Recurrent, MultifocalMycobacterium avium‐intercellulareInfection in a Patient with Interferon‐γ Autoantibody

Abstract

We describe a patient who experienced severe osteomyelitis because of Mycobacterium avium-intercellulare infection and high-titered autoantibodies against interferon-gamma. In addition to antimycobacterial chemotherapy, we treated our patient with plasmapheresis and cyclophosphamide. The treatment induced a remission after 3 years of follow-up.

Anti–IFN-γ autoantibodies in adults with disseminated nontuberculous mycobacterial infections are associated with HLA-DRB1*16:02 and HLA-DQB1*05:02 and the reactivation of latent varicella-zoster virus infection

“…7,9,11 Third, a high proportion (71%) of our patients suffered from the reactivation of latent VZV infection, a phenotype rarely reported in either MSMD patients or in patients with anti-IFN-␥ autoantibodies. [7][8][9][10][11][12][13]30 Finally and most importantly, 2 HLA alleles, DRB1*16:02 and DQB1*05:02, occurred with unexpectedly high frequencies among our patients.…”

“…9 Several subsequent case series and reports also identified small groups of patients with unusual autoantibodies of this type. [10][11][12][13] Unlike our patients, nearly half of the reported patients 7-13 had either clinical or laboratory evidence of autoimmune disease or had received steroid therapy, which can disrupt For personal use only. on May 10, 2018.…”

“…[7][8][9][10][11][12][13] In the presence of these autoantibodies, the "physiologic concentration" of IFN-␥ in response to mycobacterial infections is markedly suppressed, and the affected subjects are susceptible to disseminated mycobacterial infections, a phenotype unique to MSMD patients. [30][31][32] Patients with dNTM infections due to anti-IFN-␥ autoantibodies were first reported in 2004.…”

“…[4][5][6][7][8][9] In cases with anti-IFN-␥ autoantibody expression, disseminated NTM (dNTM) infection is the most common clinical presentation. [7][8][9][10][11][12][13] The majority of patients with anticytokine autoantibodies have associated comorbidities, either neoplastic or autoimmune. 4,9,14,15 These comorbidities and their associated therapies may render patients more susceptible to infectious diseases.…”

Mycobacterium avium Complex Cervical Lymphadenitis in an Immunocompetent Adult

“…IFN-␥ and Stat-1 signaling disregulation, while rare, causes selective holes in immunity that predispose patients to infection with NTM. This has been well illustrated in several cases of severe atypical mycobacterial infections in patients with IFN-␥ receptor deficiency and IFN-␥ autoantibody and Stat-1 defects and IL-12 receptor deficiency (2,10,13,14). Additionally, these or similar defects may be more common than have been reported.…”