol. 2007;32:18-22. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 2] [Cited by in F6Publishing: 6] [Article Influence: 0.4] [Reference Citation Analysis (0)] |
87. | Linardaki G, Katsarou O, Ioannidou P, Karafoulidou A, Boki K. Effective etanercept treatment for psoriatic arthritis complicating concomitant human immunodeficiency virus and hepatitis C virus infection. J Rheumatol. 2007;34:1353-1355. [PubMed] [Cited in This Article: ] |
88. | Alcaide AJ, Barrera MV, Habicheyn S, López N, Mendiola MV, Herrera E. Safety of etanercept therapy in a patient with psoriasis, Down’s syndrome and concomitant hepatitis C virus infection. J Eur Acad Dermatol Venereol. 2008;22:1514-1516. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 11] [Cited by in F6Publishing: 12] [Article Influence: 0.8] [Reference Citation Analysis (0)] |
89. | Piccolo D, Di Cesare A, Fargnoli MC, Paoloni M, Vecchiotti S, Peris K. Effective control of psoriasis by etanercept in a patient with HCV-related diseases. Eur J Dermatol. 2008;18:459-460. [PubMed] [DOI] [Cited in This Article: ] [Cited by in F6Publishing: 3] [Reference Citation Analysis (0)] |
90. | Collazo MH, González JR, Torres EA. Etanercept therapy for psoriasis in a patient with concomitant hepatitis C and liver transplant. P R Health Sci J. 2008;27:346-347. [PubMed] [Cited in This Article: ] |
91. | Cassano N, Vena GA. Etanercept treatment in a hemodialysis patient with severe cyclosporine-resistant psoriasis and hepatitis C virus infection. Int J Dermatol. 2008;47:980-981. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 15] [Cited by in F6Publishing: 16] [Article Influence: 1.1] [Reference Citation Analysis (0)] |
92. | Cavazzana I, Ceribelli A, Cattaneo R, Franceschini F. Treatment with etanercept in six patients with chronic hepatitis C infection and systemic autoimmune diseases. Autoimmun Rev. 2008;8:104-106. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 43] [Cited by in F6Publishing: 45] [Article Influence: 2.8] [Reference Citation Analysis (0)] |
93. | Behnam SE, Hindiyeh R, Fife DJ, Jeffes EW, Wu JJ. Etanercept as prophylactic psoriatic therapy before interferon-alpha and ribavirin treatment for active hepatitis C infection. Clin Exp Dermatol. 2010;35:397-398. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 17] [Cited by in F6Publishing: 20] [Article Influence: 1.4] [Reference Citation Analysis (0)] |
94. | Ventura F, Gomes J, Duarte Mda L, Fernandes JC, Brito C. Efficacy and safety of etanercept in patients with psoriasis and hepatitis C. Eur J Dermatol. 2010;20:808-809. [PubMed] [DOI] [Cited in This Article: ] [Cited by in F6Publishing: 2] [Reference Citation Analysis (0)] |
95. | Paradisi A, Caldarola G, Capizzi R, Siciliano M, Annichiarico E, Vecchio FM, Amerio PL, De Simone C. Safety of etanercept in patients with psoriasis and hepatitis C virus assessed by liver histopathology: preliminary data. J Am Acad Dermatol. 2010;62:1067-1069. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 21] [Cited by in F6Publishing: 22] [Article Influence: 1.6] [Reference Citation Analysis (0)] |
96. | Prignano F, Zanieri F, Milani S, Lotti T. Switch from etanercept to efalizumab in a psoriatic patient with HCV infection: a case report. Dermatol Ther. 2009;22:386-390. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 4] [Cited by in F6Publishing: 5] [Article Influence: 0.3] [Reference Citation Analysis (0)] |
97. | Richetta AG, Maiani E, Carlomagno V, Carboni V, Mattozzi C, Giancristoforo S, Calvieri S. Treatment of erythrodermic psoriasis in HCV+ patient with adalimumab. Dermatol Ther. 2009;22 Suppl 1:S16-S18. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 19] [Cited by in F6Publishing: 20] [Article Influence: 1.4] [Reference Citation Analysis (0)] |
98. | Garavaglia MC, Altomare G. Etanercept therapy in patients with psoriasis and concomitant HCV infection. Int J Immunopathol Pharmacol. 2010;23:965-969. [PubMed] [Cited in This Article: ] |
99. | Gandhi RK, Pickup T, Sheth PB. Is etanercept safe for treating plaque psoriasis in a patient with chronic hepatitis C virus infection? Arch Dermatol. 2010;146:1151-1152. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 6] [Cited by in F6Publishing: 7] [Article Influence: 0.5] [Reference Citation Analysis (0)] |
