Impaired Immune Response by Isoniazid Treatment During Intravesical BCG Administration in the Guinea Pig

Boer, Liesbeth C. De; Steerenberg, P. A.; Meijden, A.P.M. van der; Klingeren, B. Van; Jong, Wim H. de; Elgersma, Anneke; Debruyne, F.M.J.; Ruitenberg, E. J.

doi:10.1016/s0022-5347(17)36973-2

Cited by 40 publications

(12 citation statements)

References 19 publications

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“…It also commonly causes a fever and rash (Maddrey & Boitnott, 1973). On the other hand, there are observations that suggest that INH can lead to immune suppression, which include the fact that administration of INH together with intra-vesical bacillus Calmette-Guérin (BCG) therapy for superficial bladder cancer appeared to: reduce the induction of mononuclear cell infiltrate in the bladder wall, inhibit enlargement of regional lymph nodes, inhibit the increase in MHC II expression of lymph node cells and diminish systemic immunity that was induced by BCG administration (de Boer et al, 1992). Signs of immune impairment were seen even if INH was administered later on during the course of BCG therapy, or if the dose of BCG was increased.…”

Section: Discussionmentioning

confidence: 99%

Isoniazid-induced liver injury and immune response in mice

Metushi¹,

Uetrecht

2013

Journal of Immunotoxicology

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Isoniazid (INH) is associated with one of the highest incidences of idiosyncratic drug-induced liver failure of any commonly prescribed drug. The mechanism of this liver injury remains uncertain, and a valid animal model would greatly facilitate mechanistic studies. Most studies of INH-induced liver toxicity have been acute studies performed in rats with high doses of the drug, and this is very different from the idiosyncratic liver injury that occurs in humans. It has previously been demonstrated that covalent binding of INH in the liver of mice is greater than in rats and more like that in humans. Therefore, mice should be a better species in which to develop an animal model of INH-induced liver injury. Treatment of Cbl-b À/À and PD1 À/À mice, which have impaired immune tolerance, resulted in greater injury than their C57BL/6 background, but not liver failure. This suggested that the injury was mediated by the adaptive immune system; however, Rag À/À mice, which do not have competent T-and B-cells, sustained more liver injury than C57BL/6 wild-type mice. This suggested that the adaptive immune system also played a protective role. INH treatment also led to a decrease in the inflammatory cytokines IL-1a and IL-12, which suggests that the drug may have immunosuppressive properties. In short, a mouse model was developed of INH-induced liver injury in which the immune system appears to play a both protective and pathogenic role, but this study was unable to develop a model of INH-induced liver failure.

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Section: Discussionmentioning

confidence: 99%

Isoniazid-induced liver injury and immune response in mice

Metushi¹,

Uetrecht

2013

Journal of Immunotoxicology

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“…In a study by De Boer et al [9], isoniazid did not influence the growth of urothelial neoplasms in animal models. It is unknown whether iso niazid could influence the antitumour effect in man.…”

Section: Prevention Of Adverse Effectsmentioning

confidence: 88%

Practical Approaches to the Prevention and Treatment of Adverse Reactions to BCG

Meijden¹

1995

Eur Urol

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“…The prophylactic administration of isoniazid can prevent adverse effects after BCG therapy, but animal studies 16 suggest that prophylactic antituberculous drug therapy can reduce the antitumor effect as well as the immune response. Immunological studies are needed to determine the underlying pathogenic mechanism(s) of arthritis and conjunctivitis, and to search for an effective treatment or prevention of adverse events after intracavitary BCG immunotherapy.…”

Section: Discussionmentioning

confidence: 99%

Reiter?s syndrome following intravesical bacille bili� de Calmette?Gu�rin treatment for superficial bladder carcinoma: report of six cases

Murata

Adachi

Ebitsuka

et al. 2004

Modern Rheumatology

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We report the cases of six patients who developed acute Reiter's syndrome following intravesical bacille biliE de Calmette-GuErin (BCG) immunotherapy for superficial bladder cancer. After the third to eighth BCG intravesical injection, the patients developed conjunctivitis, aseptic urethritis, and polyarthritis consistent with a diagnosis of Reiter's syndrome. HLA-B27 antigen was negative in five of the patients examined. Two of the patients responded to nonsteroidal anti-inflammatory drugs for polyarthritis, and the other four responded to steroids (prednisolone 5-10 mg/day). The frequent use of intracavitary BCG may increase the incidence of BCG-induced Reiter's syndrome. Further analysis of the relationship between HLA-B and -DR alleles and arthritis should shed light on the mechanism of BCG-induced Reiter's syndrome.

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Impaired Immune Response by Isoniazid Treatment During Intravesical BCG Administration in the Guinea Pig

Cited by 40 publications

References 19 publications

Isoniazid-induced liver injury and immune response in mice

Isoniazid-induced liver injury and immune response in mice

Practical Approaches to the Prevention and Treatment of Adverse Reactions to BCG

Reiter?s syndrome following intravesical bacille bili� de Calmette?Gu�rin treatment for superficial bladder carcinoma: report of six cases

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