HHV8 infection and kaposi's sarcoma

HHV8 infection and kaposi's sarcoma

Symposium S18. Vulvar Human herpesvirus 7 in pityriasis rosea S17-7 F. Drago. Dept. Dermatology, University of Genoa, Italy The viral etiolog...

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Symposium

S18. Vulvar

Human herpesvirus 7 in pityriasis rosea

S17-7 F. Drago.

Dept.

Dermatology,

University

of Genoa,

Italy

The viral etiology of pityriasis rosea (PR) has never been demonstrated. As evidence suggests an endogenous viral reactivation, our attention was drawn to herpesviruses and in particular to human herpesvirus 6 and -7 (HHV-7). Peripheral blood mononuclear cells (PBMCs). plasma and skin from PR patients were studied by (PCR) and viral culture. 12 patients with other dermatoses and 25 healthy people were taken as controls. PR patients showed ballooning cells and syncytia in cultured PBMCs whereas controls and recovered patients did not. In the supernatant from cultured PBMCs, HHV particles in various stages of morphogenesis were disclosed by electronmicroscopy. PCR identified HHV-7 DNA in PBMCs, plasma and skin from all patients, but only in PBMCs of 5 patients tested later. Weaker signals of HHV-7 DNA were detected in PBMCs of 11 controls but not in their plasma. Skin proved negative for HHV-7 in all control specimens.

S17-8 HHV8 infection and Kaposi’s sarcoma D. Cerimele, P. Cattani’, I. Lesnoni La Parola, C. Masini, F. Cerimele’, G. Fadda’, M. Capuano. Dept. Dermafology; tlnstitute of Microbiology Catholic University Sacred Heart, Rome,

Italy

KSHV/HHVI DNA has been detected in about 100% of the samples of Kaposi’s sarcoma (KS), in 100% of body cavity based lymphomas, in 50-70% of multicentric Castleman’s disease and in scanty cases of other diseases. Serological studies have demonstrated anti-HHV8 antibodies in normal subjects with a prevalence ranging from 24% in USA, lO-20% in Italy, up to 60% in East Africa. These data have suggested that HHVI may be more widespread than it was thought before and that it could be disseminated through a route of transmission other than the sexual one. We have looked for HHVS DNA in tonsillar swabs, saliva, and urine in patients affected by classic KS. Tonsillar swabs have been positive in 14/32 (43%) of the patients, saliva specimens in 1 l/24 (45%), urine samples in 2/24 (18%). In control samples HHVS DNA has been found in 18% of PBMC, 5% of tons&u swabs and in no specimens of saliva and urine. The percentage of concordance between tonsillar swabs and saliva samples is about 80%. These results indicate that HHV8, as other herpesvirus, may be present and disseminated through the upper re piratory tract.

S18.

Vulvar disorders (HPV excluded) How normal is normal when examining a vulva?

M. Moyal-Barracco ‘s2. ‘4, rue Leon Delhomme, ‘Hipital

Ambwise

Part?, 92100

Boulogne,

75015

Paris;

France

The morphology of the vulva varies according to the specific anatomy of the patient as well as to her age and to ther obstetrical history. The knowledge of the normal aspects of

disorders

(HPV

s31

excluded)

the vulva helps to better understand its diseases and to differenciate anatomical variants from pathological processes. In case of vulvar pain, this knowledge helps to decide if what we see on the vulva is responsible for the pain or not. The iitterature about normal vulva is scarce. The material presented here comes both from clinical experience and from a study conducted in 1993 concerning the vulvar examination of 200 asymptomatic women. The morphological variations of the vestibule (vestibular papillae, red spots), the labia minora (size, Fordyce granules), the hymen (cyclic variations, tears, septae) and the clitoris (size) will be considered. The obstetrical vulva1 scars (episiotomy, paraurethral tears) will be described.

IS18 3

Lichen sclerosus in children - Genes or abuse?

Fenella Wojnarowska, Jennifer Powell. Oxford Radcftp Hospital,

Oxford,

UK

Lichen sclerosus in childhood may present to genito-urinary medicine physicians, dermatologists or gynaecologists. Frequently the possibility of sexual abuse has been raised with much ensuing trauma to the family. In our dedicated Paediatric Vulva1 Clinic we now have over 50 girls who have presented with lichen sclerosus. In more than 80% sexual abuse has been raised as a possibility prior to referral to us. This has not been substantiated in any of our cases, although there is evidence from the literature to suggest that the two may co-exist and it may be that lichen sclerosus can occur as a Koebner phenomenon. There is a strong genetic component in children with lichen sclerosus in our series, 15% have a family history, 15% have an affected sibling. There is a very high incidence of autoimmune disease within the families. We have demonstrated type linkage to HLA DQ7. These facts together suggest that there is a genetic susceptibility to lichen sclerosus and this is probably strongest in those presenting in childhood rather than in middle or old age. We have reviewed treatment and find that treatment with potent or very topical steroids is usually effective and sufficient. There does not seem to be additional benefit from the use of more potent steroids from the literature. I will outline a management scheme for these patients. The final outcome of childhood lichen sclerosus remains unclear, but previous data suggests that remission may occur in about a third. My own experience indicated improvement in symptoms but our follow-up does not yet permit a long term prognosis.

S18-4 Is vulva1 lichen sclerosus a precursor of squamous cell carcinoma? P. Carli. Institute

of Dermatology,

Universiry

of Florence,

Italy

Lichen sclerosus (LS) is a chronic, inflammatory disease occurring on skin and mainly genital mucosa. While LS at extragenital sites seems to have no potential for malignancy, a relationship between vulva1 LS and carcinoma risk has been suggested. Histological revision of peritumoral tissue has shown histological changes of LS in about 50% of vulval squamous cell c‘arcinoma (XC) samples. From such reports, an associa-