Bridging the Gap: Conference Record [Abstract book, International Conference on AIDS (12th: 1998: Geneva, Switzerland)]

572 Abstracts 32259-32262

12th World AIDS Conference

uated for intact cognitive function using the Mini-Intellect test. Patients were
subsequently screened for the presence of psychiatric disorders using the MiniInternational-Neuropsychiatric-lnterview (MINI). More specifically, anxiety was
evaluated using the Zung self-rating anxiety scale as well as the Hamilton anxiety
scale (HAM-A). The patients were also evaluated clinically and their CD4+ T-cell
counts were determined by flow cytometry.
Results: Cognitive impairment was found in several patients but none of the
patients presented with overt dementia. According to the MINI 35% of the patients
were diagnosed with a major depressive disorder. A further 3% had dysthymic
disorder while bipolar disorder was diagnosed in 6%. Concerning anxiety disorders the following was found; Panic disorder: 37%, agoraphobia: 9%, social
phobia: 15%, specific phobias: 10%, obsessive-compulsive disorder: 3% and
generalized anxiety disorder: 21%. Post-traumatic stress disorder was diagnosed
in 6 patients; in one of these patients the relevant stressor was the diagnosis of
HIV seropositivity. Thirty-two of the patients scored above the cut-off on both the
HAM-A and and the Zung scales. There was no apparent correlation between
either disease stage, or time from diagnosis, and anxiety.
Conclusions: Psychiatric comorbidity is common in HIV/AIDS patients. Anxiety
and depressive disorders were found in a large number of patients; significantly
more than what is to be expected in the general population. Treatment of these
comorbid psychiatric syndromes could lead to an improved quality of life. The
identification and treatment of psychiatric problems in HIV/AIDS patients should,
therefore, be actively pursued.
342* /32259 Discrepant immunologic and virologic responses
in HIV-infected patients receiving triple
combination therapy
Christophe Piketty1, P. Castiel1, L. Belec2, L. Weiss1, J.P. Abouker3,
M.D. Kazatchkine1. 1INSERM U430 Department of Immunology - Hospital
Broussais 96 Rue Didot - 75014 Pairs; 2Department of Microbiology - Hospital
Broussais Paris; 3lnserm SC10, Villejuif, France
Background: The addition of an HIV protease inhibitor to two dideoxynucleoside
agents results in increased CD4 cell counts, reduced plasma HIV viral load and
improved survival in patients with advanced HIV disease. Limited information is
available at present on the patterns of changes in immunologic and virologic
surrogate markers in patients treated with protease inhibitors.
Methods: We have analyzed the clinical, virologic and immunologic outcome of
a cohort of 162 protease inhibitor-naive, antiretroviral-experienced patients with
advanced HIV disease (mean CD4 cell count and plasma HIV RNA at baseline:
69 ~ 5 x 106 cells/L and 4.75 ~ 0.07 log copies/mL), treated with indinavir in
combination with two nucleoside analogues throughout a mean period of follow
up of 10.5 months.
Results: At 9 months, the mean increase in CD4 cell counts and mean decrease in plasma HIV viral load were 138.5 x 106 cells/L and 1.55 log/mL,
respectively. The proportion of patients who achieved a plasma viral load below
the threshold of detection (500 copies/mL) was 53.5% and that of patients whose
CD4 cell counts reached values above 200 x 106 cells/L, was 43.2%. Twenty one
percent of the patients exhibited discrepant virologic and immunologic responses
to treatment, of whom half failed to exhibit increases in CD4 cells >50 x 106
cells/L, despite a decrease of HIV RNA > 1 log, and half exhibited increased CD4
cell counts in the absence of virologic response The incidence of AIDS-defining
events in the latter group of patients (1/17) was similar to that of immunologic and
virologic responder patients (7/92), whereas their incidence was higher in patients
who failed to exhibit a virologic and immunologic response (2/8) and those who
failed to increase CD4 cells despite a significant decrease in viral load (4/17).
Conclusion: Our results question the relevance of the quantitative determination of viral load for monitoring the efficacy of therapy and determining changes in
the antiretroviral regimen, in a subgroup of patients who behave as immunologic
responders to antiviral therapy.
132260 Spontaneous pneumothorax (SP) etiology in patients
with HIV infection
Antonio Rivero1, F. Lozano2, A. Esteve3, A. Serrano4, E. Cordero5, F. Jimenez6,
M. Torres7. 'Unidad De Infecciosos, Hosp. Virgen De La Victoria Campus
Universitario De Teatino, S/N Malga-29010-; 2H. Virgen De Valme Sevilla; 3H.
Virgen De La Victoria Malaga; 4H. Puerta Del Mar Cadiz; 5H. Virgen Del Rocio
Sevilla; 6H. Carlos Haya Malaga; 7H. Punta Europa Algeciras, Esparia
Objective: To evaluate the SP incidence and etiology in HIV infected patients in
Andalucia, (south of Spain).
Method: We study HIV infected patients with SP. Period: 1987-1996. Analysed
data: age, sex, risk practice for HIV infection, SP etiology, CD4+ cell count,
previous CDC stage (1993), medical record of tuberculosis (TBC), Pneumocystis
carinii pneumonia (PCP), or aerosolised pentamidine use, and extension and
location of SP. It was considered as bilateral SP when a new SP was happened
between 0 hours and 4 weeks after contralateral SP.
Results: No of episodes studied: 100 of 98 patients. Sex: 90 male, 10 female.

