Polyclonal IgA Research Articles

Polyclonal Immunoglobulin E Levels Are Correlated with Hemoglobin Values and Overall Survival in Patients with Multiple Myeloma

Polyclonal IgG, IgA, and IgM immunoglobulins are often decreased in sera of patients with multiple myeloma (MM), whereas very few data are available on polyclonal IgE levels. We have determined IgE levels in a large series of MM patients at diagnosis and subjects with monoclonal gammopathy of undetermined significance (MGUS) and correlated IgE levels with survival and prognostic factors in MM. IgE were determined with a commercially available ELISA kit in 201 MM patients at diagnosis, 144 subjects with MGUS, and 77 age-matched controls. IgE levels progressively decreased from controls to MGUS and from MGUS to MM (P = 0.001). MM patients with IgE levels of >11.5 IU/mL (median) had a better survival than patients with IgE of <11.5 IU/mL (P = 0.048). The difference was even more significant when MM patients were divided according to clinical cutoff values. Patients with elevated IgE levels (>100 IU/mL) had from 2 to 3 years longer survival than those with low (<10 IU/mL) or intermediate values (10-100 IU/mL; P < 0.01). IgE levels were positively and negatively correlated with hemoglobin (P = 0.006) and beta2-microglobulin levels (P = 0.007), respectively. Univariate and multivariate analyses confirmed that high IgE levels are positive predictors of overall survival (P = 0.03 and 0.08, respectively) and strongly correlated with hemoglobin values. Because IgE levels are dependent on Th(2) responses, these data open new perspectives in the interpretation of antitumor immune responses and pathogenesis of anemia in MM.

Naturally occurring catalytic antibodies: evidence for preferred development of the catalytic function in IgA class antibodies

IgG class antibodies express catalytic activities rarely and at very low levels. Here, we studied polyclonal IgA and IgG preparations from healthy human sera and saliva for the ability to hydrolyze model peptidyl-aminomethylcoumarin (peptide-AMC) substrates. These substrates permit objective evaluation of the catalytic potential of the antibody classes with minimal effects of noncovalent interactions occurring at sites remote from the reaction center. The IgA preparations hydrolyzed Glu-Ala-Arg-AMC at rates 3-orders of magnitude greater than IgG preparations from the same individuals. The cleavage occurred preferentially on the C terminal side of a basic residue. The activity was confirmed using monoclonal IgAs isolated from patients with multiple myeloma. Active site-directed inhibitors of serine proteases inhibited the catalytic activity and were bound irreversibly by the IgA, suggesting the involvement of a serine protease-like mechanism similar to that utilized by previously described IgM antibodies. These observations suggest that mechanisms underlying B cell clonal selection favor the retention and improvement of catalytic activity in the IgA, but not the IgG compartment of the immune response.

Adaptive development of catalytic antibodies to the gp120 superantigenic site in lupus and HIV infected patients (44.43)

Abstract The B cell superantigenic site of the HIV protein gp120 (gp120SAg) is important in viral entry into host cells and gp120SAg binding IgG in the preimmune repertoire reduce the risk of infection. Like the gp120SAg binding function, the innate catalytic function of antibody (Ab) variable domains is subject to deterioration during B cell maturation, and gp120SAg binding Abs are not produced appreciably following infection. We report the selection of catalytic single chain Fv (scFv) and light chain (L chain) clones from the Ab repertoire of patients with lupus, a condition involving increased production of gp120SAg binding Abs. The Ab fragments were isolated by covalent phage selection using electrophilic gp120 analogs. Several selected fragments cleaved gp120 via a nucleophilic mechanism coordinated with noncovalent recognition of gp120(421–433), determined by electrophoretic assays. Certain clones neutralized HIV infection in cultured peripheral blood mononuclear cells (low μg/ml potency), including two scFv clones that neutralized primary clade B, C and D strains. In contrast to lupus patients, studies on polyclonal IgG and IgA from HIV infected patients did not support the presence of an amplified Ab response to gp120SAg. IgAs from a minority of infected subjects with no progression to AIDS 5.5 years following seroconversion displayed increased gp120 hydrolysis compared to rapid progressors (P&amp;lt;0.0001). These data suggest catalytic Abs as a protective anti-viral mechanism and open the way to considerations of immunogens that stimulate catalytic immunity as candidate vaccines.

