It has been reported that total serum IgE is increased in patients with alcoholic cirrhosis, but it is not clear if this fact is related to alcoholic liver disease or to alcohol intake.

To measure serum IgE in a group of chronic alcoholics with different stages of liver injury in order to elucidate if IgE increase in related to alcoholic liver damage.

Total serum IgE was determined by enzyme immunoassay in 186 chronic alcoholic patients (137 male/49 female) and 101 healthy controls. Patients and controls with known reasons for IgE elevation were excluded. Among alcoholic patients, 24 had fatty liver, 28 hepatic fibrosis, 29 alcoholic hepatitis, and 67 liver cirrhosis (38 patients were not evaluable concerning liver injury).

Total serum IgE was found to be increased in alcoholics (median 154.5 IU/mL, range 1-7329 IU/mL) with respect to healthy controls (median 20 IU/mL, range < 1-1417 IU/mL) (P < 0.001). IgE increase was moderate (180-1000 IU/mL) in 60 alcoholics (32.3%) and marked ( > 1000 IU/mL) in 27 (14.5%). Male alcoholics had higher IgE levels than females (median 191 IU/mL and range 1-7329 IU/mL vs 105 IU/mL and range 2-2189 IU/mL) ( P = 0.009). On logistic regression analysis, alcoholism, male sex and younger age (but not smoking) were independently associated with higher IgE levels. No clear relationship was noted between serum IgE and severity of alcoholic liver disease. Thus, no correlation was observed between IgE and parameters of liver function (serum bilirubin, albumin or prothrombin index). Likewise, IgE concentrations were not significantly different in patients with liver cirrhosis with respect to patients with less severe liver disease. Serum IgE was increased ( > 180 IU/mL) in 47.8% of cirrhotics and in 44% of patients without liver cirrhosis. In contrast, other immunoglobulins (IgG, IgA and IgM) were significantly correlated with liver dysfunction.

Chronic alcoholism should be considered as a cause of increased total serum IgE, regardless of the severity of the underlying liver disease.

Hypergammaglobulinemia is a well-known feature of liver cirrhosis, but studies on serum IgE in this setting are limited. The present study evaluates serum IgE concentration in a group of cirrhotic patients and examines their relationship with aetiological, clinical and analytical parameters (including liver function tests and hepatic phagocytic activity). The presence of specific IgE against common dietary antigens was also investigated. Total serum IgE was determined by enzyme immunoassay (EIA) in 52 cirrhotics (27 alcoholic and 25 non-alcoholic, including eight virus B and seven virus C-related cirrhosis, three primary biliary cirrhosis, three cryptogenic, three haemochromatosis and one Wilson's disease) and 34 healthy subjects (used as controls). Serum IgE (IU/ml) in controls was not significantly different from that of cirrhotic patients (median 42, range 2-726 vs median 86, range 2- > 1000, respectively) (P = NS). However, serum IgE among alcoholics (median 199, range 19- > 1000) was higher than that of controls (P < 0.001), virus B-related cirrhotics (median 25, range 3- > 1000) (P < 0.05), virus C-related cirrhotics (median 47, range 2-170) (P < 0.05), or non-alcoholic cirrhotics as a whole (median 23, range 2- > 1000) (P < 0.01). High IgE levels (> or = 170 IU/ml) were detected in 55.5% of alcoholics compared with only 12% of non-alcoholic cirrhotics (P < 0.01). Moreover, IgE levels were very high (> 1000 IU/ml) in six patients of the alcoholic group (22.2%) compared with only one non-alcoholic patient (4%).(ABSTRACT TRUNCATED AT 250 WORDS)

The prevalence of atopy (assessed by prick testing and serum IgE measurement), and of symptoms associated with atopy, has been defined in 122 patients with inflammatory bowel disease (IBD) and 103 age-matched controls. History analysis for atopic symptoms, and serum IgE levels, showed no differences between controls and IBD patients, or IBD subgroups (Crohn's disease, ulcerative colitis, ulcerative proctitis). Both in controls and in IBD patients, the prevalence of positive skin tests was higher in young people (aged less than 30) than in others; taking account of age distribution within the groups, there were no differences between controls and IBD patients, or subgroups, in the prevalence of positive skin tests. Our finding do not support the hypothesis that reaginic hypersensitivity plays a significant role in the pathogenesis of IBD.

Detection of IgG antibodies to Strongyloides stercoralis in sera of 29 patients with strongyloidiasis was attempted by the enzyme-linked immunosorbent assay (ELISA) using an extract of filariform larvae of S. stercoralis. The antibodies were found with a high degree of sensitivity in almost all patients. The ELISA values, however, did not correlate with the intensity of the infection or with differences in clinical and laboratory parameters. When the ELISA values of persons with Strongyloides were compared with those showing no S. stercoralis by faecal examinations, a significant difference was obtained between these two groups. The cross reactions with other helminth infections were significantly weaker than the reaction with Strongyloides infection. It was concluded that the antibodies are strongly elicited in human strongyloidiasis and that the assay provides a sensitive and specific method for diagnosis of strongyloidiasis.

