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Newly Diagnosed Pulmonary Sarcoidosis in HIV-infected Patients¹

¹ From the Departments of Radiology, Albert Einstein College of Medicine, Montefiore Medical Center, 111 E 210th St, Bronx, NY 10467 (L.B.H., G.L., A.S.); University of North Carolina School of Medicine, Chapel Hill (P.L.M.); University of Maryland, Baltimore (C.S.W.). From the 1999 RSNA scientific assembly. Received February 21, 2000; revision requested April 5; revision received May 23; accepted June 28. Address correspondence to L.B.H. (e-mail: lharamati@aecom.yu.edu).

	ABSTRACT

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PURPOSE: To determine the radiologic and clinical features of newly diagnosed pulmonary sarcoidosis in human immunodeficiency virus (HIV)–infected patients.

MATERIALS AND METHODS: Ten HIV-infected patients (seven women, three men; age range, 26–66 years; mean age, 37 years) with newly diagnosed sarcoidosis between 1989 and 1997 were retrospectively identified. Charts were reviewed for the interval between the two diagnoses, CD4 cell count, signs or symptoms, angiotensin-converting enzyme level, and initiation of highly active antiretroviral therapy (HAART). Chest radiographs (n = 10) and computed tomographic (CT) scans (n = 8) were assessed for lymphadenopathy, pulmonary nodules, focal consolidation, reticular or granular opacities (thickened interlobular septa and ground-glass opacities at CT), cysts or cavities, and fibrosis.

RESULTS: Mean interval between the two diagnoses was 3 years. Mean CD4 cell count was 213 cells per cubic millimeter. When sarcoidosis was diagnosed, eight patients had pulmonary signs or symptoms. The angiotensin-converting enzyme level was elevated in five of six patients; two developed sarcoidosis after beginning HAART. Chest radiographs revealed lymphadenopathy, pulmonary nodules, focal consolidation, reticular opacities, granular opacities, and cysts or cavities. Chest CT scans revealed lymphadenopathy, nodules, thickened interlobular septa, focal consolidation, reticular opacities, ground-glass opacities, and cysts or cavities. There was no relationship between the radiographic findings of sarcoidosis and the CD4 cell count.

CONCLUSION: The radiologic features of newly diagnosed sarcoidosis in HIV-infected patients resemble the findings of sarcoidosis in non–HIV-infected patients. In HIV-infected patients receiving HAART, sarcoidosis may be a manifestation of disease related to restoration of the immune system.

Index terms: Acquired immunodeficiency syndrome (AIDS), 60.2518 • Lung, CT, 60.1211, 60.12118 • Sarcoidosis, 60.22

	INTRODUCTION

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New-onset sarcoidosis has been described only occasionally in human immunodeficiency virus (HIV)–infected patients (1–5). Some investigators (3,4) speculate that the alteration in cellular immunity associated with HIV infection reduces the prevalence of sarcoidosis in this population. During routine clinical practice, we have encountered several HIV-infected patients who developed sarcoidosis. Two recent patients developed this condition after they were treated with highly active antiretroviral therapy (HAART) and coincidently with partial immune reconstitution. The purpose of this study was to determine the radiologic and clinical features of new-onset sarcoidosis in a group of HIV-infected patients.

	MATERIALS AND METHODS

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We retrospectively identified 10 patients with sarcoidosis diagnosed concurrently with or subsequent to the diagnosis of HIV infection at four different hospitals between 1989 and 1997. Four patients were identified during the course of clinical practice. The remaining six patients were identified by searching the hospital databases for the diagnosis of sarcoidosis and by cross-referencing the diagnosis of sarcoidosis with that of HIV infection or acquired immunodeficiency syndrome. Patients were included in the current series only if the diagnosis of sarcoidosis was made within 1 month of the diagnosis of HIV infection or subsequent to it and if the radiologic studies and clinical charts were available for review.

In each patient, material was obtained for histologic analysis and demonstrated noncaseating granulomas, a finding that was consistent with the diagnosis of sarcoidosis, with special stains being negative for acid-fast bacilli and fungus. Tissue was obtained for histologic analysis at transbronchial biopsy in eight patients, at mediastinoscopic lymph node biopsy in one patient, and at computed tomography (CT)–guided core needle biopsy of a lung nodule in one patient. The series consisted of seven women and three men, with a mean age of 37 years (age range, 26–66 years).