Significance of IgG4 in the diagnosis of mucous membrane pemphigoid

To determine the diagnostic value and frequency of tissue deposition of IgG4 in comparison to polyclonal IgG, IgA, IgM, and C3. Oral mucosal biopsies of 82 patients clinically suspected to have mucous membrane pemphigoid (MMP) were analyzed by direct immunofluorescence (IF) using polyclonal anti-human IgG, IgM, IgA, fibrin, complement C3, and anti-human IgG4 subclass monoclonal antibodies. Based on clinical, hematoxylin and eosin (H & E), and direct IF studies, 34 cases were diagnosed as MMP. The most common antibody deposited was IgG (90%), followed by C3 (82%), and IgG4 (71%). In more than half the cases of MMP, IgG4 deposition was seen in combination with IgG and or C3. Strikingly, IgG4 was the sole antibody detected in 2 cases (6%). Our results suggest that the use of monoclonal IgG4 is important in the diagnosis of MMP. We suggest adding monoclonal IgG4 to the routine panel of antibodies used in studies of cases suspected to have MMP to avoid false-negatives.

HIV-1 Envelope Triggers Polyclonal Ig Class Switch Recombination through a CD40-Independent Mechanism Involving BAFF and C-Type Lectin Receptors

Switching from IgM to IgG and IgA is essential for antiviral immunity and requires engagement of CD40 on B cells by CD40L on CD4(+) T cells. HIV-1 is thought to impair CD40-dependent production of protective IgG and IgA by inducing progressive loss of CD4(+) T cells. Paradoxically, this humoral immunodeficiency is associated with B cell hyperactivation and increased production of nonprotective IgG and IgA that are either nonspecific or specific for HIV-1 envelope glycoproteins, including gp120. Nonspecific and gp120-specific IgG and IgA are sensitive to antiretroviral therapy and remain sustained in infected individuals with very few CD4(+) T cells. One interpretation is that some HIV-1 Ags elicit IgG and IgA class switch DNA recombination (CSR) in a CD40-independent fashion. We show that a subset of B cells binds gp120 through mannose C-type lectin receptors (MCLRs). In the presence of gp120, MCLR-expressing B cells up-regulate the CSR-inducing enzyme, activation-induced cytidine deaminase, and undergo CSR from IgM to IgG and IgA. CSR is further enhanced by IL-4 or IL-10, whereas Ab secretion requires a B cell-activating factor of the TNF family. This CD40L-related molecule is produced by monocytes upon CD4, CCR5, and CXCR4 engagement by gp120 and cooperates with IL-4 and IL-10 to up-regulate MCLRs on B cells. Thus, gp120 may elicit polyclonal IgG and IgA responses by linking the innate and adaptive immune systems through the B cell-activating factor of the TNF family. Chronic activation of B cells through this CD40-independent pathway could impair protective T cell-dependent Ab responses by inducing immune exhaustion.

Pyoderma Gangrenosum Associated with Nasal Septal Perforation, Oropharyngeal Ulcers and IgA Paraproteinemia

We report a case of pyoderma gangrenosum (PG) associated with nasal septal perforation, pharyngeal ulcers and IgA paraproteinemia. A 28-year-old woman first developed painful undermined ulcers on her perianal, inguinal and axillary areas when she was 22 years old. Histological findings from the cutaneous ulcers showed dermal and epidermal infiltrate of neutrophils, which was compatible with PG. Laboratory examinations did not detect any associations of systemic diseases other than polyclonal IgA paraproteinemia. Nasal fiberscopy revealed septal perforation and multiple ulcers on her pharynx. The biopsy specimen from the pharyngeal ulcers showed a polymorphous cellular infiltrate without necrotizing vasculitis or granuloma. However, there were no atypical lymphocytes that are typically seen in nasal NK/T lymphoma. By immunohistochemical analysis, the infiltrated lymphocytes were proved to be T cells and Epstein-Barr virus encoded RNA (EBER) was not detected. No pulmonary or renal lesions resembling Wegener's granulomatosis were found. Taken together, the nasal septal perforation was considered as nasal involvement of PG.

