Serum IgA antibodies in HSV asymptomatic genital infections.

Cervico-vaginal swabs and serum samples from 81 women without herpes-associated clinical symptoms were examined for virus isolation and for the presence of IgA antibodies to herpes simplex virus (HSV) using the indirect fluorescent antibody technique. Nineteen of the 81 women were followed up for 2 years. Blood samples and swabs from cutaneous lesions were obtained from another group of 20 women (medical staff) with herpes labialis. By analysing the specific anti-HSV IgA antibodies, a higher geometric mean titre (GMT) was found in women with positive HSV-2 isolation (GMT = 380.03), as opposed to the GMT observed in women with negative HSV-2 (GMT = 63.43) or positive HSV-1 isolation (GMT = 55.15). Results from the longitudinal study also demonstrated that positive virus isolation always correlated with a marked rise in serum IgA antibody to HSV.

The role of anti-herpes specific serum IgA levels as a marker in cervical oncogenesis.

In the last few years, a great effort has been made with the aim of discovering cervical cancer etiology factor(s). At present, both HSV and HPV have been demonstrated strictly associated with cervical premalignant and malignant lesions. Nevertheless problems do exist in achieving the definitive evidence of a causative role exerted by herpes virus and/or by papilloma virus. Starting from 1984, our group studied the humoral immune response against herpes virus type two, in patients affected with CIN and invasive cervical cancer, as well as with atypical metaplasia and papilloma virus cytopathic effect at pap test, giving in 1985, the first evidence that serum levels of specific anti-herpes IgA strictly correlates both with infections and viral shedding, even when asymptomatic, as with various stages in cervical oncogenesis. This study updates our previous reports showing that IgA serum levels may be a useful marker in herpes related human diseases. Finally, data show the preliminary evidence that IgA, when levels are determined in the male partners of patients, is also useful in the screening and detection of "high risk males". These data, if further confirmed, will be of great advantage in the clinical monitoring of cervical cancer treatments, as well as in management and follow-up of preinvasive epithelial lesions of the cervix.

Ashley's hypothesis revisited.

Nowadays it is widely accepted that cervical cancer is a virus related, sexually transmitted disease, but no complete agreement exists about its etiological factors. They may be identified in HSV or in HPV or in both. Moreover, its is accepted that cervical cancer does not arises ex abrupto from normal epithelium, but often arises from the epithelia with well codified morphological lesions now defined as "Cytohistological Cervical Cancer Precursors". Epidemiological data available at the moment, also concerning risk age, suggest that two different risk classes do exist. They range respectively between 20 and 40 years and between 50 and 70 years of age. When considering sexual promiscuity, younger patients refer a higher and more intensive level than that referred by older; the latter often claim for a low level of sexual activity. Starting from this observation, as well as from clinical and histological evidence, Ashley first suggested in 1965 the existence of two different types of cervical cancer. In the Ashley hypothesis the first type, slow-growing, is often preceded by a precursor, non-invasive stage, while the second, fast-growing, rapidly invades, often without evidence of a previnvasive stage. In our series of 1,010 invasive and 210 in situ cervical cancers, indeed, two different ranges of risk-ages exist, fulfilling Ashley's hypothesis. Morphological evaluation of lesions shows that in the younger patients, invasive cancer is, in a high percentage, associated with HPV-VCE and CIN in the surroundings, while in the older, this feature is less evident.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of immunization against human chorionic gonadotropin (hCG) on transplantation of Yoshida ascitic tumour.

The human chorionic gonadotropin (hCG) is considered a marker of DNA derepression on neoplastic cells. The human chorionic gonadotropin antibodies (anti-hCG antibody) inhibit the growth of yoshida tumour cells in preimmunized recipient rats. A close relationship between the anti-hCG antibodies and tumour cell transplantation has been observed. This relationship and further experimental implications are briefly discussed.

Concerning a new pathogenetic hypothesis of the E.P.H. gestosis (note I).

The Authors, after having evaluated the literature data, report, on the basis of their clinical experience, a new pathogenic hypothesis of the E.P.H. gestosis which would be: "Disease due to missed materno-foetal adaptation:, correlated to the activation of the maternal immunocompetent system against the "not self" antigens, carried by the trophoblast and codified by the genoma of the father's origin. It is also due to missed destruction of the tunica media of the placental bed arteries and to the thromboplastinic activity of the trophoblastic cells damaged by the immunologic reaction. This disease, clinically represents, the appearance of a "temporaneous" (pre-eclampsia) or "definitive" (eclampsia) defeat of the fibrinolytic control mechanisms against a disseminated intravascular coagulopathy.

Concerning a new pathogenetic hypothesis of the E.P.H. gestosis (note II).

In this second note, the Authors report a new therapeutic protocol, based on the aetiopathogenesis, of the E.P.H. gestosis, which allows an efficient clinical control of this disease, avoiding its evolution to eclampsia.