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Biomedical subjects

G Ercilla

Publications and source records attributed to G Ercilla.

At least 37 records · Page 2Linked to original sources
PubMed1996

Hepatitis C virus-associated membranoproliferative glomerulonephritis in renal allografts.

In renal transplantation, chronic allograft nephropathy is the leading cause of long-term graft losses, transplant glomerulopathy being its glomerular form. Differential diagnosis from recurrent or de novo membranoproliferative glomerulonephritis should be established. Whether hepatitis C virus is associated with cryoglobulinemia and glomerular damage in renal allograft recipients, as in native kidneys, is not known. We identified six hepatitis C virus-infected renal allograft recipients with proteinuria higher than 1.5 g/day, microhematuria, and membranoproliferative glomerulonephritis. Virologic and immunologic studies were conducted. Low serum levels of circulating immune complexes and cryoglobulins were observed, which were type II immunoglobulin G polyclonal-immunoglobulin Mk monoclonal in all six patients. Classical serum complement pathway activation and at least one type of autoantibodies were present in all of them. Hepatitis C virus RNA was found in higher concentrations in cryoprecipitate than in serum (percentage of enrichment ranged from 341 to 18,200%). Hepatitis C virus genotype was 1b in 4 of 6 patients, 1a in 1 of 6 patients, and 2a in 1 of 6 patients. In renal histology prominent parietal diffuse deposition of immunoglobulin M was the rule. Glomerular subendothelial electron-dense deposits with fibrillar appearance were observed in the two patients in which electron microscopy provided information about glomeruli. In renal allograft recipients hepatitis C virus infection may be associated with type II cryoglobulinemia which may lead to membranoproliferative glomerulonephritis. Immunologic and virologic studies may help to differentiate hepatitis C virus-associated membranoproliferative glomerulonephritis from transplant glomerulopathy.

Adult↗
PubMed1995

Hyperinducibility of HLA class II expression of thyroid follicular cells from Graves' disease. A primary defect?

Thyroid follicular cells (thyrocytes) from Graves' disease (GD) patients' thyroid glands express HLA class II molecules "ectopically." This phenomenon has been attributed to induction by locally produced cytokines and may be relevant to disease pathogenesis. We have compared IFN-gamma-mediated induction of HLA class II in thyrocytes from glands affected with GD and a nonautoimmune disease (MNG), to investigate a possible differential regulation of HLA expression between these two pathologies. HLA induction has been measured in primary thyrocyte cultures and control autologous macrophages stimulated or not stimulated with IFN-gamma. Comparison of flow cytometric data using an improved algorithm demonstrated that expression of HLA class II molecules is more readily induced in thyrocytes from GD than from MNG thyroid glands. This higher inducibility was parallel to a faster and stronger induction of HLA class II message in GD thyrocytes but did not correlate with the levels of HLA class II or class I originally expressed by thyrocytes in the tissue or with the degree of lymphocytic infiltration of the gland. There was no association with a particular HLA class II allele or with the presence of IFN-gamma and IL-2 in the tissue, as assessed by reverse transcription-PCR. No differences in the induction of class II were found in macrophages from each group of patients. These results suggest that an intrinsic feature of thyrocytes from GD patients is an up-regulation of HLA class II expression and that this is a characteristic that may facilitate the triggering of autoimmunity to "hyperinducible" thyroid glands.

Adolescent↗
PubMed1995

Transplantation of kidneys from donors with hepatitis C antibody into recipients with pre-transplantation anti-HCV.

Hepatitis C virus (HCV) is transmitted by organ transplantation. Consequently, several organ procurement organizations have imposed a moratorium on use of organs from anti-HCV positive donors. Because of the inadequate supply of cadaver kidneys for transplantation, we adopted a policy to transplant kidneys from anti-HCV donors into anti-HCV positive recipients. During the period between March 1990 and December 1992, 24 anti-HCV positive dialysis patients received a kidney from anti-HCV positive donors (group I) and 40 anti-HCV positive patients received a kidney from anti-HCV negative donors (group II). We compared the prevalence of liver disease, anti-HCV, HCV RNA, graft and patient survival between groups. Pre-transplantation 17 of 24 (71%) patients in group I and 31 of 40 (79%) of patients in group II had serum HCV RNA. Post-transplantation follow-up was 26 +/- 8 months and 30 +/- 10 months in groups I and II, respectively. During follow-up, elevated ALT levels were present in 7 of 24 (29%) and 16 of 40 (40%) of patients in groups I and II, respectively (P > 0.05). Post-transplantation, all patients in both groups retained anti-HCV. The prevalence of HCV RNA post-transplantation was 22 of 23 (96%) patients in group I and 30 of 39 (77%) of patients in group II (P > 0.05). Graft and patient survival in group I (96% and 100%, respectively) were not significantly different from those in group II (93% and 98%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Improved detection of anti-HCV in post-transfusion hepatitis by a third-generation ELISA.