100. | Di Lernia V, Guareschi E. Successful treatment of hand and foot psoriasis with infliximab. Dermatol Online J. 2010;16:8. [PubMed] [Cited in This Article: ] |
101. | Zanni M, Missale G, Santilli D, Di Nuzzo S. Etanercept in the treatment of psoriasis and psoriatic arthritis with concomitant hepatitis C virus infection: clinical and virological study in three patients. Eur J Dermatol. 2011;21:564-567. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 7] [Cited by in F6Publishing: 11] [Article Influence: 0.8] [Reference Citation Analysis (0)] |
102. | Mederacke I, Witte T, Wedemeyer H, Meyer-Olson D. Successful clearance of hepatitis C virus with pegylated interferon α-2a and ribavirin in an etanercept-treated patient with psoriatic arthritis, hepatitis B virus coinfection and latent tuberculosis. Ann Rheum Dis. 2011;70:1343-1344. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 8] [Cited by in F6Publishing: 10] [Article Influence: 0.7] [Reference Citation Analysis (0)] |
103. | Bartalesi F, Salomoni E, Cavallo A, Corti G, Pimpinelli N, Bartoloni A, Taliani G. Chronic hepatitis C virus hepatitis and psoriasis: no longer a contraindication to interferon use in the era of biological agents? Scand J Infect Dis. 2013;45:320-323. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 5] [Cited by in F6Publishing: 7] [Article Influence: 0.6] [Reference Citation Analysis (0)] |
104. | Costa L, Caso F, Atteno M, Giannitti C, Spadaro A, Ramonda R, Vezzù M, Del Puente A, Morisco F, Fiocco U. Long-term safety of anti-TNF-α in PsA patients with concomitant HCV infection: a retrospective observational multicenter study on 15 patients. Clin Rheumatol. 2014;33:273-276. [PubMed] [Cited in This Article: ] |
105. | Di Nuzzo S, Boccaletti V, Fantini C, Cortelazzi C, Missale G, Fabrizi G, Lotti T, Hercogová J, Pagliarello C. Are Anti-TNF-α Agents Safe for Treating Psoriasis in Hepatitis C Virus Patients with Advanced Liver Disease? Case Reports and Review of the Literature. Dermatology. 2016;232:102-106. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 15] [Cited by in F6Publishing: 16] [Article Influence: 1.8] [Reference Citation Analysis (0)] |
106. | Salvi M, Macaluso L, Luci C, Mattozzi C, Paolino G, Aprea Y, Calvieri S, Richetta AG. Safety and efficacy of anti-tumor necrosis factors α in patients with psoriasis and chronic hepatitis C. World J Clin Cases. 2016;4:49-55. [PubMed] [DOI] [Cited in This Article: ] [Cited by in CrossRef: 12] [Cited by in F6Publishing: 12] [Article Influence: 1.5] [Reference Citation Analysis (0)] |
107. | Cooper S, Erickson AL, Adams EJ, Kansopon J, Weiner AJ, Chien DY, Houghton M, Parham P, Walker CM. Analysis of a successful immune response against hepatitis C virus. Immunity. 1999;10:439-449. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 610] [Cited by in F6Publishing: 622] [Article Influence: 24.9] [Reference Citation Analysis (0)] |
108. | Lechner F, Wong DK, Dunbar PR, Chapman R, Chung RT, Dohrenwend P, Robbins G, Phillips R, Klenerman P, Walker BD. Analysis of successful immune responses in persons infected with hepatitis C virus. J Exp Med. 2000;191:1499-1512. [PubMed] [Cited in This Article: ] |
109. | Abuchar A, Vitiello M, Kerdel FA. Psoriasis treated with ustekinumab in a patient with hepatitis C. Int J Dermatol. 2013;52:381-382. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 14] [Cited by in F6Publishing: 16] [Article Influence: 1.5] [Reference Citation Analysis (0)] |
110. | Juan J, Feld JJ. Hepatitis B virus and hepatitis C virus treatment and management in patients receiving immune-modifying agents. Curr Opin Rheumatol. 2014;26:395-403. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 6] [Cited by in F6Publishing: 6] [Article Influence: 0.7] [Reference Citation Analysis (0)] |
111. | Yang YW, Keller JJ, Lin HC. Medical comorbidity associated with psoriasis in adults: a population-based study. Br J Dermatol. 2011;165:1037-1043. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 111] [Cited by in F6Publishing: 124] [Article Influence: 9.5] [Reference Citation Analysis (0)] |
112. | Cohen AD, Weitzman D, Birkenfeld S, Dreiher J. Psoriasis associated with hepatitis C but not with hepatitis B. Dermatology. 2010;220:218-222. [PubMed] [DOI] [Cited in This Article: ] [Cited by in Crossref: 42] [Cited by in F6Publishing: 44] [Article Influence: 3.1] [Reference Citation Analysis (0)] |