Risk practice: 80 intravenous drug user (IDU), 10 heterosexual, 6 homosexual
and 4 other. We found at least one event that we could consider responsible for
SP in 86 cases. Etiology: bacterial 35, PCP 32, TBC 19 and other 4. Among 14
without cause: 4 of them had antecedent of TBC, 3 of TBC + PCP, and 1 TBC
+ aerosolised pentamidine use. The SP incidence was: 0.9% in HIV infected,
2.3% in AIDS, 1.2% in TBC and 3.1% in PCP. 84 cases were unilateral and 14
bilateral. CD4+ cell count: I (T4 > 500):5, II (200 < T4 < 500): 11, III (T4 <

200):73. We checked relationship among SP etiology and CD4+, risk practice
and SP extension. Etiology according to risk practice (%): IDU: bacterial 41, PCP
23, TBC 21. No IDU: bacterial 10, PCP 65, TBC 10. Etiology and extension (%).
Bilateral: bacterial 6, PCP 66, TBC 13. Unilateral: bacterial 40, PCP 26, TBC 19.
Etiology and immunity (%). T4 < 200: bacterial 28, PCP 42, TBC 19. T4 > 200:
bacterial 56, TBC 25.
Conclusions: 1 The more frequent cause of spontaneous pneumothorax in our
study is bacterial. 2 Pneumocysti carinii pneumonia is the second cause although
it is the fist in many studies. 3 Tuberculosis is and important etiology. 4 The spontaneous pneumothorax etiology in HIV infection is related with immunodeficiency
degree, risk practice and pneumothorax extension.
S32261 Two-year survey (1996-97) of pulmonary manifestations
in HIV-infected patients in an infectious disease
department in northern Italy
Matteo Bassetti, C. Bussolino, A. Di Biagio, A. Collida, A. Beltrame, V. Del Bono,
D. Bassetti. First Department of Infectious Disease, University of Genoa,
Ospedale S. martino, L. Go Rosanna Benzi 10 16132 Genova, Italy
Objective: To evaluate the incidence of pneumonia in HIV+ patients hospitalized
in our department during the years 1996-97.
Patients and Methods: We considered all the HIV+ patients hospitalized from
1/96 to 12/97 in our department and analyzed the percentage of hospitalization for
pulmonary pathology, and the type of pulmonary infection. The following parameters were evaluated for each patient: age, gender, risk factor, prophylaxis, CD4+
lymphocyte count, cultural examinations (sputum and blood culture), symptoms,
chest X-rays, antiretroviral therapy, and clinical outcome.
Results: Two hundred eighty-three HIV+ pts were hospitalized, of whom 194
in 1996 (69%) and 89 in 1997 (31%). We observed 45 pts with pulmonary manifestations (16%), 35 males and 10 females with age ranging from 27 and 55
years (mean age: 37.8 years), 7 homosexuals (15.5%), 3 heterosexuals (6.6%),
and 35 TD (77.9%). There were 28/45 tobacco smokers (>20 cigarettes/day).
Pulmonary pathology was observed in 32 pts in 1996 (16.4%) and in 13 in 1997
(14.6%). The etiology of pneumonia was P. carinii in 14 pts (31%), bacterial in
25 pts (56%), tuberculosis in 5 pts (11%), and aspergillosis in 1 (2%). Ten of the
patients with PCP had received anti-PCP prophylaxis (5 pts with TMP-SMX and 5
with pentamidine). Mean and median (range) CD4+ cells were 52 and 37 (0-146)
