PubMed Health⌕ Search

Biomedical subjects

C Betterle

Publications and source records attributed to C Betterle.

At least 19 recordsLinked to original sources
PubMed1992

Induction of autoantibodies during alpha interferon treatment in chronic hepatitis B.

Thirty-two patients with chronic hepatitis B treated with alpha interferon were tested for 12 different antibodies. Only a minority (18%) of cases developed antinuclear antibodies and none developed clinical signs of autoimmune disease. These data suggest that, at the dose regimen used, interferon therapy of chronic hepatitis B is not associated with triggering of autoimmunity.

Adult↗
PubMed1991

Expression of class I and II human leukocyte antigens by thyrocytes and lymphocytic infiltration on human thyroid tumors. An immunofluorescence study.

Surgical thyroid sections from 30 papillary carcinomas (PC), six medullary carcinomas (MC), three anaplastic carcinomas (AC), two follicular carcinomas (FC), and 16 adenomas (AD) were examined with an indirect immunofluorescence technique employing different monoclonal antibodies to evaluate the expression of human leukocyte antigen (HLA)-A, B, C (Class I) and DR, DP, DQ (Class II) by thyrocytes, together with the phenotype and distribution of inflammatory cells. Ten PC and four FC were also investigated for the presence of intercellular adhesion molecule-1 (ICAM-1). In situ deposits of immunocomplexes and circulating thyroid autoantibodies were also evaluated. An increased expression of Class I antigens was found in all PC and FC, in 33% of MC and AC, and in 31% of AD. An anomalous expression of Class II antigens was observed in 70% of PC, in 50% of FC, in 33% of AC, in 19% of AD, and in none of the MC. Expression of DP or DQ was revealed only in a portion of the DR-positive glands. A reduction of microsomal autoantigen expression was found. No ICAM-1-positive thyrocytes were detected. A moderate T-lymphocytic infiltrate was noticed only in PC, where it was correlated with DR and DP and/or DQ coexpression. B-cells and natural killer cells were virtually absent. The authors speculate that the weak Class II antigens expression, together with the partial or complete loss in microsomal autoantigen and the absence of ICAM-1 by thyrocytes, may account for the limited engagement of immunocompetent cells observed in thyroid tumors.

Adenoma↗
PubMed1991

Autoantibodies during alpha-interferon therapy for chronic hepatitis B.

The development of autoantibodies and autoimmune reactions has been reported during and after interferon (IFN) therapy. Thirteen different antibodies from the sera of 32 patients with chronic hepatitis B treated with alpha-interferon (alpha-IFN) were tested. Seventeen HBeAg-positive patients received 4.5 megaunits (MU) of recombinant IFN thrice weekly for 4 months, and 15 anti-HBe and HBV-DNA positive patients were treated with 5 MU/m2 of lymphoblastoid IFN thrice weekly for 6 months. Five patients (15%) had antinuclear antibodies (ANA) and one patient (3%) had smooth muscle antibodies before treatment. ANA appeared during IFN treatment in five (18%) of 28 previously negative patients. With discontinuation of treatment, the titer of ANA fell to undetectable levels in all patients. In contrast, none of the patients developed antibodies to endocrine organs, such as thyroid microsomal, thyroglobulin, parietal cells, pancreatic islet cell, and adrenal cortex antibodies or autoantibodies specifically associated with autoimmune liver disease such as liver kidney microsomal antibodies and antimitochondrial antibodies. There was no correlation between autoantibody positivity before therapy or autoantibody occurrence during treatment and response to IFN therapy. None of the patients developed clinical signs of autoimmune disease. These results indicate that these regimens of recombinant and lymphoblastoid IFN therapy of chronic hepatitis B are associated with a low risk of clinically significant autoimmunity.

Adult↗
PubMed1991

Islet cell surface antibodies by an ELISA method in diabetic and nondiabetic patients.

