On a rare genetic variation of plasma albumin: bisalbuminaemia.
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Biomedical subjects
Publications and source records attributed to L Bonazzi.
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A case of polyarteritis nodosa identified by the American College of Rheumatology (ACR) 1990 criteria in a 44-year-old HIV-infected man is described. The search for cytomegalovirus, HBV and B19 parvovirus infections was negative. In situ hybridization did not reveal proviral HIV-1 DNA in a skin sample. A zidovudine-associated vasculitis was excluded. Corticosteroid therapy resolved vasculitis manifestations and was well tolerated without opportunistic infections during the 10-month follow-up period. An indirect pathogenetic role of HIV as a possible cause of vascular damage cannot be excluded in our patient.
In a group of 23 patients with advanced liver cirrhosis we have found a statistically significant positive correlation (r = 0.746; p less than 0.0001) between fibronectin and prealbumin levels measured in plasma by immunonephelometric methods and found significantly lower than in healthy controls (p less than 0.001). On the contrary, no correlation of fibronectin neither to albumin nor to the presence of an enlarged spleen was observed. Since the sensitivity of prealbumin as an index of liver function is believed to be higher than that of albumin, our results support the view that the decreased fibronectin in advanced cirrhotics is mainly due to their liver failure, an enlarged spleen playing only a minor role.
The behaviour of the HBe/anti-HBe system in AVH was evaluated, using Magnius technique, by testing serum samples from 47 patients; 29 of them were followed during the clinical evolution of the disease until complete remission was achieved. HBe was more frequent in samples taken from patients in the first 7 days after the onset of jaundice (18/33 = 54%) than in samples collected later (3/14 = 21%). During the clinical evolution of the disease we could always demonstrate the disappearance of HBe not later than 12 days after the onset of jaundice. In one patient studied from the incubation period HBe disappeared before any clinical or laboratory evidence of disease. In 8/29 cases (27%) anti-HBe developed starting from the 15th day of illness, but 4 of these had had no detectable HBe during the acute phase. No significant difference could be demonstrated between HBe +ve and -ve cases in the maximum values of SGPT and bilirubin and the duration of the disease. The changing pattern of the HBe/anti-HBe system could account for the different incidences of these markers reported by many authors in AVH. Our findings support the hypothesis that HBe develops in every HBsAg +ve AVH case. Therefore, it is not the presence of HBe in the early stage, but the persistence of this marker that might be important in predicting progression to chronicity.
The risk of acquiring HIV-1 drug resistance at time of infection has become a public health problem following the widespread use of antiretroviral drugs in developed countries. Although a number of studies have reported data regarding the prevalence of HIV-1 primary resistance in developed countries over the past years, limited knowledge is available regarding the proportion of mutations related to drug resistance in antiretroviral naive subjects with chronic HIV-1 disease. In this study, we evaluated the prevalence of mutations in the reverse-transcriptase (RT) and protease region both in a representative group of recently HIV-1 infected subjects (n=68) and a cohort of chronically-infected HIV-positive patients (n=347) enrolled in the Italian Cohort of Antiretroviral Naive patients (I.CO.NA.). In recently infected individuals, the overall prevalence of mutations for nucleoside RTI (NRTIs) was 10/68 (14.7%). The distribution of mutations by calendar year were 0, 1 in 1996, 9, 3 in 1997 and 1, 0 in 1998 for NRTIs and protease inhibitors (PIs) respectively. Thymidine associated mutations were identified in six subjects (8.8%), five of whom had one mutation [41L, 70K (n=2), 215Y] and one had two mutations (67N+219Q). Four subjects (5.9%) showed the changes associated with resistance to lamivudine (184V or 118I). No non nucleoside-RTI (NNRTI) mutations were present in the study period. Primary PIs mutations (two 46L and two 82I) were present in four subjects (5.9%). Of note, mutations related to resistance to more than one class of antiretrovirals were present in one (1.5%). Among patients with chronic infection a large proportion (88.5%) carried no mutations in RT region, 11.5% individuals carried one or more mutations associated with resistance to NRTI (7.8%), or NNRTI (4.9%), with 4 patients carrying mutations to both classes. Among mutations associated with high-level resistance to RTI, T215Y was found in only 2 patients, M184V in 2 cases, T69D in another case, and K103N in only 1 patient, for a total of 6 patients (one carrying both T215Y and M184V) (1.7%). Primary mutations associated with substantial resistance to PIs were found in only 5/347 patients (1.4%); all the other patients carried only secondary mutations. Prevalence of mutations associated with high-level resistance to antiretroviral drugs is stable in recently infected individuals and low in patients with established HIV infection. The potential impact of transmitted mutations on the response to first regimen in individuals carrying transmitted mutations needs to be assessed by prospective studies.
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