Each chart was reviewed by one of four authors (G.L., A.S., P.L.M., C.S.W.) for the following information: the interval between the diagnoses of HIV infection and sarcoidosis, HIV risk factors, CD4 cell count, prior opportunistic infections, clinical signs or symptoms, serum angiotensin-converting enzyme level, and initiation of HAART.

Chest radiographs (n = 10) obtained closest to the diagnosis of sarcoidosis (within 6 weeks of the diagnosis in each patient) were reviewed for the presence of lymphadenopathy, focal parenchymal consolidation, reticular opacities, granular opacities, cysts or cavities, and fibrosis and for the size of pulmonary nodules. Chest CT scans (n = 8) were reviewed for the presence of lymphadenopathy, thickening of interlobular septa, linear opacities, focal opacities, ground-glass opacities, cysts or cavities, and fibrosis and for the size and distribution of pulmonary nodules. (Five were obtained within the same month as the diagnosis, and three were obtained 6, 10, and 11 months after sarcoidosis was diagnosed but without a new distribution of radiographic findings or new clinical manifestations at the time of CT.) Any zonal predominance (upper, middle, lower, central, peripheral) of parenchymal disease was noted on chest radiographs and CT scans.

The CT scans were obtained with a variety of techniques. Thin-section images were obtained alone or in combination with conventional images in five of eight patients who underwent CT. The chest radiographs and CT scans of each patient were reviewed at the same sitting by one of three experienced chest radiologists (L.B.H., C.S.W., P.L.M.). In seven of the patients, the images were jointly reviewed by one of the chest radiologists (L.B.H.) and a senior radiology resident (G.L.), with the differences resolved by consensus. The readers were aware of the diagnoses of HIV infection and sarcoidosis at the time the chest radiographs and CT scans were reviewed.

	RESULTS

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The median interval between the diagnosis of HIV infection and that of sarcoidosis was 3 years, with a range of 1 day to 7 years. In two patients, the diagnosis of sarcoidosis was made within the same month as but prior to the diagnosis of HIV infection. HIV risk factors were heterosexual contact (n = 3), intravenous drug use (n = 2), both (n = 3), or unknown (n = 2). The mean CD4 cell count was 213 cells per cubic millimeter (range, 25–390 cells per cubic millimeter). Six of the patients met the criteria for acquired immunodeficiency syndrome. Prior opportunistic infections had been diagnosed in five patients and included Pneumocystis carinii pneumonia (n = 3), thrush (n = 3), herpes zoster (n = 2), Mycobacterium avium-intracellulare complex lymphadenopathy, recurrent bacterial pneumonia, and Torulopsis glabrata infection (n = 1). Concurrent active disease was not known to be present at the time sarcoidosis was diagnosed.

At the time sarcoidosis was diagnosed, eight patients had one or more pulmonary signs or symptoms, as follows: shortness of breath (n = 6), cough (n = 4), chest pain or tightness (n = 3), wheezing (n = 1), and hemoptysis (n = 1). Three of these patients also had extrathoracic signs or symptoms, including rash, hepatosplenomegaly, and parotid enlargement, at presentation. Serum angiotensin-converting enzyme levels were elevated in five of the six patients tested.

Two patients developed sarcoidosis after initiation of HAART and partial immune reconstitution 4 (Fig 1) and 6 (Fig 2) years after HIV infection was diagnosed. In these patients, the CD4 cell counts increased from 11 to 126 cells per cubic millimeter within 4 months and from 26 to 199 cells per cubic millimeter within 5 months before the diagnosis of sarcoidosis was made. Another patient (Fig 3) developed a clinically diagnosed flare-up of sarcoidosis, manifested as acute ear swelling, 3 years after the diagnosis of sarcoidosis was made and shortly after initiation of HAART, which occurred, coincidently, with an increase in the CD4 cell count from 194 to 541 cells per cubic millimeter at the time of the flare-up.

View larger version (154K): [in this window] [in a new window] [Download PPT slide]   Figure 1a. Images in a 43-year-old woman (patient 9) who developed sarcoidosis 4 years after HIV infection was diagnosed and shortly after beginning HAART. (a) Posteroanterior and (b) lateral chest radiographs demonstrate bilateral hilar, subcarinal (x in b) and aorticopulmonary window lymphadenopathy. A vague parenchymal opacity is evident in the right lower lobe (arrow in a). (c) Chest CT scan at the level of the dome of the diaphragm demonstrates a 2.5-cm nodule (arrow) in the right lower lobe.