Islet cell surface antibodies (ICSA) were investigated by an ELISA method using a commercial kit in 146 subjects with and without islet cell antibodies (ICA): 28 with insulin-dependent diabetes mellitus (IDDM), 24 with noninsulin-dependent diabetes mellitus (NIDDM), 22 first-degree relatives (FDR) of IDDM patients, 31 organ-specific autoimmune patients (OSAP), 21 nonautoimmune hospitalized patients (NAP), and 20 ICA-negative normal controls. Furthermore, insulin autoantibodies (IAA) were evaluated in 87 of these subjects. ICSA were found in 11% of IDDM patients and in 14% of their FDR, in 4% of NIDDM patients, in 10% of OSAP, in 10% of NAP, and in 5% of normal controls. After absorption with rat liver powder, ICSA were detected in 7% of IDDM patients, in 5% of their FDR, in 4% of NIDDM, in 6% of OSAP, in 5% of NAP and in none of normal controls. ICSA were also detected in 4% of IAA-positive compared to 3% of IAA-negative sera. Neither correlation was found between ICSA and ICA in each group of subjects, nor between ICSA and IAA, suggesting that these autoantibodies recognize different pancreatic targets. Moreover, no significant difference was observed for ICSA prevalence in the various groups of patients studied when compared with normal controls. The prevalence of ICSA assessed by this ELISA method has been compared to that reported by other workers, who employed different techniques.(ABSTRACT TRUNCATED AT 250 WORDS)

Addison Disease↗
PubMed1991

Expression of intercellular adhesion molecule-1 (ICAM-1) on thyroid epithelial cells in Hashimoto's thyroiditis but not in Graves' disease or papillary thyroid cancer.

In order to study the possible role of antigen-independent adhesion systems in thyroid autoimmunity, we evaluated by indirect immunofluorescence the expression of lymphocyte functional antigen-1 (LFA-1) and its ligand ICAM-1 on mononuclear cell infiltrates (when present) and thyroid follicular cells of four patients with Hashimoto's thyroiditis, 30 with Graves' disease, five with papillary cancer, two with follicular adenoma, and two normal thyroid specimens. The expression of MHC class I and class II antigens was also evaluated. Most mononuclear infiltrates were LFA-1 positive, as expected. A positivity for ICAM-1 on follicular cells was observed in three out of four Hashimoto's thyroiditis specimens; such a phenomenon was totally absent in Graves' disease or any other pathological condition, or in normal tissue. MHC class II expression on thyrocytes was observed in all the patients with Hashimoto's thyroiditis, in 27 out of 30 with Graves' disease and in three out of five papillary cancer specimens.

Adult↗
PubMed1990

Immunohistochemical localization of factor X-like antigen in pancreatic islets and their tumours.

The authors have investigated by immunohistochemistry the distribution of factor X-like antigen in normal pancreatic islets and in a series of 46 pancreatic endocrine tumours. It was found that both glucagon-producing (A) cells and pancreatic polypeptide-producing (PP) cells are immunoreactive for the antigen. Benign glucagonomas and PP-omas presented the highest concentrations of immunoreactive material whose intracellular distribution was consistent with localization within cell secretory granules. Some benign insulinomas also presented factor X immunostaining in spite of the absence of the antigen in normal insulin-producing B cells. Although malignant tumours usually exhibited very low or no immunostaining, two of three malignant glucagonomas showed scattered, intensely immunoreactive cells. The factor X-like antigen identified in this study was found to differ from chromogranin A and B. The possible implications of the present findings for coagulative disorders associated with glucagonomas or diabetes are discussed.

Adenoma, Islet Cell↗
PubMed1988

Long term thyroid function after subtotal thyroidectomy for Graves' disease.

