Abstracts Vol. 1 [International Conference on AIDS (11th: 1996: Vancouver, Canada)]

Track B: Clinical Science

Mo.B.1285 - Mo.B.1289

phocytes 14x109/ I with 92% typical LGL, neutrophils 2.3x109/I, platelets 186x109/I,
hemoglobin 15g/dl. CD4 cells I.9x I09/ I. Blood leukaemic cells coexpress CD2 82%, CD3
80%, CD5 82%, CD7 71%, CD8 60%. CD57 40%, CD45RO 68%, CD45RA 63%, but not
CD I16, CD56, nor CD 19. DNA studies using TCR y probe showed( Ional rearrangement of
T-cell receptor gene. Marrow smears showed 32% of LGL. Coornbs te.t was positive with
mild hemolysis. Serum immunoglobulins levels were elevated (Ig( 13.2, igM 6.4, IgA 7.7 g/I)
Type 3 mixed cryoglobulin was detected. A serology for EBV showed elevated titers of IgG
for viral capsid and nuclear antigens. Serum complement levels were normsal Serum tested
negative for rheumatoid factor, antinuclear antibodies, HTLVI and hepatitis CV virus. One
year later he developed thrombocytopenia (I102x109/I) with anti IlbIlla antibodies.
Conclusions: The cause of clonal T LGI_ is not known.The normal counterpart of CD3, CD8,
CD57 cells are thought to represent activated CTlL of unknown antigen specificity. Retroviral
infection may represent a pathway of antigen activation. Clonal expansion ofT LGL have
been reported in HTLVI infected individuals. In HIV infection expansion of LGL have been
reported but they had a NK cell (CD I 6) phenotype and were polyclonally exparnded; to our
knowledge no cases of clonal proliferation of T-LGLs have been previously described.
M. Pulik, Centre Hospitalier d'Argenteuil, 95107 Argenteuil. France
Telephone: [phone] Fax. [phone]
Mo.B. 1285
INDUCTION OF G-CSF BY ACUTE FEBRILE INFECTION BUT NOT BY
NEUTROPENIA IN HIV-SEROPOSITIVE INDIVIDUALS.
Mauss Stefan, Steinmetz HT*,Willers R -.Jablonowski H, Haussinger D. Dept. of Medicine;
"Computer Center, Heinrich -Heine-University, Dbsseldorf; *University of Cologne, Germany
Objective: Persistent neutropenia is frequent in HIV-seropositive (HIV+) individuals particu
arly with advanced HIV-infection.The pathogenesis of this neutropenia remains unexplained
so far. G-CSF is an important factor in neutropoesis. In HIV-seronegative individuals the
endogenous G-CSF serum level seems to be regulated by a negative feed back mechanism.
However the contribution of an altered G-CSF regulation in HIV-associated neutropenia has
not been investigated yet. For this we assessed the role of endogenous G CSF in HIV associated neutropenia.
Patients and methods: Serum levels of G-CSF were determined by ELISA in a) HIV+ individuals with afebrile neutropenia (< 1000 neutrophils/pI) persisting at least four weeks
(n=-28) or b) HIV+ with acute febrile pneumonia (n= 17) and compared with c) HIVseronegative (HIV) patients with afebrile neutropenia (<1000 neutrophils/pl) due to
chemotherapy of acute myeloid leukemia (AML) (nv 17) and with d) HIV subiects with
acute febrile pneumonia (n- 17). Non neutropenic HIV+ individuals (n-75) and healthy vol
unteers (n=66) served as controls.
Results: a) HIV+ subjects with afebrile neutropenia (median = 645 neutrophils/pl, range --
9 I1-986/pIl) showed low G-CSF serum levels (median = below detection limit, range = 0 -102 pg/ml) not different from non-neutropenic HIV+ individuals (median = below detection limit, range = 0-78 pg/ml) or healthy volunteers (median -= below detection limit, range
- 0 100 pg/ml).
b) In contrast afebrile neutropenic AML patients demonstrated markedly elevated G-CSF
levels (median = 264 pg/ml, range = 0-5654 pg/ml) (p<0.0001).
c + d) On the other hand, the majority of HIV+ patients with pneurronia had increases of
G-CSF serum levels (median - I152 pg/ml) (p<0.0001) similar to HIV patients with pneumonia (median - 123 pg/ml) (p=0.98).
Conclusions: The results suggest that there is a disturbance in the induction of G-CSF by
low neutrophil counts but not febrile infection in HIV+ individuals. Ihis may be an important factor in the complex etiology of HIV-associated neutropenia. However the possible
therapeutic implications of these findings remain to be established.
Dr Stefan Mauss Klinik fbr Gastroenterologie und Infektiologie, Moorrenst. 5, Universitait
Duesseldorf 40225 Dusseldor, GermranyTel:+49/2 11/811-7805 FAX:[phone]
Mo.B. 1286
PREVALENCE OF THROMBOTIC MICROANGIOPATHY IN A COHORT OF HIV
INFECTED PATIENTS
Ripamonti D, Gregis G, Casari.S, Suardi MG, Chitoni M, *Gregornn i G. "Rossi G, Carosi
Giampiero. Clinic of Infectious and Tropical Diseases, *Clinic of Nephrology "Department
of Hematology -Brescia - Italy
Objective: To determine I) the prevalence of thrombotic rsmsicroangiopathy (TMA) in a
cohort of HIV infected patients (pts), 2) the relation ofTMA with clinical stage of HIV infec
tion and CD4 cell count and 3) to estabhlish the predictive value of hematologic abnormali
ties forTMA.
Methods: All in- and out-pts from 06/01/95 to 12/31/95 were screened for anemia, thrombocytopenia, increased serum LDH and urine abnormalities.TMA was suspected in presence of all these laboratory signs. Haptoglobin and peripheral blood smears for schistocytes
were performed in such pts to confirm diagnosis in the absence of other causes of intravascular hemolysis. Statistical analysis was performed with Relative Risk (RR) (CI 9'%) and with
Iogistic regression (univariate and multivariate analysis).
Results: 561 pts, (387 males and 172 females), mean age 33.4 ys (range 18 70) were
screened. 65.8% were drug abusers, 23.5% were heterosexuals, 9 I% were horro-bisexuals,
1.6% were both homosexuals and drug abusers.TMA was diagnosed in 8 pts, all males and
drug abusers.The following table describes the prevalence and Relative Risk of T MA.

