Abstract
Background Tuberculosis (T) may be reactivated following a primary, silent, and unknown T infection, when immunodeficiency (often jatrogenic in origin), or other risk factors (e.g. cancer, cachexia), become apparent. Post-primary T episodes were described also decades after a primary M. tuberculosis infection, in patients (p) who show apparently limited radiographic signs at chest X-ray. Some grade of immunodeficiency may also depend on the administration of associated IFN-ribavirin for an underlying chronic HCV hepatitis, as expressed by the frequent emerging of leuko-neutropenia, and altered cytokine network.
Highlights
Tuberculosis (T) may be reactivated following a primary, silent, and unknown T infection, when immunodeficiency, or other risk factors, become apparent
Some grade of immunodeficiency may depend on the administration of associated IFN-ribavirin for an underlying chronic HCV hepatitis, as expressed by the frequent emerging of leuko-neutropenia, and altered cytokine network
After 11 years, due to a progressive chronic HCV hepatitis, pegylated IFN-ribavirin were started for 7 months, until a sudden occurrence of cough-hemoptisis associated with a pulmonary lesion highly suggestive of T became apparent, in the same area where some reliquates of a primary T were demonstrated 11 years before
Summary
Tuberculosis (T) may be reactivated following a primary, silent, and unknown T infection, when immunodeficiency (often jatrogenic in origin), or other risk factors (e.g. cancer, cachexia), become apparent. Post-primary T episodes were described decades after a primary M. tuberculosis infection, in patients (p) who show apparently limited radiographic signs at chest X-ray. Some grade of immunodeficiency may depend on the administration of associated IFN-ribavirin for an underlying chronic HCV hepatitis, as expressed by the frequent emerging of leuko-neutropenia, and altered cytokine network
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