Biomedical subjects
Publications and source records attributed to M Baldi.
The clinical, radiographic and histological picture of a recently observed case of giant cell tumour of the upper maxillary is reported and some notes offered on diagnosis and treatment.
The risk of bacterial endocarditis in dentistry is examined and responsibilities for prevention clarified. A review of the principal chemotherapeutic protocols currently followed by International Cardiologist Associations is presented.
A review is given on the current knowledge of the hepatitis delta virus (HDV), the only hepatotropic non-A and non-B (NANB) virus characterized, although the infection it causes requires infection with hepatitis B virus (HBV). Studies in chimpanzees have provided the most data now available on the putative NANB agents. Histologic and electron microscopic changes occurring in HDV and NANB hepatitis have been shown to be comparable, and some biologic, epidemiologic and clinical features are similar. However, the lack of cross-protection between NANB and HDV hepatitis in cross-challenge transmission experiments and the lack of hybridization between HDV-RNA and nucleic acids from NANB material indicate that HDV and the putative NANB agents are minimally, if at all, related.
The expression of intrahepatic delta antigen (HDAg) was studied in relation to the morphologic features of HDV hepatitis and the outcome of liver disease. The study was performed in 101 patients followed up for an average of 12 years; one or more liver biopsies were available from each patient, giving a total of 167 specimens. The histologic features were assessed using numerical scores. A significant positive relation was observed between the number of HDAg-positive cells and the extent of portal inflammation (Spearman's rank coefficient 0.75). The highest degree of inflammation and intrahepatic expression of HDAg was found before the elimination of the virus, while the outcome of HDV disease was unrelated to the severity of the initial morphologic lesion. These results suggest that the individual immune response may play an important role in the pathogenesis of HDV hepatitis.
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A centric fission of chromosome 4 is described in the proband and his mother, both phenotypically normal. In addition, partial monosomy for the long arm or the short arm or both of chromosome 4 may have been present in two of the proband's sibs who died in infancy and childhood, respectively.
A paracentric inversion of chromosome 15 was observed in the father of two infants who died 29 days and 24 hours, respectively, after birth. The same inversion was found in two sisters of the proband.
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By monitoring immunobiological parameters known to be influenced by interferon (IFN), the natural killer (NK) cell activity of 10 low replication (anti-HBe) virus B-DNA (HBV-DNA) hepatitis patients receiving rIFN alpha-A, of 5 anti-HBe/delta positive hepatitis patients treated with rIFN alpha-2, and of 6 high replication (HBeAg) HBV-DNA hepatitis patients on lymphoblastoid IFN was followed-up during therapy. Overall, strong and significant (p less than 0.01) shift to increase segregated with the low replication subset; the delta positive subset was non-significantly increased (0.30 greater than p greater than 0.2); the high replication subset was depressed in a nearly significant (0.10 greater than p greater than 0.05) manner. Kinetic studies showed the activation of the first subset to follow an early steep rise and a subsequent plateau as fitted with a quadratic curve (p = 0.02); an early rise and a depression at 2 months delineated a complex cubic model (p = 0.06) in the high replication subset. The profound NK depression was clinically witnessed by a sharp rise of the aminotransferases and following drop of viremia. The study shows that i. discrete patterns of NK response as amenable to mathematical models may associate to differential patterns of virus B replication in patients responding to IFN; ii. point(s) on the NK curve may acquire clinical meaning as they coincide with a consensual or opposite shift of a clinical index.
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In an effort to define immunobiological parameters identifying "responders" vs "non-responders" to IFN among hepatitis patients, 16 patients with chronic active hepatitis were screened for changes of Natural Killer cell activity (NK). 10/16 patients replicated the hepatitis B virus (HBV-DNA positive) whereas 6/16 replicated the defective B virus associated delta virus (HDV-RNA positive). Patients received 9 MU/3x/weekly/3 months of recombinant IFN alpha A. Mean NK activity of the HBV-DNA patients rose significantly from 29.9 +/- 5.3 to 45 +/- 4.7 during therapy, whereas the 6/16 HDV-RNA positive patients did not show any significant increase of NK activity. Interestingly, individual HDV-RNA positive patients exhibiting boosted NK activity also showed improvement of disease confirmed by clearance of intrahepatic delta antigen at one year. No such a correlation was found amongst the HBV-DNA positive patients. These data indicate that in spite of widespread individual variability, IFN-mediated NK boost may herald delta clearance and help in identifying "responders" and "non-responders" in IFN trials.