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

Mo.B.1280 - Mo.B.1284

Monday, July 8, 1996

matched by CD4 cell count and date in a retrospective cohort studyThe t test and chi
square test were used for contrinuous and categorical data, respectvely to as.es possibly
significant clinical parameters associated w ith AEC > 500.
Results: There were no differences between the two cohorts with respect, age, gende r,
HIV risk category, a diarrheal lness within 4 months, parasitic infections, h st)ry of drug
allergy, presence of atopic conditrions excluding eczema (asthma, sinusitis alle i rhinitis),
patient reported rash. prior individual or total number of oppor tun;stic infections, new diagnoses within 2 months of irst AEC > 500, non HIV related mredical conditions, or total or
individual medications. The followirng parameters were assoaated with AEC 500: physician
diagnosed rash (76% vs 53%), pruntis (50% vs 20%), folliculitis (38% vs 12%), eczema (17%
vs %), and black race (52% vs 17%), p < 0.05 for all parameters. Prurigo nodularis was less
strongly assoated with AEC > 500 (p = 0. 06). Only one patient (study group) had a parasitic infection (strongylo des) known to be associated with eosinophiia.
Conclusions: Eosinophia in HIV infected patients is associated with de rmatologic conditions especially pruritis, folliculitis, and eczema but is nriot associated with other conditions
commornly as'sociated with eosinophilia includin g other atopic conditions, medications, drug
rash, drug,allergy or parasitic infections.
D J. Skiest, 5323 Harry Hines Blvd., Dallas, TX, USA, 75235 91 13 Tel: [phone]
Fax: [phone] email: SKIESTUTSW.SWMED.EDU
Mo.B. 1280
LEPROSY AND HIV COINFECTION IN AN ENDEMIC DEVELOPING COUNTRY:
HOW TO INTERPRET OCCURRENCE OF LEPROMATOUS LEPROSY IN A HIV+
HEMOPHILIAC WITH NO KNOWN CONTACT WITH LEPROSY PATIENTS?
PetriValria ', Nishio CFR, Nishio PA, takizawa CM*, Michalany NS. Federal Uni versity
of Sao Paulo, Escola Paulista de Medicina, Sao Paulo, Brazil
Issue: In spite of iamunological findings being crucial to understanding important events of
HIV disease, leprosy and HIV/AIDS confection is not sufficentlly focused as a threatening
occur erce endemic developing countries. Leprosy may occur in HIV +/AIDS paients
with no known contact with leprosy paents, iand HIV+ hemophiiacs may be at risk of
coinfection in large industrialized cities of endemic countri es, with no identification of the
source of M eprare infection. Significance of those events and clinical changes eof leprosy in
HIV+ were not clear yet.
Project: Mitsuda reaction in HIV+ was considered to presumne HFIV+ people more susceptible to leprosy in endemic countries. In a large urban centre of medium endericity (Sao
Paulo City, Brazil), and with no history of contact with leprosy patients, a white HIVI -
hemophiliac 32 years of age, having no known contact with leprosy patients, presented
cutaneous violaceous lestons mimicking Kaposi' s sarcoma (KS). Low probability of KS in
herophiliacs induced histologic examination of the nodule. Close contacts, including his
HIV+ wife, were investigated for clinical and immunological signs of leprosy
Results: Skin biopsy of the nodule disclosed typical lepromatous leprosy (as shown in photographs of clinical and histopathological aspects). Low CD4+ lymphocyte counts
(<I 100/rnrn3) corroborated signicant imnpairment of irimunocompetenrce. Source of leprosy infection was not identified among all contacts.
Lessons learned: Immunological response to M./eprae is changed in HIV+ people with
HIV/AIDS, who nay be more susceptible in endemic developing countries. Commonr clinical
signs of lepsromnatous leprosy may not exist, and it is not known if HIV+ hemophiliacs are
more susceptible to lepromatous leprosy than other HIV+- infected people.Transmission by
blood and blood products was not fully proven, in spite of the De Las Aguas experience"*.
** De Las Aguas, J. "Inoculaci6ron accidental de la lsepra por transfusion sangu(nea en gemelos
univitelinos". Revista LIeprologisa Fontilles 1967; 6(7):603- 6 I.
Valeria Petr, R. Botucatu n[ O ]740, CEP:04023 900, Sao Paulo Brazil. Escola Paulista de
Medicina Dept of Dermatology Fel55 1 1-5764305 Fax:[phone]
Mo.B.1281
MOLLUSCUM CONTAGIOSUM INFECTION IN THREE POPULATION GROUPS
Rea AJ, Goh Beng-t inc, Eldridge S**, Glover M". Departments of Genito-Urinary
Medicine*, Medical Statistcs & Epideniology", & Dermiatology **,The Royal London
Hospital, London, E! I BB, United Kingdom
Objective: To study ollusc rn cotagiosum (MC infection in patients seen in an HIIV clinic
(Gp1), compared to patients seen in a ion IIIV Genito urinary Medicine (Gp2) arid
Dermatology (Gp3) cli ics.
Methods: MC nfections seen 5 n Gp 1,2,3 from April 1993 to September 199 were retrospectively analysed. otal rnmber of clinics patients for the study period were recorded.The
data collected isnclude age, sex, I-IV status (if known) concurrent STD diagnosis, anatomical
location of MC and sexual orientation.
Results: The prevalence of MC in Gp I was 6. %, in Gp2 0.28% and in Gp3 0.2 3%. 83 % of
Gp I presented wih facil lesions compared to I patient (cardiac transplant on imruosuppressive) in Gp2 and I 3 (14%) In Gp3 of whom 7 were renal transplant patients All
anatomical sites were equally affected in childhood infection.All patients in GpI with CDC
category C ad persistent feaal lesions despite treatment compared to 3 patients in Gp2
(table). 60% of adults with genital MC had concurrent STD

