DOI: 10.1097/QAD.0b013e328010e28a

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PMID: 17148980

Issn Print: 0269-9370

Publication Date: 2007/01/02


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A delayed immune reconstitution inflammatory syndrome

Johann Cailhol; Cecilia Pizzocolo; Michel Brauner; Olivier Bouchaud; Sophie Abgrall

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Author Information: Assistance Publique Hopitaux de Paris, Departments of Infectious and Tropical Diseases

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Excerpt

The immune reconstitution inflammatory syndrome (IRIS) among HIV-infected patients initiating combination antiretroviral therapy (CART) and pretreated for an opportunistic infection is commonly described [1–3]. In the case of HIV patients receiving both antituberculous and antiretroviral drugs, it seems to be quite a frequent event, concerning 29–36% of patients [4]. In multivariate analysis, the independant reported risk factors for IRIS are disseminated tuberculosis, the timing of the initiation of CART after tuberculosis treatment, a rapid increase in CD4 cells or decrease in the viral load greater than 2 log copies/ml under CART within a month [1,5,6]. The currently admitted physiopathological basis of IRIS is a sudden CART-mediated increase in antigen-specific cells, which in turn induces an explosive response against mycobacterial antigen [3,7]. Usually IRIS occurs when the delay between antituberculous therapy and CART initiation is approximately 2 months, with a maximal reported latency of 40 weeks [8].
We describe here a case of possible IRIS occurring more than a year and a half after the initiation of antituberculous treatment.
A 43-year-old Laotian man, seropositive for HIV-1 but not yet treated, presented with pulmonary tuberculosis with a large cavity in the right upper lobe in April 2004, and soon after began his treatment with a combination including rifampicin, isoniazid, ethambutol and pyrazinamid. The absolute number of CD4 cells at the initiation of antituberculous treatment was 261 cells/μl. The patient remained contagious for 6 months, as a result of inadequate drug concentrations. The dosage was progressively increased, adapted to blood drug concentrations, until a dosage corresponding to a weight of 60 kg was reached, although the patient weighed only 35 kg. Three other antituberculous drugs were added to avoid the selection of a resistant strain during the period of inadequate drug concentration. The last positive culture of a respiratory specimen was taken in October 2005, and the strain was still responsive to all drugs.
In August, a pneumothorax was drained in the chest surgery department. In October, a fistula appeared on the scar of the drain. This event was considered as the first IRIS, even though the patient was not taking CART, and was treated successfully with steroids (1 mg/kg) for 2 months.
The antituberculous regimen was simplified to rifampicin and isoniazid in December, after clinical improvement and 2 months of negative respiratory specimen cultures.
In September 2005, 20 months after antituberculous therapy initiation, CART was introduced, using an combination of nucleoside inhibitors and efavirenz. Just before treatment initiation, the absolute CD4 cell count was 317 cells/μl, and the viral load was greater than 5.7 log10 copies/ml.
Three weeks after the initiation of CART, at the end of October, the patient noticed a fistula on the scar of the chest drain. The absolute CD4 cell count was 422 cells/μl and the viral load was 2.7 log10 copies/ml. Drug concentrations (rifampicin and efavirenz) were within the therapeutic ranges. All the microbiological specimens (from the fistula and respiratory tract) were negative for tuberculosis. A computed tomography scan did not show any evidence of tuberculosis reactivation. The fistula disappeared spontaneously in one month, at the end of November.
The patient was hospitalized in the same period to explore asthenia, weight loss and a cough lasting for a month. Semi-invasive aspergillosis was diagnosed in the sequellar cavity on the basis of microbiological and radiological findings (see Fig. 1). The specific treatment was introduced on 9 December and symptoms progressively disappeared.
The fistula could be considered as a ‘possible’ IRIS under the generally admitted definition [4,6].
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