The sensitivity of ORTHO HCV 3.0 ELISA Test System (ELISA 3) for the detection of anti-HCV was compared with the second-generation ELISA, OR-THO HCV 2.0 ELISA Test System (ELISA 2). ELISA 3 differs from ELISA 2 in that it incorporates the HCV recombinant antigen NS5, in addition to recombinant antigens derived from the NS3, NS4 and core regions of the HCV genome. Specimens tested consisted of serial bleeds obtained from 21 individuals undergoing seroconversion following acquisition of post-transfusion HCV infection. ELISA 3 demonstrated significantly greater sensitivity than ELISA 2, detecting seroconversion earlier in 24% (5/21) of cases. Although one of these cases appeared to represent early seroconversion to NS5, most of the improved sensitivity of ELISA 3 appeared to derive from increased detectability of anti-c33c.

Enzyme-Linked Immunosorbent Assay↗
PubMed1995

Markers of hepatitis C infection among hemodialysis patients with acute and chronic infection: implications for infection control strategies in hemodialysis units.

To evaluate strategies for screening patients on hemodialysis (HD) for markers of acute and chronic hepatitis C virus (HCV) infection, we studied sixty-nine patients at a single center over a 36-month period. Serum samples were tested for alanine aminotransferase (ALT) levels, anti-HCV and HCV RNA at 3-4 month intervals. Anti-HCV was tested for by EIA1, EIA2, and RIBA2. HCV RNA was detected by polymerase chain reaction (PCR). In addition, IgM antibody to the c33 antigen of HCV was detected by an experimental EIA. Of the 43 HD patients at the start of the study, anti-HCV was detected by EIA1 in 13 (30%). All EIA1 positive patients and 14 (47%) of the 30 EIA1 negative patients tested positive by EIA2. Thus, at the start of the study 27 (63%) of 43 patients tested positive for anti-HCV by EIA2. The presence of anti-HCV among EIA2 positive patients was confirmed by RIBA2 in all patients. Based on the PCR results, the sensitivity, specificity, positive predictive value and negative predictive value for EIA1 were 48%, 100%, 53% and 100%, respectively, and for EIA2 were 100%, 100%, 100% and 100%, respectively. During follow-up, 26 EIA2 negative patients began HD in the unit. Of the 42 EIA2 negative patients, five (12%) seroconverted for anti-HCV during follow-up. All five patients with new HCV infection tested positive for HCV RNA three months prior to the detection of anti-HCV by EIA2.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1994

Analysis of the contribution of the HLA system to the inheritance in the Wolfram syndrome.

The Wolfram syndrome (WS) is an autosomal recessive disorder beginning in childhood that consists of four clinical features: diabetes insipidus, diabetes mellitus, optic atrophy and deafness. Its pathogenesis remains unknown, although the tendency to develop this syndrome has been related to some class II antigens of the HLA system. We report six new cases in four families. A review of published data from the genetic features of this syndrome is performed, establishing the high frequency of the HLA-DR2 antigen in the WS (44.4%) compared with a control group (21.9%; relative risk, 2.8) and to patients with Type 1 insulin-dependent diabetes mellitus (Type 1 diabetes) (6.77%; relative risk, 9.7). We also comment the high frequency of the HLA-DQw1 antigen (85.5%) in this syndrome, without statistical significance. A familial segregation study of the HLA haplotypes has been carried out without finding correlation between the autosomal recessive pattern attributed to the WS, and the major histocompatibility complex. In conclusion, whereas HLA may increase susceptibility to the WS, as shown by the existence of an HLA-DR2 association, the major genetic influence on the inheritance of the WS must be at another locus.

Female↗
PubMed1994

Microalbuminuria development in short-term IDDM.

