The vigorous HAART-induced immune response can bring out MAC-related lesions in unusual locations (see Table 1). Necrotic subcutaneous nodules, endobronchial tumors, small bowel involvement and paravertebral abscesses have all been described (8,17,28,32,34). Histologic examination of these lesions shows an intense inflammatory response surrounding few, if any, organisms. While this inflammatory response can cause acute morbidity, it also provides long-term protection against the organism, as shown in a prospective study of patients with localized MAC infection who remained free of disease without specific anti-MAC therapy (117).
Immunologic evidence for a HAART-mediated enhanced immune response against MAC was provided by Foudraine et al (45) who described 4 patients who developed symptomatic MAC infection an average of 4 weeks after starting HAART. While all of the patients had been anergic to MAC antigens before therapy, 3 of the 4 showed a marked increase in the lymphoproliferative response to mycobacterial specific antigens at the time they presented clinically. Havlir et al (61) showed that lymphocyte proliferative responses to MAC antigens were similar in non-HIV-infected patients and HIV-infected patients with treated disseminated MAC on HAART, but significantly lower in HIV-infected patients not receiving HAART.
A brisk inflammatory response might be anticipated with the concomitant use of HAART and anti-MTB therapy in patients who are co-infected with HIV and MTB. The shift towards a Th-1 cytokine profile with increased levels of IFN-γ might be expected to alter the immune response to the mycobacterium. In fact, many such instances have been reported (27,31,48,63,67,83,98,110,113). Narita et al (110) noted transient paradoxical clinical deterioration in 36% of patients with combined HIV-MTB infections after initiation of HAART. Clinical worsening included prolonged fever of >101.5 °F, increasing respiratory symptoms, increasing lymphadenopathy, development of cutaneous lesions, and ascites. A retrospective radiologic review of cases revealed worsening radiographs in 45% of patients including increasing lymphadenopathy, lobar consolidations, and pleural effusions (43).
Since MTB in HIV-infected patients is often disseminated, the inflammatory response induced by HAART can cause significant morbidity outside the lung (48). Involvement of the central nervous system in the setting of immune reconstitution is particularly problematic. McCormack et al (98) described the paradoxical growth of an intracranial tuberculoma in a patient who developed seizures while receiving antituberculous therapy and HAART. A retrospective review of patients with both HIV and MTB treated with HAART found an 8.7% prevalence of paradoxical central nervous system lesions (63). All but 1 of the patients were symptomatic, with vasogenic edema found on neuroimaging, and required the use of glucocorticoids for resolution. Given the high morbidity that can accompany IRIS in the setting of MTB, some physicians have opted to delay the onset of HAART until anti-MTB therapy has decreased the load of organisms (24).
The time from initiation of HAART to the presentation of IRIS in patients infected with MTB is more variable than in those infected with MAC, occurring within as few as 10 days to as long as 180 days later (see Table 1). Corticosteroids have been used in anecdotal reports with good success at preventing further damage when HAART-mediated inflammation threatens vital structures, especially the central nervous system.
The positive side of the increased immune response against CMV is that it can induce a longlasting disease remission, which allows for the discontinuation of anti-CMV therapy (68,92,133). While most patients do quite well, not all patients reconstitute CMV-specific CD4+ T-cell responses (79); those patients remain at risk for recurrent CMV retinitis requiring long-term specific anti-CMV therapy.
In addition to sarcoidosis, the patient described above had worsening of cutaneous Kaposi sarcoma coincident with immune recovery due to HAART. In most cases, HAART is helpful in controlling the lesions of Kaposi sarcoma (15). However, Weir et al (141) reported a case where the initiation of HAART in a patient with known Kaposi sarcoma was followed by worsening of the Kaposi sarcoma to near-obstruction of the larynx by a large sarcoma. The authors hypothesized that an increased immune response to human herpes virus-8 resulted in inflammation and edema around a previously unsuspected Kaposi sarcoma lesion.
