Interferon-alpha treatment of hepatitis D induces tuberculosis exacerbation in an immigrant

Telesca, C.; Angélico, M.; Piccolo, Paola; Nosotti, L.; Morrone, Andrea; Longhi, Chiara; Carbone, Marco; Baiocchi, Leonardo

doi:10.1016/j.jinf.2006.12.009

Cited by 35 publications

(29 citation statements)

References 27 publications

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“…In contrast, studies in CHB have reported both favorable (16) and unfavorable results (30 However, clinically important adverse events occurred in patients with advanced liver disease, which included two cases of hepatic decompensation and one case of tuberculosis reactivation. The latter may need particular attention for patients from areas where both CDH and tuberculosis may be endemic, such as Turkey, Eastern Europe and the Middle East (10,31). It may be important to note that in the three patients in whom decompensation or tuberculosis reactivation occurred, baseline platelets counts were 74, 122 and 105x10 9 L -1 , respectively.…”

Section: Discussionmentioning

confidence: 99%

Pegylated interferon-based treatment in patients with advanced liver disease due to chronic delta hepatitis

Kabaçam

Dalekos²,

Çakalǒglu³

et al. 2012

Turk J Gastroenterol

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Amaç: ‹leri delta hepatitinde interferonlar›n güvenilirlik ve etkinli¤i araflt›r›lmam›flt›r. Çok merkezli bir klinik çal›flman›n bu alt analizinin amac›, kronik delta hepatitine ba¤l› ileri karaci¤er hastal›¤› olan ve ileri hastal›¤› olmayan hasta gruplar›n›, 48 haftal›k interferon alfa-2a (180 μgAnahtar kelimeler: Siroz, hepatitis delta, pegile interferon, tedavi Background/aims: The safety and efficacy of interferons in advanced delta hepatitis have not been explored. The aim of this subanalysis of a multicenter clinical trial was to compare the efficacy and safety of 48 weeks of pegylated interferon alpha-2a (180 μg weekly) with or without adefovir (10 mg daily) in patients with chronic delta hepatitis-induced advanced liver disease and in those with non-advanced liver disease. Materials and Met

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Section: Discussionmentioning

confidence: 99%

Pegylated interferon-based treatment in patients with advanced liver disease due to chronic delta hepatitis

Kabaçam

Dalekos²,

Çakalǒglu³

et al. 2012

Turk J Gastroenterol

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“…Highly virulent strains of M. tuberculosis induce higher levels of Type I IFNs 20. There are reports of TB reactivation during IFN-α treatment for hepatitis C viral infection 24. The increase in Type I IFNαβ-inducible transcripts in the blood of active TB patients (Fig.…”

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confidence: 95%

An interferon-inducible neutrophil-driven blood transcriptional signature in human tuberculosis

Berry¹,

Graham²,

McNab³

et al. 2010

Nature

1,612

169

1,983

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Tuberculosis (TB), caused by infection with Mycobacterium tuberculosis (M. tuberculosis), is a major cause of morbidity and mortality worldwide and efforts to control TB are hampered by difficulties with diagnosis, prevention and treatment 1,2. Most people infected with M. tuberculosis remain asymptomatic, termed latent TB, with a 10% lifetime risk of developing active TB disease, but current tests cannot identify which individuals will develop disease 3. The immune response to M. tuberculosis is complex and incompletely characterized, hindering development of new diagnostics, therapies and vaccines 4,5. We identified a whole blood 393 transcript signature for active TB in intermediate and high burden settings, correlating with radiological extent of disease and reverting to that of healthy controls following treatment. A subset of latent TB patients had signatures similar to those in active TB patients. We also identified a specific 86-transcript signature that discriminated active TB from other inflammatory and infectious diseases. Modular and pathway analysis revealed that the TB signature was dominated by a neutrophil-driven interferon (IFN)-inducible gene profile, consisting of both IFN-γ and Type I IFNαβ signalling. Comparison with transcriptional signatures in purified cells and flow cytometric analysis, suggest that this TB signature reflects both changes in cellular composition and altered gene expression. Although an IFN signature was also observed in whole blood of patients with Systemic Lupus Erythematosus (SLE), their complete modular signature differed from TB with increased abundance of plasma cell transcripts. Our studies demonstrate a hitherto under-appreciated role of Type I IFNαβ signalling in TB pathogenesis, which has implications for vaccine and therapeutic development. Our study also provides a broad range of transcriptional biomarkers with potential as diagnostic and prognostic tools to combat the TB epidemic.

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“…In 2007, Telesca et al reported a case of a young Romanian patient who developed a severe exacerbation of pulmonary tuberculosis during IFN-a treatment of chronic hepatitis D. They proposed that IFN-induced weight loss and anorexia may have played an important role in promoting clinical manifestations of tuberculosis in some patients. 25 Sabbatani et al also reported an unexpected observation of severe pulmonary tuberculosis after a 7-month combined pegylated IFN-ribavirin for chronic HCV infection. They recommended that the enlargement of IFN indications needs careful evaluation for previous (usually missed) tuberculosis, to prevent or avoid its possible reactivation.…”

Section: Discussionmentioning

confidence: 97%

Cutaneous Granulomas Associated With Interferon Therapy

El‐Khalawany

Mohammad

Aboeldahab

et al. 2016

The American Journal of Dermatopathology

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Treatment with interferon (IFN) could be associated with variable cutaneous adverse reactions. The aim of this study was to describe the clinicopathological spectrum of cutaneous granulomas associated with IFN therapy and identify the causal relation between IFN therapy and granulomatous reactions. The study included 18 patients (16 males and 2 females) with an average age of 48 years. Clinically, most of the lesions were solitary (83.3%) and located on the face (44.4%) and/or trunk (38.9%). The lesions were commonly presented as nodules (33.3%) or plaques (27.8%) with a common size of 5-10 cm. Granulomatous reactions were localized to the injection site in 4 cases, distributed on other body areas (remote granuloma) in 11 cases, and associated with lung involvement (systemic granuloma) in 3 cases. Histologically, injection site granuloma showed suppurative reaction in 75% and sarcoidal reaction in 25%. Remote granuloma showed tuberculoid reaction in 27.3%, interstitial in 27.3%, and sarcoidal in 45.4%. Systemic granuloma showed sarcoidal reaction in all cases. After withdrawal of IFN, only 3 lesions showed spontaneous complete clearance, whereas most of the lesions (83.3%) showed only partial improvement. Our results suggested that IFN is not a causal agent of all associated cutaneous granulomas but it mostly provokes the appearance of granulomatous reactions in susceptible individuals. Findings that prove this concept include the formation of granuloma in body sites away from the injection site, the heterogeneous pattern of granuloma both clinically and histologically, and incomplete clearance of most of the lesions after withdrawal of IFN.

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Interferon-alpha treatment of hepatitis D induces tuberculosis exacerbation in an immigrant

Cited by 35 publications

References 27 publications

Pegylated interferon-based treatment in patients with advanced liver disease due to chronic delta hepatitis

Pegylated interferon-based treatment in patients with advanced liver disease due to chronic delta hepatitis

An interferon-inducible neutrophil-driven blood transcriptional signature in human tuberculosis

Cutaneous Granulomas Associated With Interferon Therapy

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