This investigation was performed to determine the possible significance of the IgE levels in intestinal secretions for the recognition of type I food allergy (immediate hypersensitivity). Four groups of individuals were studied and compared with each other: (1) healthy controls and patients with gastrointestinal disorders not affecting the small intestine; (2) patients with small intestinal disease; (3) patients with various manifestations of allergy but without food intolerance; and (4) patients with atopic sensitivity to foods. Despite the presence of proteolysis in the intestinal fluid, a statistically highly significant increase of the intestinal IgE level was observed in patients of group 4 with type I food allergy and in patients of group 3 as compared with normals. This was associated with an increase in the serum IgE level. An increased synthesis of the IgE in the lamina propria of the small intestine is most probable, but not yet adequately established.

The cell-mediated and humoral immune responses were assessed in 15 patients with Crohn's disease and in 28 age-matched control subjects by means of several in vivo and in vitro methods. The disease activity in most patients was absent or moderate. Studying cellular immunocompetence we investigated the skin reactivity to various recall antigens (Candida, Trichophytin, Mumpsantigen, Streptokinase-Streptodornase, PPD), the primary immune response to Dinitrochlorobenzene (DNCB) and Keyhole Limpet Hemocyanin (KLH), and the lymphocyte transformation induced by mitogens (Phytohemagglutinin, Concanavaline A, Pokeweed Mitogen) and specific antigens. Humoral immunity was studied by measuring immunoglobulins, isohemagglutinins, and the antibody response to KLH. In addition, complement components and (in 10 patients) the proportions of T- and B-lymphocytes in the peripheral blood were evaluated. Cutaneous responsiveness to Candida, Mumps-antigen, SK-SD, and DNCB as well as the cellular immune response to KLH were impaired in patients with Crohn's disease (significance was reached for SK-SD, DNCB, and the mean area of induration). The lymphocyte transformation test with PHA, ConA, and PWM revealed normal results. For specific antigens (PPD, SK-SD, KLH) a good correlation could be demonstrated between delayed hypersensitivity and the in vitro lymphocyte responsiveness. Humoral immunity was not unequivocally impaired in Crohn's disease. Five patients with Crohn's disease proved constantly decreased total absolute lymphocyte counts in peripheral blood. The proportions of T- and B-lymphocytes and the complement-levels were corresponding to those in normal controls. No correlation was found between immunological and clinical parameters. In conclusion, patients with Crohn's disease exhibited a partial impairment of the cellular immune response, whereas humoral immunity was not affected. However, it remains to be elucidated whether this immune defect represents a basic pathogenetic factor in the onset of the disease.

Thirty-nine patients with ulcerative colitis and 35 with Crohn's disease have been investigated for evidence of reaginic hypersensitivity and compared with control subjects. There was no difference in the frequency of a personal or family history of atopy or in serum IgE levels. Similarly, no overall difference was noted in prick test responses to 21 allergens. However, further analysis of prick test responses showed that patients with inflammatory bowel disease responded more frequently to food allergens. This was highly significant when compared with healthy controls (p less than 0.001). The relevance of this finding to the aetiology of inflammatory bowel disease is discussed.

In 20 patients suffering for several years from serious chronic relapsing Crohn's disease the following immunological tests were carried out: (1) in-vitro stimulation of blood lymphocytes by PHA-P, (2) identification of T and B cells by formation of spontaneous rosettes and complement receptor rosettes, (3) effect of Crohn's serum on mixed lymphocyte reaction (MLR) of normal allogeneic lymphocytes, (4) in-vitro phagocytosis and intracellular killing of E. coli by polymorphonuclear granulocytes. The results indicate an immune defect of lymphocyte function and the effect of humoral factor(s) on T cell mediated immune reactions: (1) Lymphocyte stimulation by PHA-P was reduced significantly in Crohn's disease. In PHA-P dose response, maximal stimulation has shown a decrease and a shift to higher doses. (2) An increase in the absolute number of B cells caused a decrease in the mean percentage of T cells. The absolute number of T cells did not differ significantly from those of the controls. (3) Crohn's serum has shown an inhibitory effect in MLR of normal lymphocytes. (4) No impairment of phagocytosis or intracellular killing by polymorphonuclear granulocytes has been observed. The results suggest a symptomatic immune defect syndrome in a wasting disease. There is no evidence of a primary immune defect in Crohn's disease.

Three aspects of immunological function were studied in patients with Crohn's disease and ulcerative colitis (inflammatory bowel disease): atopic status and serum IgE levels; serum concentration of C-reactive protein; and C3 activation. The incidence of atopy, assessed by prick testing with common allergens, did not differ in patients with inflammatory bowel disease from healthy controls. 12 of 39 patients with Crohn's disease and 5 of 20 with ulcerative colitis, among whom were some non-atopic subjects, had elevated serum levels of IgE. Serum levels of C-reactive protein in patients were significantly greater than normal, even in those in whom the disease was clinically quiescent. Symptomatic patients with Crohn's disease had significantly higher levels than similar patients with ulcerative colitis and in Crohn's disease the levels correlated well with an overall assessment of severity and disease activity. Although conversion of C3 was detected in fresh serum samples from inflammatory bowel disease patients and not controls, only minimal traces were present in just 7 of 89 samples of EDTA--plasma from 47 patients; this finding did not correlate with disease activity. However, there were low titres of immunoconglutinin in the sera of some patients, but not in controls, suggesting that complement activation may be occurring in vivo.