Because hepatitis C virus (HCV) and HIV have similar routes of acquisition, there is a large patient population who are co-infected, with estimates ranging from 30%-50% (37). How HAART affects HCV levels and the immune response to HCV has not been definitively answered (126,147). Because antiretrovirals may cause hepatotoxicity, differentiating direct drug toxicity from immune-induced exacerbations of hepatitis is difficult. HAART induces a transient rise in HCV RNA and alanine aminotransferase (ALT) after 2 weeks of therapy, perhaps because of an increase in cytotoxic CD8+ T lymphocytes causing immune-mediated hepatocyte destruction (140). In most cases, HCV RNA levels return to baseline within 3 months (124,129).
Two patients who were anti-HCV negative before beginning HAART developed hepatitis and became anti-HCV positive after treatment; retrospective analysis of pretherapy serum by PCR revealed HCV (66). Zylberberg et al (147) described a patient with HCV infection who had marked hepatic decompensation approximately 7 months after beginning HAART. Liver biopsy revealed marked hepatic necrosis and inflammatory activity, with an increase in hepatic CD8+ T lymphocytes that mirrored the patient’s overall immune reconstitution. There was no evidence of drug-induced hepatotoxicity, such as an eosinophilic infiltrate, nor was there evidence for a direct HCV effect, such as fibrosing cholestasis. In another case, symptomatic cryoglobulinemia developed after 3 months of HAART in a patient with HCV infection (107).
Similar diagnostic and therapeutic dilemmas appear after initiation of HAART in patients co-infected with HIV and hepatitis B virus (HBV). In the absence of HAART, co-infected patients have higher levels of HBV DNA polymerase, less spontaneous clearance of HBeAg, and lower levels of ALT compared with patients infected with HBV alone (54). This suggests that the immune suppression mediated by HIV allows for increased HBV replication and decreased clearance by the immune system. How HAART influences the immune response to HBV is still being investigated, with 1 study (132) showing an 8.5% incidence of severe hepatic cytolysis, as defined by ALT >200 IU/L, among treated co-infected patients. Whether this was due to drug toxicity or an immune-mediated attack on viral infected hepatocytes is not clear. Carr et al (22) described an HBV-infected patient who had symptoms of acute hepatitis after initiation of HAART. At the time that HAART was stopped for fear of drug-induced hepatitis, serologic evaluation revealed that HBeAg had been cleared and titers of anti-HBc and anti-HBe had increased. In numerous other cases, transient rises in HBV DNA levels have occurred in conjunction with clinical hepatitis following initiation of HAART (94,96,123,139). Continuation of therapy led to the appearance of a variety of hepatitis B antibodies with clearance of HBsAg and resolution of the hepatitis.
The diagnosis of IRIS in patients with HCV or HBV is problematic. Many patients can be expected to have transient increases in liver enzymes in the first few weeks after starting HAART. Whether this represents interactions between the hepatotropic viruses and HIV or between the immune system and virusinfected hepatocytes is still under investigation. Physicians caring for these patients need to be aware of this interaction so that HAART is not stopped unnecessarily. Such patients need to be observed closely since there is a significant potential for both immune-mediated and drug-induced hepatotoxicity. Only liver biopsy may be able to clarify the pathogenesis.
The development of progressive multifocal leukoencephalopathy (PML) in advanced HIV disease has been associated with a mean survival time measured in months. The use of HAART, while not preventing the development of PML in all patients, has been shown to increase survival significantly in patients with PML (3,137), presumably because of an increased immune response to the JC virus, the causative organism. With HAART, levels of JC virus in the CSF decrease and levels of antibody to JC virus increase (35,55). Nevertheless, an inflammatory PML variant has developed in several patients treated with HAART, with MRIs of these patients showing contrast enhancement, suggesting a strong inflammatory component (29,82). Biopsy of these lesions has revealed extensive demyelination with surrounding inflammation consisting of lymphoplasmoid cells. In marked contrast to the usual course of PML, all the patients described who developed PML in the setting of immune reconstitution have had either improvement or at least stability of their neurologic deficits.