Prof Giarnpiero Carosi. Clinic of Infectious Diseases. Ospedale Civile di Brescia. Piazzale
Spedali Civili Brescia - Italy
Mo.B. 1287
ACUTE MYELOMONOCYTIC LEUKEMIA ASSOCIATED WITH HIV INFECTION AND
GRANULOCYTE COLONY-STIMULATING FACTOR THERAPY
Gonzalez-Garclia I, Lorenzo A, Jimenez-Yuste V*, De Castro M*, Jimenez C'", Mar tin MP*,
Herranz Pr. Fernandez-Capitnin C, Pena JM. Servicios de Medcina Interna. "Hematologia y
-"Dermatologia. H. La Paz. Universidad Autanoma. Madnrd. Spain.
Introduction: Patients with HIV infection firequently have myelodysplastic syndrome but
acute mieloid leukemia is unusual. If these alterations are related to HIV infection of bone
mairrow progenitor cells, antiretroviral therapy or viral coinfections are unknown, Acute
mieloid leukemia has developed after the administration of Granulocyte colony-stimulating
factor (G-CSF) in patients with myelodysplastic syndrome or congenital neutropenia.
Object: A case of acute myelomonocytic leukemia (M4) associated with HIV infection and
G-CSf treatment is presented
Case Report: A 32 year-old white woman was diagnosed in OCT/94 of HIV infection and
oral candidiasis wsshen she has 230 CD4 lymphocytes/mm3. In JAN/95 she developed severe
neutropenia (fewer than 200 neutrophils/mm3) and mild anernmia while she was receiving
zidovudine. In FEB/95 a myelodysplastic syndrome was diagnosed by bone marrow exami
nation as neutropenia and anemia did nrot improve after zidovudine withdrawal. In JUN/95.
while she was receiving G-CSF treatment, acute rnmyelomonocytic leukemia (M4) with cuta
neous infiltrations and 70 percent blasts on peripheral blood tests was observed. G-CSF
therapy was stopped and cutaneous lesions and blast crisis disappeared. In SEP/95 without
relation to G-CSF therapy, new acute leukemic systemic manifestations reappeared and the
patient died of septic shock in OCT/95.
Conclusions: Patients with HIV infection can develop acute mieloid leukemias. Special sur
veillance may be necessary in those receiving hermatopoietic growth factors. It remains
uncertain whether G-CSF therapy contributes to leukemogenesis or to the progression to
acute leukemia in such patients.
Dr. J. Gonzalez-Garcia. Ciudad Pegaso C/Cuatro No3, I odcha. 28022 Madrid. Spain.
telephone/Fax: [phone]
Mo.B. 1288
ANTI-BETA2 GLYCOPROTEIN I AND ANTI-CARDIOLIPIN ANTIBODIES IN HIV
POSITIVE PATIENTS.
Sirera Guillem, Reverter JC*,Teixid6 M*,TAssies D*, Romeu J. Raventos A,Tural C, Segura A.
Font J'", Ordinas A*, Clotet B. AIDS Unit, Hospital Germans Trias i Pujol, Badalona: and
*Hemotherapy and Hemostasis Unit, and "*Systemic Autoimrnune Diseases Unit, Hospital
Clinic, Barcelona, Spain.
Objective: Anti-cardiolipin antibodies (aCL) are associated with thrombosis in autoimmune
diseases but not in AIDS patients. A 50 kDa serum cofactor, identified as Bf2-glycoprotein I
(l2GPI), enhances aCL activity in autoimmune diseases and antibodies anti- B2GPI (a
B2GPI) had been found.We developed an ELISA to study the prevalence of a B2GPI in HIV
positive patients and its relationship with aCL.
Methods: Sixty five AIDS positive patients were studied (6 I male/ 4 ferrmale). CDC stage
were A1 in 20 patients, B2 in I17, and C3 in 28. Four CDC C3 patients had disseminated
tuberculosis, 3 Pneumocystis cannii pneumonia, I 3 cytomegalovirus infection, and 8 Kaposi's
sarcoma.Twenty eight patients were intravenous drug abusers, 32 homosexuals, and 5 het
erosexuais. Ihirty patients were receiving anti-retroviral treatment. None of these patients
