The journal of allergy and clinical immunology. In practice · 2014
Rituximab and immune deficiency: case series and review of the literature.
Клинический случайСтатьяОбзорНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Kaplan Blanka, Kopyltsova Yelena, Khokhar Amrita, Lam Fung, Bonagura Vincent
Аннотация
BACKGROUND: As the indications and use of rituximab continue to expand, the reports of long-term effects of anti-CD20--mediated B-cell depletion on the immune system accumulate.
OBJECTIVE: We report a group of patients with immunodeficiency who were treated with rituximab and present their immunologic data.
METHODS: A retrospective chart review identified patients with immunodeficiency who received rituximab for treatment of their primary disease and required immunoglobulin replacement therapy (IGRT). Pre-IGRT immunoglobulins, specific antibodies, B-cells, and B-cell phenotype were recorded and analyzed.
RESULTS: We identified 11 patients with immunodeficiency who received rituximab and required IGRT. Two of these patients were diagnosed with common variable immunodeficiency before rituximab treatment. Nine other patients had hypogammaglobulinemia and did not achieve an adequate response to polysaccharide vaccine. There was a significant delay in B-cell recovery. B-cell phenotypes identified predominantly naive B cells in the blood of these patients with significant decrease in switched and memory B cells.
CONCLUSION: There are patients with persistent B-cell dysfunction long after rituximab treatment was discontinued. Some of these patients required IGRT. These patients should be distinguished from patients with primary immunodeficiency diseases. Routine baseline B-cell numbers and serum immunoglobulin levels before starting immunomodulatory therapy are required to help distinguish primary immunodeficiency diseases from secondary rituximab-induced, transient, and, at times, prolonged immune suppression. Periodic monitoring is prudent to identify immune recovery. Post-rituximab B-cell phenotyping may help identify the patients who will develop persistent immune dysfunction caused by an unidentified underlying disease or the prolonged effect of rituximab treatment.
OBJECTIVE: We report a group of patients with immunodeficiency who were treated with rituximab and present their immunologic data.
METHODS: A retrospective chart review identified patients with immunodeficiency who received rituximab for treatment of their primary disease and required immunoglobulin replacement therapy (IGRT). Pre-IGRT immunoglobulins, specific antibodies, B-cells, and B-cell phenotype were recorded and analyzed.
RESULTS: We identified 11 patients with immunodeficiency who received rituximab and required IGRT. Two of these patients were diagnosed with common variable immunodeficiency before rituximab treatment. Nine other patients had hypogammaglobulinemia and did not achieve an adequate response to polysaccharide vaccine. There was a significant delay in B-cell recovery. B-cell phenotypes identified predominantly naive B cells in the blood of these patients with significant decrease in switched and memory B cells.
CONCLUSION: There are patients with persistent B-cell dysfunction long after rituximab treatment was discontinued. Some of these patients required IGRT. These patients should be distinguished from patients with primary immunodeficiency diseases. Routine baseline B-cell numbers and serum immunoglobulin levels before starting immunomodulatory therapy are required to help distinguish primary immunodeficiency diseases from secondary rituximab-induced, transient, and, at times, prolonged immune suppression. Periodic monitoring is prudent to identify immune recovery. Post-rituximab B-cell phenotyping may help identify the patients who will develop persistent immune dysfunction caused by an unidentified underlying disease or the prolonged effect of rituximab treatment.