The anecdotal nature of the reports of IRIS precludes firm recommendations regarding therapy. At this stage, the most important step is probably to recognize IRIS as a possible explanation for new symptoms; this can help to minimize invasive diagnostic procedures and allow for the early use of therapeutic agents. The most extensive experience with antiinflammatory agents in the literature has been in the treatment of M. tuberculosis, C. neoformans, and CMV. These organisms have a predilection for the central nervous system, which has little tolerance for inflammation. In the case of CMV ocular disease, corticosteroids have been used in both local and systemic fashions with encouraging results (72,74,131). Long-term, aggressive anti-CMV treatment to decrease CMV antigen has also been advocated (84). Systemic corticosteroids have been used in the treatment of IRIS involving M. tuberculosis infection, especially in the setting of intracranial tuberculomas with surrounding edema (27,48,63,67,98,110).
The use of pharmaceutical interventions other than steroids has been limited. Mild cases of inflammation might respond to nonsteroidal antiinflammatory drugs (NSAIDs), which could be used by themselves or in conjunction with corticosteroids. The use of other antiinflammatory therapies, such as thalidomide, is currently being investigated.
We describe clinical features and essential laboratory data in 24 patients who underwent paradoxical clinical deterioration while receiving highly active antiretroviral therapy (HAART) for the treatment of human immunodeficiency virus (HIV) infection. The patients had responded to antiretroviral therapy as defined by increased CD4+ T cell lymphocyte counts and reductions in HIV viral loads. In 14 of 24 patients, the deterioration was attributable to a response to an infectious agent proven to be present before starting HAART. While 8 of the remaining 10 patients developed inflammation against microbes that had not been clinically recognized before starting HAART, it seems likely that these organisms were already established before the institution of therapy. Two of these patients had mycobacterial disease of the colon, 2 had symptoms secondary to disseminated cytomegalovirus, 1 had lymphadenitis in association with Bartonella infection, and 1 had an atypical pneumonia in response to Pneumocystis carinii. Presumably latent infections with herpes viruses were responsible for symptoms in 2 cases; 1 patient developed severe periproctitis secondary to herpes simplex while another had progressive Kaposi sarcoma, a disease associated with human herpes virus-8. Of the final 2 patients, 1 had worsening of sarcoidosis, a disease in which CD4+ T lymphocytes play a central role in pathogenesis, while the other developed an autoimmune disorder (Graves disease), which may have been related to the production of autoreactive T lymphocytes occurring during immune reconstitution. We propose that a restored capacity of the host to mount an inflammatory response against persistent microbial antigens or self-antigens led to the development of symptoms in these patients; we call this constellation of events the immune reconstitution inflammatory syndrome (IRIS).
We found reports of an additional 158 cases of IRIS. We discuss here the literature on the basic science of immune reconstitution engendered with HAART, along with microbial-specific immune responses that occur following HAART. The preponderance of cases occurred in association with Mycobacterium avium complex (28 cases), Mycobacterium tuberculosis (34 cases), cytomegalovirus (19 cases), or herpes zoster (38 cases). Other associated diseases included Cryptococcus neoformans meningitis and lymphadenitis, Kaposi sarcoma, Hepatitis B, Hepatitis C, progressive multifocal leukoencephalopathy, Graves disease, and sarcoidosis. For some presentations, such as sarcoidosis, cryptococcal meningitis, and herpes zoster, the clinical manifestations were quite similar to the same disease occurring in the absence of HAART. Other presentations, such as localized Mycobacterium avium complex lymphadenitis, cytomegalovirus vitreitis, and inflammatory PML, were unique to patients with immune reconstitution. Anecdotal reports suggest that there may be some benefit from treatment with antiinflammatory drugs if the inflammatory response compromises vital structures or has caused substantial systemic symptoms.
The advent of HAART has improved the prognosis of persons infected with HIV. Clinicians involved in the care of these patients need to be aware of the potential, however, for this therapy to cause a paradoxical decline in clinical status. While the search for new infectious processes must be diligent and the possibility of drug toxicity needs to be evaluated, it is important to recognize that improved immune function, itself, can be the source. In IRIS, the need to ameliorate the signs and symptoms of immune reconstitution has to be balanced with the desire to maintain the patient on long-term, effective anti-HIV therapy. With increasing recognition of patients with IRIS, it may now be possible to initiate clinical trials to determine the most appropriate approach to treatment.
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