Mo.B. 1282
SYMPTOMATIC SYSTEMIC CD8 LYMPHOCYTOSIS IN HIV-I INFECTION:A
COHORT STUDY
B. Jarrousse. ( L_):,,. Cohen,V Zeller, P Berlureau, J.P Arene, L. Guillevin.
Department of Ie,I': iane, Hfpital Avicenne, Universite Paris-Nord, FRANCE
Objective: To descrbe t,,linical, immunologic features and outcome of symptomatic diffuse infiltratve CD8 ly:np'sucytosis resembling Sjogren syndrome in a monocentric cohort
of HIV-i infected patients.
Patients: Consecutive sample of 8 patients
Results: Among 171 patients with increased numbers of CD8 lyrmphocytes (> 1000/pL), 8
patients (6 black, 2 caucasian) including 3 men and 5 women (average age 32) developed
clinical symptoms resembling Sjogren syndrome: 7 had bilateral parotid gland enlargement, 7
had xerostomia and/or xerophtalmia. All of the 8 patients had generalized lymphadenopathy 6 had frank respiratory symptoms related to lymphocytic interstitial pneumonitis (3
cases) or diffuse bronchiolitis (3 cases), 3 had lymphocytic infiltration of the gastrointestinal
track and one had aseptic meninrgitis. Galliumn scanning showed abnormal salivary gland
uptake in all of the 4 tested patients. Minor salivary gland biopsies showed grade 4 lymphocytic infiltration according to the Chisholm and Mason criteria in 4 patients. BAL fluid analysis showed CD8 lymphocytic alveolitis in 4 patients. At onset of symptoms, blood lymphocytes count was 2205 + 736/pL, mean CD4 cells count was 313 ~ 182/pL and CD8 cells
count was 1459 ~ 541/pL( with increase of CD8CD38+ cells in 6 cases). None of the
patients had antinuclear antibodies. Cryoglobulinemia was detected in 3 patients. HTLV I
ELISA testing was negative rin all patients. During a follow-up of 30 ~ 20,9 months, two
patients developed an opportunistic infection and one patient died of septic shock. None of
the patients developed lymphoid malignancy Benefit of antiretroviral therapy was observed
on sicca symtoms anrid parotid gland ernlargement.The use of oral corticosteroids was associated with transient or sustained remission of respiratory symptoms in 3 casens.
Conclusion: Clinically significant systemic CD8 lymphocytosis remains very uncommonin
adults infected with HtIV, predominantly observed among the black patients.This disorder
previously reported in strong association with HLA-DRS, may involve a genetically host
immune response to HIV.
B.Jarrousse, H6pital Avicenne, I 25, rue de Stalingrad 93009 Bobigny, France
phone: 33 I 48 95 53 51 ifax: 33 48 95 54 50
Mo.B.1283
POLYARTERITIS NODOSA IN AN HIV-INFECTED PATIENT WITH CASTLEMAN'S
DISEASE: POTENTIAL ROLE OF KSHV AND EFFICACY OF TREATMENT WITH
IMMUNOGLOBULIN.
Lesueur Arnaud-. Salmon D", Blanche P*, Essam E5, Dupin N*, Clauvel JP*5, Sicard D*.
*Service de medecine interne hopital Cochin Paris France, "*Service de dermatologie hopital Tarnier Paris France, **Service d'hematologie, h6pital St Louis Paris France
Case report: A 49 year old seropositive homosexual male patient presented in September
92 with fever, associated with multiple lymphadenopathy splenomegaly and pancytopenia.
CD4 cell count was 200/mm3.
I- After 5 months of unexplained fever, multicentric Castleman's disease was diagnosed
after splenectomy, on histopathological study of lymph nodes and spleen. 31 courses of
Vinblastine (6mg) at 21I-day intervals over 2 years were given with good effect on the systemic symptoms and lymphadenopathyTheVinblastine was ceased in April 95 due to the
appearance of a rapidly progressive, painfiul, asymmetrical peripheral neuropathy affecting all
four limbs, and replaced by Interferon (3 MU 3 times weekly).The Castleman's disease
remained quiescent under this treatment for 10 months.
2-The polyneuropathy progressed despite the cessation ofVinblastine treatment, and a
neuromuscular biopsy was performed in September 95.The diagnosis of polyarteritis
nodosa affecting the muscle vasculature and epineurial vessels was made.There were no
renal, digestive or articular manifestations of PAN. HBV and Parvovirus B I9 serology
demonstrated past infection; HCV and HTLV I serology were negative. KSHV detection by
PCR in circulating mononuclear cells was positive ins December 1995, as is seen in the
majority of HIV-linked cases of CastIeman's disease. PCR investigation of the nerve biopsy is
in process at time of writing. No other viral agent capable of triggering PAN was found.
Interferon therapy was continued, and a monthly treatment of intravenous imnmunog lobulin
(2g/kg) was commenced with good results; pain relief and arrest of the progression of the
peripheral neuropathy were achieved following the first treatment.
Conclusion:We report a case of Castleman's disease associated with KSHV Polyartentis
nodosa with neuromuscular manifestations developed secondarily in this patient. A causative
role of KSHV or interferon treatment n this disorder cannot be ruled out.To our knowledge, this is the first reported case of PAN in an HIV-infected patient successfully controlled
over a long term (5 nrths at time of writing) by immunoglobulin treatment. Such a treat
ment is interesting in this clinical situation since it does not aggravate the immunodeficiency.
A Lesueur, Departement de medecine interne, hopital Cochin 27 rue du faubourg Saint
Jacques 75014 Paris France TEL et FAX: [phone]
Mo.B. 1284