had positive specific luetic serology aCL and a 32GPI were determined by ELISA. In the a
(32GPI assay, microtiter plates coated with purified human B2GPI were incubated with dilut
ed sera and revealed with peroxidase conjugated anti human immunoglobulins. Intra and
interassay coefficients of variation ranged between 7 and I 2%.
Results: thirty one patients (47.7%) had aCL (30 IgG and I IgM). In stage AI prevalence of
aCL was 55.0%, in stage B2 58.8%. and in stage C3 35.7% (NS). aCL prevalence in patients
with Kaposi's sarcoma (62.5%) was higher than in the remainder stage C3 patients (25.0%)
(p=0.04). None of the patients with and without aCL had a B2GPI.
Conclusions: aCL in AIDS patients are not associated with a (32GPI in contrast with
autoimmune diseases.These results provide an indirect evidence on the heterogeneity of
the aCL_ phenomena and could explain its different association with thrombotic rnisk
Guillem Sirera, AIDS Unit. Hospital Germans,Tirias i Pujol. Crtc Canyet s/n. Badalona. 089 '
Barcelona. Spain.Tel: [phone] ext 341. fax: [phone]
Mo.B. 1289
WALDENSTROM'S MACROGLOBULINEMIA IN AN HIV POSITIVE PATIENT
WITHOUT EVIDENCE OF EBV ASSOCIATION
DenisejSgsr M.D. Northeastern Ohio Universities College of Medicine
Objectives: To describe the first case of Waldenstrom's macroglobulinemia in an HIV infect
ed patient, to present the course of this usually benign malignancy and to explore a possi
ble assocration with EBV
Methods: A 52 year old Caucasian man, known to be HIV positive since 1988 with a stable
CD4 cell count in the low 100s for 2 years, presented with a very insidious onset of symptoms over 4 months. Nonspeciic fatigue, dizziness, headaches myalgias especially with
severe thigh pain was associated with weight loss. Normal laboratory and radiologic studies
included amylase. liver panel, barium GI studies and brain MRI. Eventually he was noted to
have nginal type chest pain, acute shortness of breath with diffuse rales and rncreasing leg
pain with leve: Routine, mycobacterial, fungal and cytomegalovirus cultures were negative. A
rising total protein from 7.6 to i 2. I over 3 months prompted a serum protein elec
trophoresis which demonstrated a 6 gm IgM kappa band. Bone marrow evaluation co
tirmed the diagnosis of a low grade lymphocytic plasmacytoma, consistent with
WAaldenss romn's macroglobulinema.
Results: Plsrnapheresis lead to improvement in headaches, Shest pain, shortness of breath,
and body pairns which were presumably due to hypervisosity Although fludarabine carrues
a igh success rate with this plasracytoma, he failed to respond to therapy Evaluation fo
EBV by gene probe and antibody studies was negative. HCV, which is speculated to be
associated with Waldenstrom's, was not detected by RIBA Antibody assay

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Clinical n~ of
stage pts
no-AIDS pts 44
AIDS pts 1 19
total 561
"CI 95:5.2 209.3

Cases of Prevalence RR CD4 cell n~ of
TMA count pts
S 0.22% i > 50/mmc 483
7.95 26~ < 50/mmc 78
8 I4% total 561
"* CI 95% 54 3-48

Cases of Prevalence RR
TMA
7 9 s 434

Anemia and thrombocytopenia had predictive value in multivarite arnalysis: Hemoglobin:
OR 0.40, Cl 0.2-0.8; Platelets: OR. 0.96. Cl 0.93-0.99.,
Conclusions: 1) Global prevalence ofTMA in HIV infected pts is low 2) Relative Risk of
TMA is much higher in AIDS pts with severe immunosuppression (CD4 < 50/mmc).
3) Anemia has the strongest predictive value forTMA.