View larger version (178K): [in this window] [in a new window] [Download PPT slide]   Figure 1b. Images in a 43-year-old woman (patient 9) who developed sarcoidosis 4 years after HIV infection was diagnosed and shortly after beginning HAART. (a) Posteroanterior and (b) lateral chest radiographs demonstrate bilateral hilar, subcarinal (x in b) and aorticopulmonary window lymphadenopathy. A vague parenchymal opacity is evident in the right lower lobe (arrow in a). (c) Chest CT scan at the level of the dome of the diaphragm demonstrates a 2.5-cm nodule (arrow) in the right lower lobe.

View larger version (138K): [in this window] [in a new window] [Download PPT slide]   Figure 1c. Images in a 43-year-old woman (patient 9) who developed sarcoidosis 4 years after HIV infection was diagnosed and shortly after beginning HAART. (a) Posteroanterior and (b) lateral chest radiographs demonstrate bilateral hilar, subcarinal (x in b) and aorticopulmonary window lymphadenopathy. A vague parenchymal opacity is evident in the right lower lobe (arrow in a). (c) Chest CT scan at the level of the dome of the diaphragm demonstrates a 2.5-cm nodule (arrow) in the right lower lobe.

View larger version (136K): [in this window] [in a new window] [Download PPT slide]   Figure 2a. Images in a 37-year-old woman (patient 7) who developed sarcoidosis 6 years after HIV infection was diagnosed and shortly after beginning HAART. (a) Posteroanterior chest radiograph demonstrates bilateral pulmonary nodules, focal areas of consolidation, and cavities (greater on the right side), with an upper lung predominance. (b) Chest CT scan at the level of the hila demonstrates nodules and confluent opacities with a predominantly peribronchovascular distribution. There are small bilateral thick-walled cavities (arrow).

View larger version (149K): [in this window] [in a new window] [Download PPT slide]   Figure 2b. Images in a 37-year-old woman (patient 7) who developed sarcoidosis 6 years after HIV infection was diagnosed and shortly after beginning HAART. (a) Posteroanterior chest radiograph demonstrates bilateral pulmonary nodules, focal areas of consolidation, and cavities (greater on the right side), with an upper lung predominance. (b) Chest CT scan at the level of the hila demonstrates nodules and confluent opacities with a predominantly peribronchovascular distribution. There are small bilateral thick-walled cavities (arrow).

View larger version (170K): [in this window] [in a new window] [Download PPT slide]   Figure 3a. Images in a 32-year-old woman (patient 5) who developed sarcoidosis 7 years after HIV infection was diagnosed. (a) Posteroanterior chest radiograph obtained when sarcoidosis was diagnosed demonstrates bilateral small nodules in the lung parenchyma that are greatest in the left apex and right lower lobe. There is a suggestion of right paratracheal, aorticopulmonary window, subcarinal, and bilateral hilar lymphadenopathy. (b) Posteroanterior chest radiograph obtained 10 months later demonstrates that the lung parenchymal disease has a similar distribution but is more extensive and confluent. The lymphadenopathy is similar in extent and distribution. (c) Chest CT scan at the level of the inferior hila obtained at the same time as b demonstrates bilateral small nodules in the lower lobes, with confluent opacity in the right lower lobe. There is a 5-mm nodule (arrow) in the right upper lobe abutting the minor fissure.

View larger version (155K): [in this window] [in a new window] [Download PPT slide]   Figure 3b. Images in a 32-year-old woman (patient 5) who developed sarcoidosis 7 years after HIV infection was diagnosed. (a) Posteroanterior chest radiograph obtained when sarcoidosis was diagnosed demonstrates bilateral small nodules in the lung parenchyma that are greatest in the left apex and right lower lobe. There is a suggestion of right paratracheal, aorticopulmonary window, subcarinal, and bilateral hilar lymphadenopathy. (b) Posteroanterior chest radiograph obtained 10 months later demonstrates that the lung parenchymal disease has a similar distribution but is more extensive and confluent. The lymphadenopathy is similar in extent and distribution. (c) Chest CT scan at the level of the inferior hila obtained at the same time as b demonstrates bilateral small nodules in the lower lobes, with confluent opacity in the right lower lobe. There is a 5-mm nodule (arrow) in the right upper lobe abutting the minor fissure.

