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

550 Abstracts 32149-32153

12th World AIDS Conference

CD16, CD25, CD56 negative, and CD57 positive. On cluster analysis the group
could be divided into 2 subgroups on the basis of whether the CD8 counts were
above or below 2.5 x 109/i.
All patients tested were negative for HTLV-1 infection. CD8 counts above 2.5 x
109/1 were sustained for between 9 and 22 months, with spontaneous variations
noted.
Conclusion: CD8 lymphocytosis in this group of HIV positive patients represents both monoclonal and polyclonal expansion of T-large granular lymphocytes
with a highly characteristic immunophenotype (CD3+, CD4-, CD8+, CD16-,
CD56-, CD57+). A subgroup showed marked CD8 lymphocytosis, the majority
containing monoclonal CD8 populations. Hypergammaglobulinaemia, and in one
case, paraproteinaemia were associated features. Our data suggest this is a
benign reactive condition, the mechanism of which we are investigating.
32149 Reversal of neutropenia in AIDS patients with CD4 cells
count below 50 treated with combined antiretroviral
therapy including protease inhibitors (PI)
Jacques Gilquin. Fondation Hospital St. Joseph, 185 Rue Raymond Losserand,
75014 Paris, France
Neutropenia is reported in over 50% of AIDS patients (P). Multiple aetiologies may be associated: ineffective granulopoiesis, antineutrophilic antibodies,
cytotoxic effects of drugs, vitamin deficiencies, opportunistic infections and malignancies. Myeloid growth factors are often required to stimulate the granulopoiesis
but they have only a transient effect. Recent data suggest that PI may correct
HIV related haematological disorders.
We report on the reversal of long lasting neutropenia (>9 months) in three AIDS
patients with CD4 counts of <50 cells/mm3 treated with stavudine + lamivudine
+ (ritonavir or indinavir). The three patients had Granulocyte-colony stimulating
factor (G-CSF) dependent neutropenia and recurrent bacterial infections. Normal
absolute neutrophil counts (ANC) were observed at 5 months of antiviral therapy and persist after one year of follow-up. The three patients could stop their
supportive therapy.
Data at baseline and at 5 months of PI therapy:

P Age/sex CD4+ Viral load Duration of
increase reduction cytopenia prior
(cells/mm3) (log 10/mL) PI therapy
1 36/M 2-632 >2.3 3.5 years
2 60/F 5-112 2.3 9 months
3 49/M 1 83 1.4 5 years

ANCs at ANC at
baseline 5 months of
(cells/mm3) PI therapy
200-800 4500
150-400 1300
100-700 5000

32151 Idiopathic CD4+ T-cell lymphocytopenia (ICL): Experience
in the West Midlands, UK
Andrew J. Winter1, M. Shahmanesh2, T. Mughal3, H. Nelson4,
D.S. Kumararatne5. 1Dept. of GU Medicine, 2Whittall St. Clinic, Birmingham;
30ncology Dept., Royal Preston Hospital, Preston; 4 Dermatology Dept., Queen's
Hospital, Burton Ontrent; 5lmmunology Dept., Heartlands Hospital, Birmingham,
UK
Background: Since 1990 we have fully evaluated five patients with idiopathic
CD4+ T-cell lymphocytopaenia. We present the demographic and clinical findings
below.
Case Sex Age at Subsequent Latest counts Medical conditions
No. diagnosis follow-up (x 109/1)
(y) (m) CD4 CD8
1 F 16 80 m 0.08 0.14 Multiple plantar and palmar warts since 1988;
Cervical and vaginal condylomata since 1994
2 F 20 53 m 0.10 0.69 Disseminated genital condylomata since 1990
3 F 35 26 m 0.49 0.20 Recurrent vaginal candidiasis since 1993;
Severe pneumonia x7 since June 1995;
Severe cellulitis x4 since May 1996
4 M 19 17m 0.13 0.51 Osteomyelitis July 1996;
Primary high-grade bone lymphoma June 1997
5 M 46 91 m 0.05 0.16 Auto-immune haemolytic anaemia 1988;
(deceased High-grade B-cell lymphoma November 1995
May 1997) (Case report in press in Br J Hosp Med)
Conclusions: We have investigated five patients with ICL. All patients had
normal immunoglobulins, normal purine and pyrimidine metabolism, and were
negative for HIV-1 antibody and HIV-1 DNA by PCR. Two patients have persistent
HPV infection: one has been helped by topical imiquimod. Two patients have
developed high-grade lymphoma (one a primary bone lymphoma) of which one
has died. One patient presents with recurrent aggressive septic shock but has
normal in-vitro neutrophil function.
32152 The aetiology and natural history of neutropenia in HIV
disease
David Moore, S. Portsmouth, T. Benepal. Kobler Centre, Chelsea & Westminster
Hospital, 369 Fulham Road, London SW, England
Background: Neutropenia occurs often in HIV disease and seems to be well
tolerated. As the natural history is ill defined, this study aimed to define the
course of neutropenic episodes by serially measuring the absolute neutrophil
count (ANC) from the onset of neutropenia. Demographic and clinical data were
also collected.
Methods: In all adult patients with neutropenia (ANC < 1000/mm3) serial
ANCs were performed weekly (after 6 weeks, fortnightly) until the ANC rose
to >1000/mm3. Subjects on cytotoxic chemotherapy or with no prior ANC
>1000/mm3 were excluded. All prior ANCs, CD4/CD8 counts, drug therapy
and illnesses were recorded.
Results: 77 patients were enrolled over a 6 month period. 71 (92%) took at
least one drug known to cause neutropenia and 29 (38%) were taking 3 or more
myelosuppressive drugs. Lamivudine and cotrimoxazole +/- zidovudine were
taken by 30 subjects (39%). In 41 of the 77 patients the episode of neutropenia
was their first recorded (mean number of previous ANCs = 18), occurring at a
median CD4 count of 90 (range 2-700). Median ANC prior to neutropenia in this
group was 1900/mm3, higher than for those with prior neutropenia (1400/mm3;
p < 0.001), recorded a median of 5 weeks earlier in both groups. 21 patients
were deemed unevaluable for the natural history analysis, mainly due to excessive delays between ANCs. Median duration (12 days) and median nadir
ANC (800/mm3) of neutropenic episodes was similar for the two groups. Only 6
infections occurred, none life threatening and only 2 culture positive. Significantly
lower ANC nadirs (p = 0.02) and CD4 counts (p = 0.009) were found in those with
infection, who were also more likely to have had previous episodes of neutropenia
(p = 0.004). Neutropenia duration did not predict risk of infection (p = 0.7).
Conclusions: Neutropenia tends to occur late in HIV disease, is usually attributable to drug therapy, generally transient and well tolerated even when drugs
are continued. ANC nadir and CD4 count determine infection risk better than
duration of neutropenia.
32153 Evaluation of granulocyte reserve in AIDS neutropenia by
steroid challenge test to predict the response to G-CSF
Daniele Scevola, Roberto Brustia, Poma Gianluigi, Tosini Giampero. Clinica
Malattie Infettive IRCCS Policlinico S. Matteo 27100 Pavia, Italy
Objective: To study the granulocyte kinetic induced by a steroid challenge test
of 200 mg hydrocortisone i.v. injected in AIDS neutropenic patients in order to
predict the response to G-CSF.
Design: Open clinical study