cells/lI for pts with PCP, 77 and 21 (3-610) cells/pil for bacterial pneumonia, 93
and 85 (3-232) cells/p l for pts with tuberculosis. The incidence of symptoms in
our study population was: fever (96%), asthenia (82%), cough (48%), chest pain
(46%), dyspnea (28%), and cyanosis (6%). At the time of hospitalization 8 (17%)
of the pts had never received antiretroviral therapy, 22 (48%) were treated with
AZT, 13 (28%) were treated with the combination of two nucleoside analogs, and
2 (4%) with triple therapy (2 nucleoside analogs + 1 protease inhibitor). Sixteen
(35%) patients had exitus during hospitalization.
Conclusions: The incidence of hospitalization for pneumonia has remained
unchanged, in spite of the decrease of the number of pts hospitalized for HIVrelated pathologies, likely due to HAART efficacy. Bacterial pneumonia represents
the most frequent cause of hospitalization among pulmonary pathology, followed
by pneumocystosis, (particularly in patients with CD4+ <200 cells/tl), and tuberculosis. The occurrence of such pathologies appears correlated with the lack of
HAART treatment.
32262 | Bacterial pneumonia in HIV-infected patients
Lorenzo Minoli, L. Cocchi, R. Giacchino, V. Broletti, R. Maserati. Infect Dis
Dept-Policlinico San Matteo Via Taramelli 5 Pavia, Italy
Background: Even if since 1993 bacterial pneumonias (BPs) represent an AIDSdefining illness, the knowledge about this infection lies far behind the one available
for the majority of other opportunistic infections in HIV-infected individuals.
Methods: This retrospective analysis included all the clinical charts of HIV+
pts discharged from our Institution between 1/92 through 12/97 with a diagnosis
of BP (TB and atypical mycobacteria BP excluded). Isolates from any pertinent
source (i.e. blood, sputum, pleural fluid and others) were considered for causative
agent (CA) identification and susceptibility studies.
Results: Out of 120 identified cases (representing 18.7% of discharged HIV+
pts in that period) we were able to recover reliable data on 98 pts (69 m, 29
f; mean age: 33 yrs; 67 IVDA, 16 eterosex, 7 gay m, 3 hemophiliacs, 5 undetermined). Mean CD4+ cell count at diagnosis was 122/mcL (0-1050). Chest
X-ray showed a segmental or lobar infiltrate in the majority of cases (87%). Four
pts had homolateral pleural effusion. Unilateral or bilateral pleural effusion were
present in 25 (25.5%) pts; 9 subjects had nodular lesions and 4 cavitary lesions.
Two patients also showed lymphoadenopathy. CAs resulted to be S.aureus (14
cases), Paeruginosa (11), S.pneumoniae (6), R.equi (4), Enterobacter spp. (3),
K.pneumoniae (3) plus one case each of E. coli, Peptostreptococcus spp, Enterococcus spp. CA was not identified in 55% of cases and Dx was done on clinical
grounds.
Conclusion: This retrospective study demonstrated a high prevalence of

S.aureus BPs (8 out of 14 cases by MRSA), the causative role of otherwise rare
agents such as R.equi and the overall typical appearance of chest X-ray studies
(even if pleural involvement resulted relatively frequent).