View larger version (122K): [in this window] [in a new window] [Download PPT slide]   Figure 3c. Images in a 32-year-old woman (patient 5) who developed sarcoidosis 7 years after HIV infection was diagnosed. (a) Posteroanterior chest radiograph obtained when sarcoidosis was diagnosed demonstrates bilateral small nodules in the lung parenchyma that are greatest in the left apex and right lower lobe. There is a suggestion of right paratracheal, aorticopulmonary window, subcarinal, and bilateral hilar lymphadenopathy. (b) Posteroanterior chest radiograph obtained 10 months later demonstrates that the lung parenchymal disease has a similar distribution but is more extensive and confluent. The lymphadenopathy is similar in extent and distribution. (c) Chest CT scan at the level of the inferior hila obtained at the same time as b demonstrates bilateral small nodules in the lower lobes, with confluent opacity in the right lower lobe. There is a 5-mm nodule (arrow) in the right upper lobe abutting the minor fissure.

	DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

The scarcity of cases reported in the literature (1–5) and the necessity for our search of hospital databases to include a long interval suggests that, in fact, new-onset sarcoidosis occurs only rarely in HIV-infected patients. The current series, which included 10 HIV-infected patients with newly diagnosed pulmonary sarcoidosis, is, to our knowledge, the largest to date. The range of radiologic and clinical features of sarcoidosis in this group of HIV-infected patients resembles the spectrum of radiologic findings of sarcoidosis described typically in non–HIV-infected patients.

Bilateral hilar and mediastinal lymphadenopathy is the most frequently described (6–9) radiographic finding in sarcoidosis, occurring in 70%–90% of patients. Lymphadenopathy was similarly present in 70% of the HIV-infected patients in this series. On chest radiographs, lung parenchymal disease is evident in about half of the cases of newly diagnosed sarcoidosis (6,7,9). Ninety percent of patients in the present series had lung parenchymal abnormalities on the chest radiograph. The dominant lung parenchymal abnormalities in sarcoidosis, described (6,7,9) in about 75% of cases, are small nodules and reticulonodular opacities. These findings were present on eight (80%) of 10 chest radiographs in this series. Large nodules and areas of consolidation were described in 10%–20% of cases and were present in 30% of patients in this series.

At chest CT, small nodules ranging in size from 2 to 10 mm are the most frequently reported lung parenchymal abnormalities in sarcoidosis, occurring in 50%–100% of cases. The nodules are usually distributed along the bronchovascular bundles, subpleurally, and in the interlobular septa (10–17). In the present series, small nodules were evident in seven (88%) of eight patients and had a subpleural and peribronchovascular distribution in all patients. Thickening of the interlobular septa was also present in the majority of patients with small nodules. Linear opacities are found in 32%–88% of patients with typical sarcoidosis and occurred in three (38%) of eight patients in this series. Ground-glass and focal opacities are described (10-17) in 16%–75% and 44% of cases and were present in four (50%) and in five (62%) of eight patients, respectively, in this series.

Cysts or cavities may be a manifestation of honeycombing, cavitation, cystic bronchiectasis, or preexisting bullae or pneumatoceles (9). Cavitation is a rarely described feature in sarcoidosis but was evident in one patient in the present series. Another patient in this series had thin-walled upper lobe-cysts, which may have been related to a prior episode of P carinii pneumonia or to preexisting bullae rather than to sarcoidosis. Pulmonary fibrosis was not present in any patient in this series. Fibrosis is described (7,9,10,12,15–17) in up to 38% of cases of sarcoidosis. The presence of fibrosis is usually a reflection of the duration of disease. Its absence in this series can be largely attributed to the new diagnosis of sarcoidosis and perhaps to the fact that HIV-infected patients usually receive close follow-up care. Thus, the patients in this series may have received a diagnosis of sarcoidosis earlier than did other patients.

The spectrum of clinical signs and symptoms of sarcoidosis in the present series is similar to that seen in typical sarcoidosis (9), although the patients in this series were more frequently symptomatic. Eighty percent of patients in this series were symptomatic at the time sarcoidosis was diagnosed, compared with about half of the patients with typical sarcoidosis (9).

All of the symptomatic patients in this series had pulmonary signs or symptoms, which are described (9) in one-third of patients with typical sarcoidosis. The range of pulmonary signs and symptoms was typical of sarcoidosis and included shortness of breath, cough, chest pain, and wheezing. One patient (10%) in this series had hemoptysis, which is described (9) in 6% of patients with sarcoidosis. Three of the patients in this series (all of whom had pulmonary symptoms) had extrathoracic signs or symptoms. These signs or symptoms included a rash, hepatosplenomegaly, and parotid enlargement. In typical sarcoidosis, cutaneous involvement is described (9) in 20%–30% of patients, hepatosplenomegaly in 20%, and parotid swelling in 60%. The serum angiotensin-converting enzyme level was elevated in five (83%) of six tested patients in this series and is described (9) to be elevated in up to 90% of patients with typical sarcoidosis.

