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

544 Abstracts 32118-32122

12th World AIDS Conference

patients. In this study the influence of gastrointestinal (GI) symptoms, duration
of symptoms and presence of intestinal pathogens in HIV as factor of survival in
2700 HIV patients should be examined.
Methods: In a prospective study of HIV patients (70% AIDS) with GI symptoms, 397 patients were found (by stool examination or endoscopic biopsies) to
carry enteropathogens. Main findings were Cytomegalovirus (26.9%), Candida
(20.7%), Herpes (10.8%) and M. avium complex (8.4%). Factors of survival (enteropathogen, duration of symptoms, variety of symptoms, complications) were
determined by life table analysis and log rank test.
Results: Weight loss (p < 0.01) and dysphagia (p < 0.05) were found to
be factors of reduced survival, whereas abdominal pain, diarrhea, retrosternal
pain or vomiting were not significantly different. Multiple symptoms are factors
of reduced survival in comparison to a single symptom (p < 0.01). While stool
enteropathogens do not mean a poor prognosis, bioptic findings (CMV, Candida,
Mycobacteria) are significant factors (p < 0.01). In addition, duration of symptoms (acute vs. chronic symptoms) did not show significant differences (p >
0.05). In cases of life-threatening complication following enteric infection, only GI
perforation is a factor of short survival, while GI obstruction or bleeding are not
significantly different.
Conclusion: Intestinal enteropathogens in HIV infection (e.g. Cytomegalievirus, Candida or mycobacteria) predict shorter survival and should therefore
be prevented or checked early. Some single GI symptoms (or multiple symptoms)
and intestinal perforation are relevant factors for the prognosis, too. Since infections diagnosed by biopsy (CMV, Candida, M. avium) influence the survival (but
not stool findings), endoscopy in symptomatic patients is recommended.
32118 1 HBs seroconversion of a precore hepatitis B virus mutant
infection with lamivudine-containing anti-HIV regimen
Francois Raffi1, Jerome Hoff2, F. Bani Sadr1, M. Gassin2. 1Maladies Infectieuses
Et trolicales Hotel-Dieu 44035 Nantes Cedex 01; 2Laboratoire Virologie
Hotel-Dieu, Nantes, France
Background:Chronic B hepatitis due to precore hepatitis B virus (HBV) mutants
are often of bad prognosis in immunodeficient patients. Precore HBV mutant is
suspected on the association of a HBe seroconversion (Ac HBe) with detection
of the HBV genome (HBV-DNA) in the serum. Chronic B hepatitis in HIV infected
patients poorly respond to alpha-interferon (IFN). Although lamivudine (3TC) has
promising activity on HBV infection in HIV patients, experience on precore HBV
mutant infection is lacking
Case Report: A 35 year-old man wich asymptomatic HIV infection was diagnosed in 1994 with a precore HBV mutant co-infection. Liver biopsy disclosed
a chronic active hepatitis. Six months alpha-IFN therapy failed to improve liver
transaminases nor serum HBV-DNA. Anti-HIV therapy was initiated in August
1996, including zidovudine, zalcitabine, and ritonavir, and led to persistent control
of plasma HIV RNA (4.9 loglo at baseline, <400 copies/ml since the second month
of treatment) and rise of CD4 cell count (from 316 to >600/mm3). In October
1996, HBV-DNA was 4140 pg/ml; zalcitabine was changed to lamivudine (150
mg bid): HBV-DNA fell under the limit of detection by molecular hybridization (10
pg/ml) and ALAT normalized after a transient elevation (18 x N). Seroconversion
from HBs Ag to HBs Ac at a protective rate (80 IU/ml) occurred in December
1997, at which time transaminases were normal and HIV RNA < 400 copies/ml.
Conclusion: Lamivudine, as part of an anti-HIV treatment including a protease
inhibitor, induced a dramatic decrease of the HBV replication and a resolution
of the HBV infection despite 2 factors of bad response to IFN treatment: HIV
infection and precore HBV mutant.
32119 Esophageal disease in AIDS
Dirce Bonfim Lima1, E.J.S. Silva2, P.R.A. Pinho1, D.D.P. Paiva1. 1Universidade
do Estado Rio de Janeiro, Rua Rodolpho de Souza 105 Vila Isabel Rio de
Janeiro-RJ-ZC 20551-270; 2Minestbrio da Saude, Rio de Janeiro, RJ, Brasil
Objectives: To evaluate esophageal involvement in AIDS patients with upper
gastrointestinal symptoms.
Design: Retrospective study.
Methods: In this study, between 1985 and 1996, adult patients with confirmed
HIV infection, upper gastrointestinal and esophageal symptoms underwent upper
gastrointestinal endoscopy primarily with Olympus fiberscopes and later Fujinon
video endoscopes. Biopsies were performed in all cases with standard biopsy
forceps. At least seven specimens were obtained from each lesion. They were
fixed in 10% formalin and stained with Hematoxylin and Eosin (H & E), Gomori
methenamine silver for fungi and Fite for acid-fast organisms.
Results: Two hundred and fifty six patients with the average age 38.8 years
and standard deviation 9.2 were submitted to esophagogastroduodenoscopy.
One hundred and seven patients had esophageal disease diagnosed (41.7%).
The endoscopy showed: Whitish plaques appearing as dense confluent exudates
diffuse in the esophagus whose biopsy revealed Candida esophagitis (42 cases
39%). Ulcers with raised borders and poor necrotic bases whose biopsy revealed
Cytomegalovirus esophagitis (14 cases 13%), Herpes simplex esophagitis (6
cases 5.6%), non-Hodgkin's Lymphoma (1 case 1%), Papillomavirus esophagitis