Between 1973 and 1980, 93 patients with Graves' disease underwent subtotal thyroidectomy by the same surgeon (the size of thyroid remnant was 4 g per side). No case of operative mortality, no case of thyroid storm nor of surgical complications occurred. Three months after surgery 40% of patients were euthyroid, 25% had overt hypothyroidism, 35% had subclinical hypothyroidism. In the following yr important variations of thyroid function were observed. The number of patients with subclinical hypothyroidism decreased slowly (22% and 9% at 3 and 6 yr, respectively), and some became euthyroid, some hypothyroid, others relapsed. Seven patients had recurrent hyperthyroidism. In particular at 3 yr 45% of patients were euthyroid, 28% had overt hypothyroidism, 22% had subclinical hypothyroidism, 4% had recurrence; at 6 yr 56% were euthyroid, 32% had overt hypothyroidism, 9% had subclinical hypothyroidism, 3% had recurrence. Four out of the 8 patients operated under 20-yr-old became hypothyroid in comparison with only 2 out of the 15 patients over 50-yr-old. Relapses were present only in patients operated at less than 40-yr and only in females. No correlation was found between thyroid lymphocytic infiltration and thyroid function after surgery, nor between the presence of antithyroid antibodies and hypothyroidism. All cases who relapsed had high TMA titers both before and after operation. This study confirms the need for accurate follow-up after subtotal thyroidectomy for Graves' disease.

Adolescent↗
PubMed1988

The natural history of adrenal function in autoimmune patients with adrenal autoantibodies.

Adrenal autoantibodies (AA) were found in 23 of 2571 (0.9%) patients with organ-specific autoimmune diseases, in one of 632 first-degree relatives of insulin-dependent diabetic patients, and in none of 375 normal controls. In AA-positive subjects the prevalence of human leucocyte antigens (HLA)-A1, -B8 and -DR3 was significantly higher with respect to the general population. Two groups were followed (15 subjects persistently positive for AA and 51 negative subjects) for a mean period of 3.2 years. Yearly tests were made for AA and adrenal function. Of the 15 subjects persistently positive for AA, six developed Addison's disease after a period varying from 6 months to 10 years. Of the 51 subjects initially negative, two became positive during follow-up, and one of these developed Addison's disease 15 months later. In contrast, all the remaining 49 persistently negative subjects maintained normal adrenal function tests. Overall, of the 17 positive subjects, seven (41%) developed Addison's disease, three (18%) showed various degrees of subclinical adrenocortical failure and the remaining seven maintained normal glandular function. In the positive patients the yearly incidence of detriment in adrenal function was 19%. Patients who developed Addison's disease showed significant association with HLA-B8 phenotype. The development from normal adrenocortical function to overt Addison's disease seemed to progress through four distinct stages of functional impairment: increased plasma renin activity with normal/low aldosterone (stage 1), low cortisol response after i.v. administration of ACTH (stage 2), increased ACTH (stage 3), and low basal cortisol (stage 4).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Complement-fixing gastric parietal cell autoantibodies. A good marker for the identification of type A chronic atrophic gastritis.

Using an indirect immunofluorescence (IIF) technique, gastric parietal cell autoantibodies of IgG class (GPCA-IgG) were found in 2% of a normal population, in 5-26% of organ-specific autoimmune subjects and in 100% of patients with pernicious anaemia. With the exception of subjects with alopecia, there was a significantly increased prevalence of GPCA-IgG in autoimmune patients with respect to normal controls. GPCA of IgA class were detected in 22% of GPCA-IgG positive subjects, whereas GPCA of IgM class were uncommon. One-hundred and fifteen subjects underwent gastroscopy and body mucosal biopsy. Histopathological findings of chronic atrophic gastritis (CAG) were present in 71% of GPCA-IgG positive autoimmune patients without pernicious anaemia, in 100% of GPCA-IgG positive patients with pernicious anaemia, and in 20% of GPCA negative autoimmune patients. Complement-fixation test was performed in 46 GPCA-IgG positive subjects without pernicious anaemia using the IIF method. Twenty-nine patients (63%) were found to fix complement fractions till C9 (CF-GPCA) together with properdin factor, and in 25 of them (86%) the histological examination of body gastric mucosa disclosed a CAG (P = 0.0003 versus GPCA-IgG positive/CF negative controls). No significant difference was observed for the prevalence of CAG in GPCA-IgG positive/CF negative subjects with respect to GPCA-IgG negative control group. We conclude that the presence of CF-GPCA represents a useful immunological marker in the identification of CAG, while no predictive value seems to be associated with non-complement fixing GPCA-IgG.