UNLABELLED: To assess risk factors associated with microalbuminuria development in short-term evolution insulin-dependent diabetes mellitus (IDDM) we undertake a cross-sectional study with retrospective examination of the 34 patients diagnosed with IDDM between 1982 and 1983 and followed up for at least 7 years in an outpatient endocrinology clinic. MAIN MEASURES: (1) At IDDM diagnosis: age, sex, parameters of metabolic control (fasting glycemia, HbA1), islet-cell antibodies, insulin autoantibodies, endogenous insulin secretion (EIS) and HLA type. (2) At 1 year evolution: EIS re-evaluation. (3) From IDDM diagnosis (every 3-4 month): body mass index, insulin schedule and dose, and parameters of metabolic control. (4) At 7-year evolution: 24-h urinary albumin excretion (UAE) and arterial blood pressure measurements on two consecutive outpatient controls. Microalbuminuria was defined as UAE above 30 micrograms/min on the two consecutive measurements. After 7-year follow-up, 8 (23.5%; 95% Cl: 9.3 to 37.7%) patients developed microalbuminuria. Their metabolic control was worse (7 years mean HbA1: 10.7 vs. 9.7%; P = 0.04) and 1 year EIS lower (1.9 vs. 7.6 ng/ml.10 min; P = 0.03) than in normoalbuminuric patients. They also had higher prevalence of 'high-normal' arterial blood pressure (P = 0.03) and diabetic retinopathy (P = 0.01) than normoalbuminuric patients did. Stepwise logistic regression analysis showed that diabetic retinopathy was the only independent and significant risk factor related to microalbuminuria development (P = 0.01). We conclude that in subjects with short-term evolution IDDM, microalbuminuria development was associated with glycemic control, EIS and arterial blood pressure levels, however the strongest association was found with diabetic retinopathy occurrence.

Adolescent↗
PubMed1992

Influence on survival of p24 antigen levels in patients with AIDS or advanced AIDS related complex treated with zidovudine.

In a prospective study sixty-eight patients consecutively diagnosed as having AIDS or advanced ARC who were started on zidovudine therapy were followed up for a median period of 725 days. In the 20 patients who had a baseline p24 antigen level above 20 pg/ml, there was a statistically significant trend towards reduction of the p24 antigen levels after the first month of treatment. The median time of survival of the 68 patients was 702 days and the median symptom-free period was 510 days. Treatment with zidovudine significantly reduced the p24 antigen levels. However, the life expectancy and the symptom-free period were not statistically different in the patients with p24 antigen levels always below or with levels always above two arbitrarily chosen cut-off points of 20 pg/ml and 50 pg/ml, respectively.

AIDS-Related Complex↗
PubMed1992

Non-association between 9.2 KB PvuII RFLP and seronegative spondyloarthropathies in Spain.

Several studies of DNA restriction fragment length polymorphism (RFLP) in ankylosing spondylitis (AS) have been carried out. The association between a recently identified class I HLA 9.2 kb PvuII RFLP and AS remain controversial. In order to evaluate this possible association in an Euro-Caucasian population, the genomic DNA of 42 AS patients and 18 patients with Reiter's syndrome (RS) and 42 healthy controls was analysed. Non-association between 9.2 kb PvuII RFLP and AS or RS was observed. As described previously, a strong association between this fragment and HLA-A3 and/or HLA-A9 antigens was demonstrated. A study of two families showed that this RFLP segregates with HLA-A3 and/or HLA-A9 and independently of the HLA-B27. Our findings support the view that the 9.2 kb PvuII fragment is not universally associated with AS.

Arthritis, Reactive↗
PubMed1991

Immunogenetic findings in cutaneous lupus erythematosus.

The serologic features and histocompatibility antigen associations of 93 patients with cutaneous lupus erythematosus are reported. Of them, 37 had chronic cutaneous lupus erythematosus and 56 had subacute cutaneous lupus erythematosus. Subacute cutaneous lupus erythematosus with an annular pattern occurred in 32 patients; 24 had a papulosquamous morphology. Sixty percent of patients with annular subacute cutaneous lupus erythematosus had anti-Ro antibodies. The incidence of this antibody in the other two groups was lower. In addition, patients with annular skin lesions had significant antigen association with HLA-B8 (37.5%; relative risk, 4.6) and HLA-DR3 (59.4%; relative risk, 4.3). There were no significant differences among chronic cutaneous lupus erythematosus and subacute cutaneous lupus erythematosus of the papulosquamous type and the control population for any HLA loci. Thus only patients with annular skin lesions represent a homogeneous subgroup in which there is a striking concordance of anti-Ro antibodies and the HLA-B8 and HLA-DR3 phenotypes.

Acute Disease↗
PubMed1990

Hepatitis C virus antibodies in chronic alcoholic patients: association with severity of liver injury.