IgA antibodies to human tissue transglutaminase: audit of routine practice confirms high diagnostic accuracy

Background: The diagnostic accuracy of IgA tissue transglutaminase antibodies (TGA) for coeliac disease (CD) has been assessed following the introduction of the test into routine practice in 2002. Methods: Specificity was assessed in serum samples received from 1554 adults for routine coeliac serology. The population for assessing sensitivity was 75 consecutive new adult diagnoses of CD. TGA was measured by enzyme-linked immunoassay using human tissue transglutaminase as antigen. Concordance between TGA and endomysial antibody (EMA) was also assessed. Results: The prevalence of new diagnoses of CD in the population tested was 2.8% with similar proportions of new diagnoses in males and females. The positive predictive values at a cut-off of 3 units/mL were 0.77 for samples from Primary Care and 0.92 for samples from Hospital sources, with a sensitivity of 92%. At TGA <3 units/mL, EMA was usually negative; when TGA was >4.9 units/mL, EMA was rarely negative. Conclusions: We have assessed the role of TGA in routine clinical practice and confirmed high diagnostic accuracy. Sensitivity (92%) is identical to the sensitivity for EMA. IgA deficiency should be excluded in samples showing low absorbance readings in the TGA assay and interference from monoclonal and polyclonal IgA should be excluded in samples with slightly raised TGA levels and negative EMA. TGA is recommended as the first-line serological test for coeliac disease.

The significance of stress hormones (glucocorticoids, catecholamines) for eruptions and spontaneous remission phases in psoriasis.

In an earlier paper, it was described how acute eruptions of psoriasis may be produced in phases of immune deficiency and in the presence of bacterial antigen-releasing inflammatory foci, whereas clinical spontaneous remissions are produced in phases of immunologic activity. Therefore, it was of interest to investigate whether the stress hormones cortisol/epinephrine are involved in triggering such deficiency and activity phases. During a series of investigations lasting up to 3 years in 95 patients, the following were determined: cortisol/epinephrine levels, polyclonal serum immunoglobulins IgM, IgG, and IgA, total serum IgE, complement C3 and C4 proteins, T cells and subpopulations, as well as streptococcal titers ASO/ADNase B, severity index (PASI) RESULTS: Phases of clinical inactivity are associated with the mechanism, "immunologic regulation," where antibacterial titers are elevated, but all other parameters are unremarkable. Eruption phases (in 32 of 95 patients) showed absolute increases in serum cortisol levels and antibacterial titers, and decreases in serum epinephrine (adrenaline) levels. Phases of spontaneous remission (in 25 of 32 patients) showed, in contrast to the eruption phases, absolute increases in serum epinephrine levels, and significant falls in serum cortisol levels and bacterial titers. On the basis of these results, the participation of the immune system is confirmed in the pathogenesis of psoriasis, which is subject to control by higher neurohormonal systems. Cortisol may be involved in the clinical eruption phase, and epinephrine in the remission phase. Both hormones are true antagonists and have important effects on the human immune system if produced in excess via the pituitary-adrenal axis. Infection with Streptococcus pyogenes is an additional trigger for the dermatosis.

Antibodies to porcine pancreatic amylase in inflammatory bowel disease. Characterization and prevalence.

It has been proposed that the immunoglobulins in some naturally occurring macroamylases may primarily directed to animal amylase. This would suggest that there may also be an antibody to animal amylase with inability to bind endogenous amylases in circulation. On the basis of this assumption, an antibody to porcine pancreatic amylase (PPA) was investigated in sera from patients with inflammatory bowel disease (IBD): ulcerative colitis (UC) and Crohn's disease (CD), because serum antibodies to various dietary antigens have been demonstrated to be a significantly prevalent in patients with IBD. This investigation took advantage of the abilities of serum to inhibit specific activity of added PPA and to form an artificial macroamylase with the PPA. As expected, such antibodies to PPA were detected frequently in patients with CD (19/50, 38%), rarely in patients with UC (1/50, 2%) and not at all in normal controls (0/30). There were two different types of antibodies differing in their reaction with PPA; one was an enzyme-inhibiting antibody and another an enzyme-noninhibiting antibody. The former seemed to be of monoclonal or oligoclonal IgG whereas the latter was of polyclonal IgG and IgA or polyclonal IgG alone, and both were detected in almost cases. The presence of the antibodies specific for CD suggests that the antibodies may play an etiological role in CD, of which the etiology is still unknown.

