Augmentation of antitubercular therapy with IFNγ in a patient with dominant partial IFNγ receptor 1 deficiency
Abstract Osteomyelitis due to Mycobacterium bovis Bacille Calmette–Guerin (BCG) often develops in patients with interferon-γ receptor 1 (IFNγR1) deficiency. In these patients, susceptibility appears to be caused by impaired interleukin-12- and IFNγ-mediated immunity. Here we report the case of a one...
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| Veröffentlicht in: | Clinical immunology (Orlando, Fla.) Fla.), 2014-03, Vol.151 (1), p.25-28 |
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| creator | Takeda, Kanako Kawai, Toshinao Nakazawa, Yumiko Komuro, Hisako Shoji, Kensuke Morita, Kumiko Katsuta, Tomohiro Yamamoto, Matsuri Miyairi, Isao Ohya, Yukihiro Ishiguro, Akira Onodera, Masafumi |
| description | Abstract Osteomyelitis due to Mycobacterium bovis Bacille Calmette–Guerin (BCG) often develops in patients with interferon-γ receptor 1 (IFNγR1) deficiency. In these patients, susceptibility appears to be caused by impaired interleukin-12- and IFNγ-mediated immunity. Here we report the case of a one-year-old girl with dominant partial IFNγR1 deficiency who suffered from lymphadenitis and multiple sites of osteomyelitis due to BCG infection. She was allergic to isoniazid and rifampicin – the prescribed standard treatment – and required prior desensitization therapy. She was subsequently treated with these drugs, but her symptoms did not improve. IFNγ therapy was added to the antitubercular therapy, increasing the serum level of IFNγ and leading to the resolution of the lymphadenitis and osteomyelitis. In conclusion, high dose IFNγ therapy in combination with antitubercular drugs led to resolution of BCG infection in a patient with dominant partial IFNγ deficiency. |
| doi_str_mv | 10.1016/j.clim.2014.01.004 |
| format | Article |
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In these patients, susceptibility appears to be caused by impaired interleukin-12- and IFNγ-mediated immunity. Here we report the case of a one-year-old girl with dominant partial IFNγR1 deficiency who suffered from lymphadenitis and multiple sites of osteomyelitis due to BCG infection. She was allergic to isoniazid and rifampicin – the prescribed standard treatment – and required prior desensitization therapy. She was subsequently treated with these drugs, but her symptoms did not improve. IFNγ therapy was added to the antitubercular therapy, increasing the serum level of IFNγ and leading to the resolution of the lymphadenitis and osteomyelitis. In conclusion, high dose IFNγ therapy in combination with antitubercular drugs led to resolution of BCG infection in a patient with dominant partial IFNγ deficiency.</description><identifier>ISSN: 1521-6616</identifier><identifier>EISSN: 1521-7035</identifier><identifier>DOI: 10.1016/j.clim.2014.01.004</identifier><identifier>PMID: 24509072</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Allergy and Immunology ; Antitubercular Agents - therapeutic use ; Drug Therapy, Combination ; Female ; Gene Expression ; Humans ; Infant ; Interferon-gamma - therapeutic use ; Interferon-γ ; Interferon-γ receptor 1 deficiency ; Interleukin-12 - genetics ; Interleukin-12 - immunology ; Isoniazid - therapeutic use ; Mendelian susceptibility to mycobacterial diseases ; Mycobacterium bovis - immunology ; Mycobacterium bovis - pathogenicity ; Mycobacterium bovis Bacille Calmette–Guerin ; Osteomyelitis ; Osteomyelitis - complications ; Osteomyelitis - drug therapy ; Osteomyelitis - immunology ; Receptors, Interferon - deficiency ; Receptors, Interferon - immunology ; Rifampin - therapeutic use ; Tuberculosis, Lymph Node - complications ; Tuberculosis, Lymph Node - drug therapy ; Tuberculosis, Lymph Node - immunology ; Virus Diseases - complications ; Virus Diseases - drug therapy ; Virus Diseases - immunology</subject><ispartof>Clinical immunology (Orlando, Fla.), 2014-03, Vol.151 (1), p.25-28</ispartof><rights>Elsevier Inc.</rights><rights>2014 Elsevier Inc.</rights><rights>Copyright © 2014 Elsevier Inc. 