The prevalence of hepatitis C virus antibody and its relationship to the severity of liver disease in chronic alcoholic patients has been assessed, using a recently developed enzyme immunoassay and confirmed by a recombinant immunoblot assay, in 144 patients (mean age +/- S.D. = 44.4 +/- 11.3 yr) who had consumed greater than 80 gm/day ethanol for greater than 5 yr. Hepatic disease was evaluated by clinical and biochemical studies and by liver biopsy when appropriate. In addition, 76 liver biopsy specimens from these patients were analyzed to determine whether liver lesions were similar in alcoholic patients with and without hepatitis C virus antibodies. According to clinical and histological features alcoholic patients were divided into five groups: normal liver (45 patients), fibrosteatosis (20 patients), alcoholic hepatitis (14 patients), cirrhosis (61 patients) and chronic hepatitis (4 patients). Hepatitis C virus antibodies were present in 35 alcoholic patients (24.3%). The prevalence of hepatitis C virus antibodies correlated with the severity of liver injury: 2.2% in patients without liver disease, 20% in those with fibrosteatosis, 41.4% in those with alcoholic hepatitis and 42.6% in those with cirrhosis. Hepatitis C virus antibodies were found in one of the four patients with chronic hepatitis (p less than 0.001). Furthermore, patients positive for hepatitis C virus antibodies with normal liver or fibrosteatosis showed higher serum bilirubin and gamma-globulin concentrations and lower aminopyrine breath test scores than did patients negative for hepatitis C virus antibodies with normal liver or fibrosteatosis. Similar differences between patients with and without hepatitis C virus antibodies were observed in patients with alcoholic hepatitis or cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Non-hemolytic transfusion reactions of the febrile type].

The results of a hundred cases of febrile non haemolytic transfusion reactions are presented. We used the techniques that would best identify the different causes of these reactions. Most of these antibodies were anti HLA. Platelet and granulocyte-specific antibodies were seldom detected. The nature of the antibodies was specified by their different reactivity with the cells of various donors, by applying a panel of cells from typed donors and by absorption experiments. The study of the donor sera enabled us to elucidate the causes of some reactions. Nevertheless, in a significant percentage of cases it was not possible to determine the cause of the reaction, especially in the case of reactions secondary to platelet transfusions. Finally, we analyzed the reasons that could account for these phenomena.

Blood Platelets↗
PubMed1989

Prevalence of antibodies to hepatitis C virus in Spanish patients with hepatocellular carcinoma and hepatic cirrhosis.

The prevalence of antibodies against hepatitis C virus (HCV) was investigated in 96 patients with hepatocellular carcinoma, 106 patients with liver cirrhosis without evidence of cancer, and 177 controls without liver disease. 75% of patients with hepatocellular carcinoma had HCV antibodies (anti-HCV), a significantly higher proportion than that observed in patients with cirrhosis (55.6%), or controls (7.3%). The prevalence of anti-HCV was significantly higher in patients with alcoholic cirrhosis and hepatocellular carcinoma (76%) than in patients with alcoholic cirrhosis alone (38.7%) whereas in patients with cryptogenic cirrhosis there was no significant difference between those with and without primary liver cell cancer (81.4% and 77.5%, respectively). These results indicate that HCV infection may have a role in the pathogenesis of hepatocellular carcinoma, even in patients with chronic liver disease apparently related to other agents such as alcohol, and that this recently identified hepatitis virus may be found in a large proportion of patients with cryptogenic cirrhosis.

Aged↗
PubMed1989

Correlation between residual beta-cell function and islet cell antibodies in newly diagnosed type I diabetes. Follow-up study.

To establish whether there is a correlation between the autoimmune response to the islets and beta-cell function during the initial stages of type I (insulin-dependent) diabetes, and islet cell antibody (ICA) titer and C-peptide levels (fasting and glucagon stimulated) were determined in 39 newly diagnosed patients at onset of diabetes and every 3-6 mo for 2 yr. ICAs were detected in 74% of the patients, and beta-cell function was detected in 84% of the patients at onset. The ICA+ and ICA- groups had similar C-peptide values at diagnosis and at 3 mo, but from 6 mo on, the ICA+ group consistently showed a tendency to lose C-peptide secretory capacity more quickly when assessed by fasting and glucagon-stimulated C-peptide levels (ICA+ vs. ICA- fasting C-peptide levels at 18 and 24 mo, P = .013 and .017, respectively; ICA+ vs. ICA- glucagon-stimulated C-peptide levels at 6, 18, and 24 mo, P = .023, .007, and .028, respectively). The initial ICA titer had the highest predictive value on the outcome of beta-cell function (P = .04), and patients with complement-fixing ICAs did not behave differently from the general ICA+ group. This correlation between beta-cell function and ICA titer supports the role of autoimmunity in the pathogenesis of type I diabetes and has important implications for the design of immunotherapy trials.

Adolescent↗