Reconstitution lymphadenitis has been described recently in a number of HIV-infected patients who were co-infected with M avium-intracellulare complex (18) or tuberculosis (19,20) and who began treatment with HAART. These patients developed fever and lymphadenopathy coincidently with the antiretroviral therapy–induced partial immune reconstitution. Their signs and symptoms were attributed to an exuberant immune response to a previously established infection. This phenomenon has been described as a disease related to restoration of the immune system.

The relationship between initiation of HAART and new-onset sarcoidosis in two patients and a sarcoidosis flare-up in one patient in the present series is intriguing. The chest radiographic and CT findings in the two patients who developed sarcoidosis after initiation of HAART in the present series were somewhat atypical. One of these patients had cavitary nodules without lymphadenopathy. In addition to histopathologic analysis that yielded confirmatory findings, she underwent extensive evaluation for mycobacterial and fungal infection, which was unrevealing. The other patient had large nodules associated with lymphadenopathy.

Three cases of new-onset sarcoidosis or a sarcoidosis-like pulmonary disorder have recently been described (4,5) in HIV-infected patients receiving HAART. In two of these patients, diffuse small nodules without lymphadenopathy were depicted at chest radiography and at CT. The other patient had bilateral hilar and mediastinal lymphadenopathy without lung parenchymal disease. Findings in these cases suggest that antiretroviral therapy–induced partial immune reconstitution may increase the likelihood that HIV-infected patients will develop sarcoidosis as a disease related to restoration of the immune system.

This series is limited by its retrospective nature and by the small number of patients included in it. In addition, it is possible that undiagnosed concurrent illness or alternative diagnoses may have been responsible for the clinical, radiologic, and histopathologic findings that were attributed to sarcoidosis in these patients. This dilemma arises in all cases of sarcoidosis, which is a diagnosis of exclusion, even in typical cases. In HIV-infected patients, this limitation is accentuated by their predisposition to the development of a variety of opportunistic conditions. However, this limitation is mitigated by the fact that the patients in this series underwent a thorough and unrevealing work-up for other diagnoses.

Bilateral hilar and mediastinal lymphadenopathy associated with pulmonary nodules ranging in size from less than 5 mm to greater than 1 cm was the dominant chest radiographic and CT finding of newly diagnosed sarcoidosis in this series of HIV-infected patients. In non–HIV-infected patients, these findings would lead to strong consideration of a diagnosis of sarcoidosis. However, in HIV-infected patients, it is important to note that infectious diseases with similar manifestations may be present. Tuberculosis, infection with M avium-intracellulare complex, histoplasmosis, and cryptococcosis occur with increased frequency in HIV-infected patients and often demonstrate hilar and mediastinal lymphadenopathy associated with pulmonary nodules (21). Because of their higher frequency of occurrence, infections would be more likely than sarcoidosis to cause these radiologic findings in HIV-infected patients. Less commonly, HIV-associated neoplasms, such as lymphoma, Kaposi sarcoma, and metastatic cervical cancer, can also have a similar radiologic appearance (21).

In summary, we describe findings in 10 HIV-infected patients who developed new-onset pulmonary sarcoidosis. In two, sarcoidosis developed after initiation of HAART. The radiologic features of sarcoidosis in this series were similar to those previously described for sarcoidosis in non–HIV-infected patients. The diagnosis of sarcoidosis, although uncommon, should be considered in HIV-infected patients who develop lymphadenopathy and pulmonary nodules, and sarcoidosis may be a manifestation of disease related to restoration of the immune system.

	ACKNOWLEDGMENTS

 
The authors thank Seymour Sprayregen, MD, for his careful review of the manuscript and Eleanor J. Murphy for her assistance with manuscript preparation.

	FOOTNOTES

 
Abbreviations: HAART = highly active antiretroviral therapy, HIV = human immunodeficiency virus

Author contributions: Guarantor of integrity of entire study and study concepts, L.B.H.; study design, G.L., L.B.H.; definition of intellectual content, all authors; literature research, G.L., A.S.; clinical studies, all authors; data acquisition and data analysis, all authors; statistical analysis, L.B.H.; manuscript preparation, all authors; manuscript editing, L.B.H., P.L.M., C.S.W.; manuscript review, all authors.

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