Fosfomycin, an antibiotic, possessed TGF- β-like immunoregulatory activities

The regulatory effects of fosfomycin (FOM) were correlated closely with the multifunction of TGF-β in the modulation of immune responses in vivo and in vitro. LPS-induced polyclonal IgM and IgG antibody responses were depressed at 3 days after the initial culture and subsequently enhanced at day 10 by FOM or TGF-β. Neither FOM nor TGF-β inhibited LPS-induced IgA antibody responses, whereas dexamethasone (DX) reduced polyclonal IgM, IgG and IgA antibody responses wholly. The suppression of antibody responses and Mv1Lu cell proliferation induced by FOM or TGF-β was partly overcome with soluble TFG-β receptors (sRIII). Oral, i.v. and i.p. administration of FOM exhibited similar enhanced SRBC-specific antibody responses to that seen after oral administration of TGF-β. The addition of FOM and latent TGF-β inhibited the proliferation of Mv1Lu cells, but FOM did not lead to an increase in plasmin activities, which convert latent to active TGF-β, and further the expression of TGF-β receptors on the cell surface. In addition, FOM failed to enhance TGF-β secretion. These findings suggest that immunomodulation of FOM results in increased sensitivity of cells to TGF-β.

Acute motor axonal neuropathy with high titer IgG and IgA anti-GD1 a antibodies following Campylobacter enteritis

We describe the first two European cases of acute axonal motor neuropathy with both IgG and IgA anti-GD1a antibodies following Campylobacter enteritis. Both patients acutely developed severe weakness without sensory involvement, had antibodies to Campylobacter jejuni and polyclonal IgG and IgA titers ≥ 12 800 to GD1a at onset, which decreased during follow-up. Serial electrophysiologic studies showed: 1, normal or only slightly slowed motor conductions; 2, evidence of a progressive loss of excitability and conduction failure in nerve fibers undergoing axonal degeneration in intermediate nerve segments and evidence of distal axonal involvement in one nerve; 3, normal sensory conductions, sensory potential amplitudes and somatosensory evoked potentials. Although we cannot exclude that axonal degeneration followed demyelination, we think that anti-GD1a antibodies account for the axonal involvement because GD1a is present in the axolemma and exposed at the node of Ranvier and in nerve terminals. The exclusive motor involvement could be explained by the fact that GD1a has a different internal structure in motor and sensory fibers.

Distribution of monoclonal antibodies in intestinal and urogenital secretions of mice bearing hybridoma 'backpack' tumours.

Mice bearing IgA hybridoma 'backpack' tumours have been used to demonstrate that secretion of a single monoclonal IgA can protect against mucosal infection, but the relevance of this model to normal IgA protection is not clear. The authors analysed the distribution of specific monoclonal and total antibodies in bile, local intestinal secretions, cervical-vaginal secretions, urine and serum of mice bearing anti-cholera toxin (CT) IgA and IgG backpack tumours, with and without bile duct ligation. Backpack tumours resulted in high levels of both anti-CT and total IgA or IgG in serum, and IgA (but not IgG) in bile. Secretions recovered by absorbent filter 'wicks' from mucosal surfaces throughout the intestines of backpack tumour mice contained significant concentrations of monoclonal anti-CT IgA, but total IgA levels were as in normal mice. Neither monoclonal nor total IgA levels on mucosal surfaces were altered by bile duct ligation. Furthermore, anti-CT monoclonal IgA levels in local intestinal secretions of backpack tumour mice were comparable to specific polyclonal IgA levels previously elicited by mucosal immunization with CT. Thus, IgA-mediated protection against enteric challenge in the backpack tumour model may be a valid predictor of protection provided by natural mucosal immunization in vivo. High monoclonal IgA levels in bile, urine and the female genital tract, however, may not reflect the situation in normal immunized mice.

Specificity of an Enzyme-1 Inked Immunosorbent Assay for Dog Ige Antibody to Japanese Cedar (Cryptomeria Japonica) Pollen

ABSTRACT We developed a fluorometric enzyme-linked immunosorbent assay (ELISA) for allergen-specific IgE in dogs with the use of monoclonal anti-dog IgE; we assayed IgE antibody to Japanese cedar pollen in the sera of dogs with Japanese cedar pollinosis. To assess the specificity of this ELISA, a pooled serum sample from pollinosis dogs was subjected to gel chromatography. The peak of anti-pollen allergen IgE activity was different from the peaks of total IgA, IgG and IgM. When IgE antibody positive serum was heated at 56°C for 4 h, antibody activity was markedly reduced. Furthermore, polyclonal anti-dog IgA, IgG and IgM did not interfere with anti-pollen allergen IgE activity in the ELISA. From these results, this assay is considered to have a high specificity for dog IgE.