(6 cases 5.6%), three of them confirmed by immunoperoxidase staining. Raised
purple lesions (3 cases 3%) whose biopsy showed Kaposi's sarcoma. There
were 35 idiopathic ulcers (32.8%) and three of them healed with zidovudine
treatment.
Conclusion: Opportunistic esophageal disease was diagnosed endoscopically
in 41.7% of our patients with AIDS and upper gastrointestinal symptoms. Candida

esophagitis is the most common cause of symptomatic disease, followed by
Cytomegalovirus esophagitis. Idiopathic esophageal ulceration was present in 35
of 107 patientswith dysphagia. Molecular biology methods would be the ideal
technique for maximum diagnostic yield.
32120 1 Evaluation of HIV infection's influence on natural course
of chronic C hepatitis
Anita Olczak, Waldemar W.H. Halota, Ewa E.T.S. Topczewska-Staubach,
Maegorzata M.P. Paweouska, Arkadiusz A.K. Kuziemski. Department of
Infectious Diseases, UL Floriana 12 85-030 BYDGOS2C2, Poland
The aim of the study was assessement of potential influence of HIV-1 infection
on natural history of chronic C hepatitis. Investigations were performed in two
20-persons groups of patients with chronic C hepatitis. In one of them were
included patients coinfected HIV-1, in the asymptomatic stage of infection (CD4
between 200-500/mm3). To the second belong HIV-seronegative, HCV-infected
patients. Investigations were perform during two years. Morphological examinations of the liver have been done at the begining and in two, one years intervals
(three times). Liver biochemical tests were performed sistematically. Diagnosis
of HCV infection is based on positive immunoenzymatic tests and HCV-RNA in
sera. We have used Scheuer classification for morphological assessement. HIV
infections were diagnosed with Western-Blot.
Results: The course of chronic C hepatitis was similar in both examined groups.
They were not any statistically significant differences between biochemical examinations' results (ALT, bilirubin, alkaline phosphatase, prothrombin index). Total
immunoglobulins concentration was higher in group HIV coinfected. They were
no any essential differences in the liver pictures of analysed patients.
Conclusion: Asymptomatic HIV infection do not change natural course of
chronic C hepatitis.
321211 Association of parasitic infections and Salmonella
cholerauis bacteremia in HIV infected persons
Carlos H. Ramirez-Ronda1, C.R. Rivera-Vazquez, J. Figueroa, S. Saavedra,
C.R. Ramirez-Ramiezrez. San Juan VAMC - Univ. Puerto Rico School Medicine,
San Juan; 181 Mirador St, Paseo Alto, San Juan, PR, Puerto Rico (USA)
Purpose: To present the association of S. cholerasuis bacteremia with concomitant infections with Giardia lamblia and Blastocystis hominis.
Methods/Results: Two HIV+ patients presented to our institution with a clinical
picture of fever, sepsis, diarrhea and abdominal cramps. A 39 y/o male HIV+
person with history of IVDA, on ddl+d4T with CD4 cell count of 209, was in his
usual state of health when he developed sudden onset of fever, chills, epigastric
abdominal pain, diarrhea, non productive cough and later felt prostrated. On examination he was clinically septic with stable vital signs and no specific physical
findings. Blood culture grew S. cholerasuis and stool culture was negative but the
stool showed abundant Blastomyces hominis. He was treated with ciprofloxacin
and continued on TMP-SMX, he recovered. A second patient is a 36 y/o male
HIV+ person with history of IVDA, taking d4T, 3TC and saquinavir with a CD4
of 230, on TMP-SMX prophylaxis that presented with exacerbation of his loose
stools and abdominal cramps and fever. The patient was clinically septic and blood
cultures grew S. cholerasuis, stool examination revealed large amounts of Giardia
lamblia. He was treated and recovered. Both patients share the consumption of
raw eggs, prepared in a punch (as an extra nutritive supplement).
Conclusions: Salmonella cholerasuis has been reported in bacteremias in
HIV+ patients, the association of heavy intestinal parasitation and ingestion of
punch with raw eggs makes these cases particular. The possibility that heavy
parasitic infestation even with non penetrating parasites, can result in increased
inflammation and a greater chance for invasion of the bacteria to the blood stream
is raised.
32122 Helicobacter pylori infection in HIV positive patients with
antral gastritis
Zofia Przedlacka, J. Firek, Z. Kaminski, P. P. Pulik, B. Gorecka, G. Cholewiska,
A. Horban. 37 Wolska St, Warzawa 01-201 AIDS Diagnosis & Therapy Center,
Poland
Backgrounds: The aim of the study is to evaluate the prevalence of Helicobacter
pylori infection in HIV positive patients with chronic antral pathology and to find the
correlation between Helicobacter pylori infection and cellular immunodeficiency
or antibiotic therapy.
Methods: Forty eight HIV positive patients (mean age 37.3), that underwent
upper endoscopy and antral biopsy with histopathological diagnosis of chronic
gastritis or ulceration were retrospectively compared to the group of 217 patients
(mean age 49.6) not at high risk of HIV infection, with the similar histopathology
findings. The tissue samples were additionally stained for Helicobacter pylori
detection and examined by one pathologist. Cellular immunity was measured by
CD4 count.
Results: Helicobacter pylori was identified in biopsy specimens from 18 of 48

(37.5%) HIV positive patients, while in 105 of 217 (48.4%) controls, that was not
statistically significant. Helicobacter pylori was present in tissue samples in 9 of
25 (36%) HIV infected patients with CD4 count under 200/mm3 and in 9 of 23
(39%) with CD4 count over 200/mm3. Only 2 of 13 (15.4%) patients with current
antibiotic therapy and 16 of 35 (45.7%) without such a therapy were positive for
Helicobacter pylori.