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In these patients, susceptibility appears to be caused by impaired interleukin-12- and IFNγ-mediated immunity. Here we report the case of a one-year-old girl with dominant partial IFNγR1 deficiency who suffered from lymphadenitis and multiple sites of osteomyelitis due to BCG infection. She was allergic to isoniazid and rifampicin – the prescribed standard treatment – and required prior desensitization therapy. She was subsequently treated with these drugs, but her symptoms did not improve. IFNγ therapy was added to the antitubercular therapy, increasing the serum level of IFNγ and leading to the resolution of the lymphadenitis and osteomyelitis. In conclusion, high dose IFNγ therapy in combination with antitubercular drugs led to resolution of BCG infection in a patient with dominant partial IFNγ deficiency.</description><subject>Allergy and Immunology</subject><subject>Antitubercular Agents - therapeutic use</subject><subject>Drug Therapy, Combination</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Humans</subject><subject>Infant</subject><subject>Interferon-gamma - therapeutic use</subject><subject>Interferon-γ</subject><subject>Interferon-γ receptor 1 deficiency</subject><subject>Interleukin-12 - genetics</subject><subject>Interleukin-12 - immunology</subject><subject>Isoniazid - therapeutic use</subject><subject>Mendelian susceptibility to mycobacterial diseases</subject><subject>Mycobacterium bovis - immunology</subject><subject>Mycobacterium bovis - pathogenicity</subject><subject>Mycobacterium bovis Bacille Calmette–Guerin</subject><subject>Osteomyelitis</subject><subject>Osteomyelitis - complications</subject><subject>Osteomyelitis - drug therapy</subject><subject>Osteomyelitis - immunology</subject><subject>Receptors, Interferon - deficiency</subject><subject>Receptors, Interferon - immunology</subject><subject>Rifampin - therapeutic use</subject><subject>Tuberculosis, Lymph Node - complications</subject><subject>Tuberculosis, Lymph Node - drug therapy</subject><subject>Tuberculosis, Lymph Node - immunology</subject><subject>Virus Diseases - complications</subject><subject>Virus Diseases - drug therapy</subject><subject>Virus Diseases - immunology</subject><issn>1521-6616</issn><issn>1521-7035</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc-OFCEQh4nRuOvqC3gwHL1MWwU0PZMYk83G1U02elDPhKYLl7H_CbRmnsv38JmkndGDB0-Q4vdVha8Ye4pQIaB-sa9cH4ZKAKoKsAJQ99g51gI3Dcj6_umuNeoz9iilPQDUQuiH7EyoGnbQiHM2Xy6fBxqzzWEa-eS5HXPIS0vRLb2NPN9RtPOBfw_5jt9cv_v5g4eRWz4XoGDHejcNYSxgqcYcbH8KRnI05yly5B354ArgDo_ZA2_7RE9O5wX7dP3649Xbze37NzdXl7cbpxDzhmrZiFZ3ohaNkq2yO2Gp861sBZQnb7Umb9W2Rt_5rbY7BdKhVL71ElXbyAv2_Nh3jtPXhVI2Q0iO-t6ONC3JYA24leuUEhXHqItTSpG8mWMYbDwYBLOaNnuzmjaraQNoiukCPTv1X9qBur_IH7Ul8PIYoPLLb4GiSb8NUBeKmGy6Kfy__6t_8BIZg7P9FzpQ2k9LHIs_gyYJA-bDuut11ajKmmGn5S_PLKYn</recordid><startdate>20140301</startdate><enddate>20140301</enddate><creator>Takeda, Kanako</creator><creator>Kawai, Toshinao</creator><creator>Nakazawa, Yumiko</creator><creator>Komuro, Hisako</creator><creator>Shoji, Kensuke</creator><creator>Morita, Kumiko</creator><creator>Katsuta, Tomohiro</creator><creator>Yamamoto, Matsuri</creator><creator>Miyairi, Isao</creator><creator>Ohya, Yukihiro</creator><creator>Ishiguro, Akira</creator><creator>Onodera, Masafumi</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20140301</creationdate><title>Augmentation of antitubercular therapy with IFNγ in a patient with dominant partial IFNγ receptor 1 deficiency</title><author>Takeda, Kanako ; Kawai, Toshinao ; Nakazawa, Yumiko ; Komuro, Hisako ; Shoji, Kensuke ; Morita, Kumiko ; Katsuta, Tomohiro ; Yamamoto, Matsuri ; Miyairi, Isao ; Ohya, Yukihiro ; Ishiguro, Akira ; Onodera, Masafumi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c411t-e5372b6d252743b4a92aedfb3b20537fa66efa4851fdf86a9403c134fbf314b73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Allergy and Immunology</topic><topic>Antitubercular Agents - therapeutic use</topic><topic>Drug Therapy, Combination</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Humans</topic><topic>Infant</topic><topic>Interferon-gamma - therapeutic use</topic><topic>Interferon-γ</topic><topic>Interferon-γ receptor 1 deficiency</topic><topic>Interleukin-12 - genetics</topic><topic>Interleukin-12 - immunology</topic><topic>Isoniazid - therapeutic use</topic><topic>Mendelian susceptibility to mycobacterial diseases</topic><topic>Mycobacterium bovis - immunology</topic><topic>Mycobacterium bovis - pathogenicity</topic><topic>Mycobacterium bovis Bacille Calmette–Guerin</topic><topic>Osteomyelitis</topic><topic>Osteomyelitis - complications</topic><topic>Osteomyelitis - drug therapy</topic><topic>Osteomyelitis - immunology</topic><topic>Receptors, Interferon - deficiency</topic><topic>Receptors, Interferon - immunology</topic><topic>Rifampin - therapeutic use</topic><topic>Tuberculosis, Lymph Node - complications</topic><topic>Tuberculosis, Lymph Node - drug therapy</topic><topic>Tuberculosis, Lymph Node - immunology</topic><topic>Virus Diseases - complications</topic><topic>Virus Diseases - drug therapy</topic><topic>Virus Diseases - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Takeda, Kanako</creatorcontrib><creatorcontrib>Kawai, Toshinao</creatorcontrib><creatorcontrib>Nakazawa, Yumiko</creatorcontrib><creatorcontrib>Komuro, Hisako</creatorcontrib><creatorcontrib>Shoji, Kensuke</creatorcontrib><creatorcontrib>Morita, Kumiko</creatorcontrib><creatorcontrib>Katsuta, Tomohiro</creatorcontrib><creatorcontrib>Yamamoto, Matsuri</creatorcontrib><creatorcontrib>Miyairi, Isao</creatorcontrib><creatorcontrib>Ohya, Yukihiro</creatorcontrib><creatorcontrib>Ishiguro, Akira</creatorcontrib><creatorcontrib>Onodera, Masafumi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical immunology (Orlando, Fla.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Takeda, Kanako</au><au>Kawai, Toshinao</au><au>Nakazawa, Yumiko</au><au>Komuro, Hisako</au><au>Shoji, Kensuke</au><au>Morita, Kumiko</au><au>Katsuta, Tomohiro</au><au>Yamamoto, Matsuri</au><au>Miyairi, Isao</au><au>Ohya, Yukihiro</au><au>Ishiguro, Akira</au><au>Onodera, Masafumi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Augmentation of antitubercular therapy with IFNγ in a patient with dominant partial IFNγ receptor 1 deficiency</atitle><jtitle>Clinical immunology (Orlando, Fla.)</jtitle><addtitle>Clin Immunol</addtitle><date>2014-03-01</date><risdate>2014</risdate><volume>151</volume><issue>1</issue><spage>25</spage><epage>28</epage><pages>25-28</pages><issn>1521-6616</issn><eissn>1521-7035</eissn><abstract>Abstract Osteomyelitis due to Mycobacterium bovis Bacille Calmette–Guerin (BCG) often develops in patients with interferon-γ receptor 1 (IFNγR1) deficiency. In these patients, susceptibility appears to be caused by impaired interleukin-12- and IFNγ-mediated immunity. Here we report the case of a one-year-old girl with dominant partial IFNγR1 deficiency who suffered from lymphadenitis and multiple sites of osteomyelitis due to BCG infection. She was allergic to isoniazid and rifampicin – the prescribed standard treatment – and required prior desensitization therapy. She was subsequently treated with these drugs, but her symptoms did not improve. IFNγ therapy was added to the antitubercular therapy, increasing the serum level of IFNγ and leading to the resolution of the lymphadenitis and osteomyelitis. In conclusion, high dose IFNγ therapy in combination with antitubercular drugs led to resolution of BCG infection in a patient with dominant partial IFNγ deficiency.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>24509072</pmid><doi>10.1016/j.clim.2014.01.004</doi><tpages>4</tpages></addata></record> |
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| subjects | Allergy and Immunology Antitubercular Agents - therapeutic use Drug Therapy, Combination Female Gene Expression Humans Infant Interferon-gamma - therapeutic use Interferon-γ Interferon-γ receptor 1 deficiency Interleukin-12 - genetics Interleukin-12 - immunology Isoniazid - therapeutic use Mendelian susceptibility to mycobacterial diseases Mycobacterium bovis - immunology Mycobacterium bovis - pathogenicity Mycobacterium bovis Bacille Calmette–Guerin Osteomyelitis Osteomyelitis - complications Osteomyelitis - drug therapy Osteomyelitis - immunology Receptors, Interferon - deficiency Receptors, Interferon - immunology Rifampin - therapeutic use Tuberculosis, Lymph Node - complications Tuberculosis, Lymph Node - drug therapy Tuberculosis, Lymph Node - immunology Virus Diseases - complications Virus Diseases - drug therapy Virus Diseases - immunology |
| title | Augmentation of antitubercular therapy with IFNγ in a patient with dominant partial IFNγ receptor 1 deficiency |
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