A case of virus associated hemophagocytic syndrome and malignant histiocytosis: sometimes a difficult distinction.

The differential diagnosis among hemophagocytic syndromes and particularly between the virus-associated hemophagocytic syndrome (VAHS) and the malignant histiocytosis (HM) is quite easy in typical cases. Difficulties of interpretation may sometimes ensue when viral-bacteriologic work-ups indicative of VAHS are negative and/or morphologic histiocytic aberrations indicative of HM are missing. The authors present a case of hemophagocytic syndrome with the latter characteristics and discuss the differential diagnosis.

[Guidelines for management of genital herpes infection in the experience of a health care center for sexually transmitted diseases in Buenos Aires (Argentina)]. / Pautas para el manejo de la infección herpética genital en la experiencia de un centro de atención de ETS en Buenos Aires (Argentina).

During two years all clinical genital lesions compatible with herpes simplex virus (HSV) etiology were studied systematically through intent of virus isolation in BHK cells. Isolation of virus was confirmed in 85% of the 206 cases studied. All seems to indicate that around the 20% of the isolations belong to the type HSV1 and the rest to the type HSV2. Viral Antigen demonstration, by direct and/or indirect technics with antibodies poly or monoclonals shows to be less sensitive than the virus isolation. The systematic study of these sexually transmitted disease revealed two indicative results: 5.32 cases of Gonococia per each case of HSV were confirmed. It seems to be a possibly relation for the actual epidemiology moment of our country. The other is the need, specially in younger people, to explore systematically syphilis, not only in all the genital ulcers, also in presence of a typical clinical of HSV.

Clinical significance of fibrinopeptide A in acute lymphocytic and non-lymphocytic leukaemia.

Fibrinopeptide A (FPA) was systematically investigated in 74 patients with acute leukaemia at different stages of the disease (50 with non-lymphocytic leukaemia, ANLL; 24 with lymphocytic leukaemia, ALL). At diagnosis, 75% of the cases had high FPA levels (86% in ANLL and 54% in ALL) with significantly higher levels in ANLL than in ALL (13.4 vs 4.4 ng/ml; p less than 0.001). Patients with DIC (20 cases in ANLL and 1 case in ALL) had significantly higher levels (p less than 0.001). FPA levels were neither correlated with fibrinogen or FDP levels nor with blast cell count. During chemotherapy, median FPA did not show significant changes whereas, at the end of therapy, a return toward normality was generally observed both in ALL and ANLL apart from the group of patients with acute promyelocytic leukaemia. Among the 24 patients who entered post-remission follow-up (13 ANLL and 11 ALL), 10 cases out of the 11 relapsing (6/6 with ANLL and 4/5 with ALL) had increased FPA 1 to 2 months before the ascertainment of the relapse. However, 16% and 9% of the samples obtained on different occasions, respectively from ANLL and ALL cases in maintained first remission, showed FPA above the normal limit. This study demonstrates that subclinical activation of blood coagulation, as indicated by high FPA level, is common both in lymphocytic and non-lymphocytic leukemia and suggests that this phenomenon is related to disease activity.

One year follow-up study of T-cell subsets and incidence of seropositivity for HTLV-I and HTLV-III antibodies in patients treated "on demand" or sporadically with clotting concentrates.

A 1-year follow-up study of the T-cell subset abnormalities was carried out in 16 severe haemophilia A patients, treated "on demand" with an average amount of 500 U/kg/yr of factor VIII concentrate (group A) and in 15 mild haemophiliacs or von Willebrand patients treated only sporadically with less than 3000 U of factor VIII and no longer exposed to any other blood component in the 2 years preceding the beginning of the study (group B). In group A, 50% and 70% of patients showed a reduced or inverted T 4/T 8 ratio, respectively, at the beginning and at the end of follow-up. These values were of 30% and 20% in patients of group B, suggesting a long-lasting effect of concentrate therapy on T-cell subsets. The low T 4/T 8 ratio was mainly due to an increase of suppressor cells. None of the patients was found positive for anti HTLV-I, whereas 3 patients, all belonging to the group A, showed antibodies against HTLV-III. Thus, in these patients, HTLV-III seems not to be the only cause of low T 4/T 8 ratio.