Regulation of complement activity by immunoglobulin. I. Effect of immunoglobulin isotype on C4 uptake on antibody-sensitized sheep erythrocytes and solid phase immune complexes.

Intravenous Ig, composed principally of IgG, prevents complement attack by inhibiting C3 and C4 uptake onto target cells and tissues. Using two different models, Ab-sensitized SRBC and BSA-anti BSA solid phase immune complexes, we have examined the complement inhibitory capacity of three Ig classes (IgG, IgM, IgA) focussing on inhibition of C4 uptake. It was found that on both a weight and molar basis, monomeric serum IgA and IgM were far more active than IgG (weight efficiency ratios were 1.0, 20.8, and 236.3, and molar efficiency ratios 1.0, 24.0, and 1382.9 for polyclonal IgG, IgA1, and IgM, respectively). Monoclonal IgM were less active than polyclonal IgM (50% inhibition was achieved in SRBC model by 0.022, 0.30, 1.6, and 1.6 mg/ml of polyclonal IgM and monoclonal IgM from patients Lew, Will, and Pri). Secretory IgA was less active than serum IgA1 and similar in inhibitory activity to IgG (weight and molar efficiency ratios 1.5 and 0.6 compared with IgG). All tested preparations were less active in the solid phase immune complex model than in the sensitized cell model. A mixture of Igs of different isotypes was somewhat more active than any isotype alone. These results suggest that polyclonal serum IgA and IgM can also be considered for active therapy in diseases accompanied by the activation of classical complement pathway.

非溶血性輸血副作用惹起患者より検出された同種抗ＩｇＡ抗体について

We used an enzyme-liked immunosorbent assay (ELISA) using polyclonal IgA purified from pooled plasma as an antigen for the screening of anti-IgA antibodies in sera from patients with nonhemolytic transfusion reactions (NHTRs). Among 154 patients referred to our laboratory from April 1994 to January 1995, two were positive for anti-IgA IgG antibodies. Specificites of the anti-IgA antibodies were examined by immunoblotting. Anti-IgA2m(1) and anti-IgA1 were detected in one case each. Sera from both patients contained normal levels of total IgA. In one case, a 43-year-old woman with chronic myelogenous leukemia showed urticaria followed by wheezing dyspnea and fever one hour after the start of platelet concentrate (PC) transfusion. In the other case, a 45-year-old woman with aplastic anemia complained of itching, urticaria, facial edema and nausea immediately after the start of PC transfusion. No antibodies against HLA, platelet-specific antigens or irregular antibodies against red blood cell antigens were detected in either patients' sera collected before transfusion or in the transfused blood in these cases. These findings suggested that these NHTRs might have been caused by subclass and allotype-specific anti-IgA antibodies. These results show that ELISA and Western blotting are useful in the detection of anti-IgA antibodies responsible for NHTRs.

Effects of orally administered Clostridium butyricum MIYAIRI 588 on mucosal immunity in mice

The activation of local mucosal immunity by Clostridium butyricum MIYAIRI 588 (CBM588) was investigated in germ-free mice. An increase of polyclonal IgA production in the small intestine or secretion into the intestinal lumen was observed in mice mono-associated with CBM588 and fed a diet containing killed vegetative cells of CBM588 (VCBM). However, fecal IgA of anti-CBM588 was rarely formed in mice administered CBM588 during 6 weeks from administration. Cholera toxin was administered orally to SPF mice fed a diet containing CBM588, and IgA secretion of anti-cholera toxin was enhanced in mice fed a VCBM diet. In addition, the production of IgA, IgM and IgG in Peyer's patch cell culture was increased in the presence of VCBM. These results suggest that oral administration of CBM588 stimulates polyclonal mucosal immune activity and shows adjuvant activity for anti-cholera toxin.

IL-15 has stimulatory activity for the induction of B cell proliferation and differentiation.