HIV (GpI

HIV CDC

's 469 P e umprve iV
n y a t ire paitients

CD3+ CD8+ CD 16- CLONAL LARGE GRANULAR LYMPHOCYTE LEUKAEMIA
isite P5e,,5,n ir AND HIV INFECTION
Pulik Marc, Lionnet F, Genet R Petitdidier C, Jary L, Fourcade C,Touahri T Department of
Haematology, Argenteuil, France
2 ( 00x) (0%) Objective: To report a case of clonal CD3+ CD8+ CD I 6- large granular lymphocyte
t(15% 1(25s') leukaemia (TF-LGL) in an HIV-infected patient.Tcells derived leukaemias are very unusual in
S(0q 3 (00% association with HIV infection.
i 69 (9857%) Methods: Surface immunophenotyping of the lymphocytes was performed with flow
cytometry using a broad panel of lymphoid-associated monoclonal antibodies.The DNA
Sused for gene rearrangement studies, by polymerase chain reaction, was extracted from.... mononuclear cells preparation.
an those in Gp2&3.The Results: A 46 year-old man had thrombocytopeni a in 1987 Evaluation showed an adequate
ig enumber of megakaryocytes and a shortened platelet life-span. He tested negative for HIV
antibodies. A splenectomy was performed. Platelets count normalized. In 12/93, an
hemogram disclosed lymphocytosis (I I.4x109/I) and HIV testing was positive in 03/94. He
eclhapel, I ondon E I I BB, UK was referred for evaluation. Clinical exam was unremarkable. Blood counts revealed: lym
Conclusions: The period prevalence of MC is greater in GpI t h
facial location of MC in adults is a predictor of HIV positivia ty hav
of immunosuppressron.
Dr BT Gih, A's rnass KiFl -entre, Roya I ondo n ospitrl,Whit

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