Adolescent↗
PubMed1987

Islet cell and insulin autoantibodies in organ-specific autoimmune patients. Their behaviour and predictive value for the development of type 1 (insulin-dependent) diabetes mellitus. A 10-year follow-up study.

To evaluate the behaviour and predictive value of islet cell and insulin autoantibodies in patients with organ-specific autoimmune diseases, we followed 21 non-diabetic subjects for a mean period of 84 +/- 27 months. Ten patients were persistently seropositive for complement-fixing islet cell antibodies and high titres of immunoglobulin G islet cell antibodies (greater than or equal to 1:8). The prevalence of persistent insulin autoantibodies in this group was 67%. Seven patients (70%) developed Type 1 (insulin-dependent) diabetes mellitus after a latency period of 2-60 months. The predictive value of complement-fixing islet cell antibodies was 65%, and in the presence of both complement-fixing islet cell and insulin autoantibodies the predictive value rose to 76%. Eleven patients were seronegative for complement-fixing islet cell antibodies and had low immunoglobulin G islet cell antibodies titres (less than 1:8) that were either persistent or transient, or that fluctuated during follow-up. The prevalence of persistent insulin autoantibodies in this group was 45%; only one subject developed Type 1 diabetes. The predictive value of persistent islet cell antibodies (complement-fixing positive/negative) was 54%, and it rose to 70% when both islet cell and insulin autoantibodies were present. Individuals with only insulin autoantibodies or immunoglobulin G islet cell antibodies did not develop diabetes mellitus. A high frequency of HLA-DR3 and/or DR4 was found in patients who developed diabetes mellitus. Thus, the presence of both islet cell and insulin autoantibodies in patients with organ-specific autoimmune disease appears to confer the highest risk of progression toward Type 1 diabetes.

Adolescent↗
PubMed1987

Thyroid autoantibodies: a good marker for the study of symptomless autoimmune thyroiditis.

In 3737 subjects without clinically thyroid disorders we evaluated the incidence of thyroid microsomal and thyroglobulin antibodies. These autoantibodies were found in 7% of a normal population, in 9% of patients with various non-autoimmune diseases, and in 11-16% of groups who either had or were at risk for autoimmune diseases: patients with IDDM, vitiligo, alopecia areata, idiopathic hypoparathyroidism, Addison's disease, and first-degree relatives of IDDM patients. Functional thyroid evaluation with TRH test was performed in 197 seropositive subjects and 144 seronegative controls. One-quarter (26%) of the subjects with thyroid autoantibodies showed functional abnormalities on TRH testing, whereas only 2.8% of the 144 seronegative controls showed subclinical hypothyroidism. After an observation period of 12-44 months, 102 persistently seropositive subjects were reassessed and 31% of them showed an impairment in TRH test response.

Adult↗
PubMed1987

Detection of insulin autoantibodies using an ELISA technique in first-degree relatives of IDDM patients and in autoimmune patients.

We have improved an ELISA technique for the detection of IgG and IgM class IAA demonstrating the sensitivity and the specificity of antigen-antibody reaction. In sera of 135 first degree relatives of IDDM patients and of 128 autoimmune patients "at risk" for IDDM either positive or negative for islet cell antibodies (ICA), the prevalence of IAA IgG/IgM in all groups studied was significantly (p less than 0.001) higher than in controls, but the highest frequency of IAA was observed in the ICA-positive subjects. A similar association was also observed in complement-fixing ICA (CF-ICA) positive subjects. Future prospective studies will be necessary to establish the role of IAA as marker of B-cell damage.

Adolescent↗