The identification and cloning of the novel cytokine IL-15 were recently described. IL-15 is produced by a wide range of cell types, with the highest levels of IL-15 mRNA being detected in epithelial lines, monocytes, muscle, and placenta. Although it has no sequence identity with IL-2, IL-15 shares many of the T cell-stimulatory activities described for IL-2. We have examined IL-15 for its ability to stimulate B cells and have compared its activity with that of IL-2. IL-15 costimulates proliferation of B cells activated with immobilized anti-human IgM or phorbol ester, but has no stimulatory effect on resting B cells. In combination with recombinant CD40L, IL-15 is a potent inducer of polyclonal IgM, IgG1, and IgA secretion, but does not cause production of IgG4 or IgE. The activity of IL-15 in B cell proliferation and differentiation assays is comparable with that of IL-2. Studies that used neutralizing Abs have demonstrated that, for signal transduction in B cells, IL-15 uses the beta-chain of the IL-2R complex but, unlike IL-2, does not require the alpha-chain. IL-2 is required for the generation of a human primary Ag-specific in vitro response using sheep erythrocytes as Ag. Of all cytokines examined, only IL-15 has the capacity to replace IL-2 in this system, although only partially. In summary, IL-15 has comparable activity with IL-2 for the induction of B cell proliferation and differentiation and uses at least some of the components of the IL-2R complex to mediate its effects.

An enzyme immunoassay for the determination of anti-IgA antibodies using polyclonal human IgA

An enzyme immunoassay (EIA) for screening and quantitation of serum anti-IgA antibodies of IgG class is described. This method is based on the use of purified polyclonal human serum IgA as the coating antigen and a commercial alkaline phosphatase-conjugated anti-human IgG as the detecting antibody. Nonspecific reactions were minimized by blocking vacant protein binding sites with bovine serum albumin and by using individual sample blanks. The IgA specificity of a positive antibody finding was confirmed by testing inhibition: pooled normal human serum inhibited the binding of specific antibodies by over 80%. The same degree of inhibition could also be demonstrated by a commercial myeloma IgA preparation and by the IgA used for coating but not by IgA-deficient serum (< 0.05 mg/l). On the basis of the mean anti-IgA antibody titre in EIA, a value of 12000 arbitrary units of anti-IgA per litre (AU/l) was assigned to a patient serum used as standard in the assay. Anti-IgA results obtained by EIA and haemagglutination correlated well, which makes it possible to compare earlier HA results with those obtained now by EIA. The measuring range of the assay was 0.6–27 AU/l and the lowest quantifiable concentration 7 AU/l. The dilution requirement for serum was 1 16 . The interassay coefficients of variation for control sera with antibody levels from 35 AU/l to 3770 AU/l varied from 9 to 12%.

IgG isotype-specific auto-antibodies bind preferentially to cross-linked membrane Ig.

Under equilibrium conditions, the affinities of five anti-IgG2a mAb isolated from virus-infected mice were comparable to other high-affinity auto-antibodies. Similar to rheumatoid factors, these anti-IgG2a auto-antibodies bound to aggregated or complexed IgG2a with 50 to 1500-fold higher avidity than their monomeric counterparts. Despite their high functional affinity to IgG2a, flow cytometric analysis revealed no binding or marginal mAb binding to four distinct lines of B cells expressing different densities of membrane-anchored IgG2a. If, however, surface IgG2a was cross-linked by polyclonal light chain-specific antibodies, IgM and IgA mAb binding resulted, and was detected as an increase in mean fluorescence intensity compared with isotype-matched control antibodies. The binding of one IgM mAb to cross-linked IgG2a patches of the cell surface was also visualized by confocal microscopy. Pretreatment of cells with aggregated IgG2a caused increased fluorescence intensity, demonstrating that the IgM and IgA mAb were also able to interact with IgG2a aggregates bound on the B cell surface via Fc gamma RIIB. It also permitted efficient co-ligation of the aggregated B cell receptors (BCR) with Fc gamma RIIB-fixed immune complexes known to deliver a negative signal in B cell activation. Cross-linking of IgG2a complexes bound to Fc gamma RI on macrophages or dendritic cells with antigen-specific BCR and/or T cells via their Fc gamma RIIB may accelerate the physical contact of cells involved in the antigen-specific response.(ABSTRACT TRUNCATED AT 250 WORDS)

Simultaneous macroamylasemia and macrolipasemia

The first case of the simultaneous presence of macroamylasemia and macrolipasemia in a patient with gluten enteropathy (celiac disease) is described. Both macroenzymes were formed by association of polyclonal IgA with amylase and lipase. Both macroenzymes had molecular masses > 300 kDa.