Methods: After giving informed consent, 32 AIDS patients with absolute neutrophil count (ANC) < 1.0 x 109/L received i.v. a single dose of 200 mg hydrocortisone as steroid challenge test. WBCs and differential counts were obtained
before and hourly for 8 hr after administration. The response to G-CSF 1 microgram/kg/s.c./day was evaluated daily for 10 days.
Results: Extent and duration of neutropenia were associated with drug toxicity
and opportunistic infections involving bone marrow. A more impaired response to

Conclusion: these data suggest that combined antiretroviral regimen including
PI may be effective in the treatment of severe long lasting neutropenia in AIDS
patients.
32150 Immune thrombocytopenic purpura in HIV-infected
children
Maria Jose Mendes', N.P.M. Rubini, A.V.P. Cordovil, F.S. Sion, M.C. Magalhaes,
A.J. Almeida, C.A. Morais-De-Sa. University of Rio de Janeiro; 'Rua Visconde
De Piraja, 568/Apto. 601, Ipanema, Rio De Janeiro, RJ, Brazil
Objectives: Describe the prevalence rate of immune thrombocytopenic purpura
(ITP) in a population of HIV- infected children and investigate the clinical evolution
and relationships of ITP in association with HIV infection.
Methods: We studied retrospectively all the cases of ITP ocurring in children
diagnosed as HIV-infected in our Pediatric Immunology Clinic within the period
of 1986 and 1997. The following aspects were analysed: rate of ITP, correlation
between the development of ITP and the CDC classification, clinical evolution of
ITP and the therapeutic response. The data collected was analysed in accordance
to descriptive statistics methodology.
Results: We observed a ITP prevalence rate of 3.9% (6/154). One of the
patients in the study was lost to follow-up. ITP was the initial clinical manifestation
in 2 (40%) patients and in 3 it occurred between 4 months and 7 years after the
onset of the disease. All the patients, at the time of the ITP, were classified in
the following categories: B1, B2 and B3, with CD4 counts ranging from 123 to
1500 cells/mm3 (median, 600 cells/mm3). All patients presented total remission
of the clinical picture in a variable period of 15 days to 15 months (mediam,
4 months). The treatments used were: intravenous immunoglobulin (IVIG) in 5
patients, steroid therapy (STER) in 4 and danazol in 1, in the following manner:
3 patients were treated with IVIG+STER, 1 with IVIG+STER+ danazol and 1 with
IVIG alone. One patient died one year after the occurrence of ITP with Lymphocitic Interstitial Pneumonitis and pulmonary lymphoma. All the other patients
had favourable outcomes, maintaining there clinical classifications, and surviving
until the end of the study for periods ranging from 6 months to 7 years (median,
2 years).
Conclusions: In our data base we observed that: (1) the prevalence rate of
ITP was 3.9%, (2) a significant percentage of the patients had ITP as initial
clinical manifestation of HIV infection, (3) ITP occurs predominantly in patients
with moderate clinical manifestations and a mild to moderate decline in their
immune function, and (4) the clinical evolution and therapeutic response of ITP
was satisfactory, not being a major cause of any worsening in the clinical picture
or death.