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Results for “Hypergammaglobulinemia”

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At least 19 recordsLinked to original sources
PubMed1998

Influence of microbial stimulation on hypergammaglobulinemia and autoantibody production in pristane-induced lupus.

Pristane induces a lupus-like syndrome characterized by autoantibody production and glomerulonephritis in nonautoimmune strains of mice. Although it has been suggested that this syndrome results from nonspecific immune activation, there is little evidence so far that B cells are activated nonspecifically by pristane or that this promotes autoimmunity. In this study, we examined whether polyclonal hypergammaglobulinemia occurs in pristane-induced lupus, and its relationship to the production of anti-DNA, nRNP/Sm, and Su autoantibodies. In conventionally housed mice, there was a marked increase in total IgM and IgG3 2 weeks after i.p. pristane injection, followed by increased IgG1, IgG2a, and IgG2b levels. IgM levels were higher in pristane-treated specific pathogen-free (SPF) mice than in conventionally housed mice, whereas IgG and IgA levels were reduced. Pristane induced anti-nRNP/Sm and Su autoantibodies in SPF mice, but their onset was delayed and levels were lower than those in conventionally housed mice. There was no consistent relationship between total IgG1, 2a, and 2b hypergammaglobulinemia and production of anti-nRNP/Sm and Su autoantibodies. Moreover, the total Ig levels were similar in the anti-nRNP/Sm-positive and -negative groups. In contrast, production of IgM anti-ssDNA antibodies paralleled IgM hypergammaglobulinemia in some, but not all, mice. These studies indicate that pristane-induced lupus is associated with marked hypergammaglobulinemia, the magnitude of which is influenced by the microbial environment. However, anti-nRNP/Sm and Su autoantibody production is at least partly independent of polyclonal B cell activation. The data strongly suggest that pristane-induced lupus is not exclusively the consequence of nonspecific immune stimulation. They also point to the importance of microbial stimulation in the development of hypergammaglobulinemia in this inducible lupus model.

Animals↗
PubMed2003

Mechanisms of hypergammaglobulinemia and impaired antigen-specific humoral immunity in HIV-1 infection.

Hypergammaglobulinemia and defective humoral immunity are hallmarks of HIV-1 infection. Naive B cells have been recently suggested as the major source of hypergammaglobulinemia in chronic viral infections. We recently reported that HIV-1-infected patients carry low levels of memory B cells. Here we studied whether defects in the naive and memory B cells in HIV-1-infected patients translated into hypergammaglobulinemia and defective humoral immunity against specific antigens. Naive B cells from HIV-1-infected patients exhibited abnormal expression of the activation/differentiation markers CD70 and leukocyte-associated Ig-like receptor (LAIR-1). Activated naive B cells from patients showed a significant increase in the intracellular immunoglobulin G (IgG) content ex vivo and this activated phenotype correlated to hypergammaglobulinemia and to the ability of naive B cells from patients to secrete IgG in vitro. We analyzed the levels of antibodies to tetanus toxoid, measles, and HIV-1 in relation to memory B cells and observed a significant reduction of antigen-specific antibodies in patients with low-memory B lymphocytes. Nevertheless, hypergammaglobulinemia and levels of polyspecific self-reactive antibodies were comparable in patients with normal and low memory B cells. We conclude that reduction of memory B lymphocytes in HIV-1 infection correlates with defective humoral immunity and that hyperactivated naive B cells may represent the source of abnormal IgG production in HIV-1 infection. Our results may be relevant to the design of HIV-1 therapeutical vaccines and to the clinical management of HIV-1-infected patients.

Adult↗
PubMed1988

Predominance of the IgG1 subclass in the hypergammaglobulinemia observed in pre-AIDS and AIDS.

In addition to the well-known T-cell dysfunctions in AIDS, hypergammaglobulinemia, mostly IgG, and autoimmune phenomena indicate that B cells are also involved. Reports of HIV-infected and activated B cells suggest T cell-independent B-cell abnormalities. In order to assess the IgG subclasses involved in hypergammaglobulinemia, we examined all four IgG subclasses in sera and in vitro with an enzyme-linked immunosorbent assay (ELISA). The in vitro studies included 7-day cultures of mononuclear cells and highly purified B cells stimulated with a T cell-independent polyclonal B-cell activator (Klebsiella pneumoniae, KlebsM). Cultures were done with cells from seven patients with AIDS, seven patients with persistent generalized lymph node enlargement and HIV antibodies, and normal controls. In vivo, hypergammaglobulinemia was found to be restricted to the IgG1 subclass. In vitro, high spontaneous levels of IgG were not elevated significantly under stimulatory conditions, as demonstrated by the measurement of all four IgG subclasses in the culture supernatants. In vitro, hypergammaglobulinemia also resulted from IgG1. These results indicate that there are B-cell abnormalities in pre-AIDS and AIDS, in that the B-cell preactivation in vivo resulting in hypergammaglobulinemia is restricted to IgG1.

AIDS-Related Complex↗
PubMed1986

Systemic plasmacytosis. A syndrome of peculiar multiple skin eruptions, generalized lymphadenopathy, and polyclonal hypergammaglobulinemia.

A description is given of two patients with peculiar multiple skin eruptions, asymptomatic generalized lymphadenopathy, and polyclonal hypergammaglobulinemia. Both patients were admitted to our hospital for further evaluation of an increased erythrocyte sedimentation rate and hypergammaglobulinemia discovered during routine medical examinations. Despite various investigations, the underlying disease causing the hypergammaglobulinemia was not found. Histologic examination disclosed dense perivascular infiltration of plasma cells in the dermis. In the lymph nodes, considerable plasma cell infiltration was found from the cortex to the medulla. These plasma cells were mature and showed no cellular atypism. The association of peculiar multiple skin eruptions, lymphadenopathy, and polyclonal hypergammaglobulinemia, which we have called "systemic plasmacytosis," signifies a new syndrome that can be differentiated from diseases reported previously.

Adult↗
PubMed2001

The influence of placental malaria infection and maternal hypergammaglobulinemia on transplacental transfer of antibodies and IgG subclasses in a rural West African population.

Two hundred thirteen mother-baby pairs in The Gambia were studied to determine the influence of placental malaria infection and maternal hypergammaglobulinemia on transplacental antibody transfer. Antibody transfer for herpes simplex virus 1 (HSV-1), respiratory syncytial virus (RSV), and varicella-zoster virus (VZV) was significantly reduced by placental malaria infection by 69%, 58%, and 55%, respectively. Maternal hypergammaglobulinemia was associated with a significant reduction in antibody transfer for HSV-1, RSV, VZV, and pneumococcus by 89%, 90%, 91%, and 88%, respectively. In addition, placental malaria infection was associated with a significant reduction in transfer of IgG1, IgG2, and IgG4 (P<.01, P=.01, and P=.03, respectively) but not of IgG3 (P=.59). Maternal hypergammaglobulinemia significantly impaired the transfer of IgG1 and IgG2 (P=.01) but not of IgG3 or IgG4 (P=.62 and P=.59, respectively). Placental malaria infection and maternal hypergammaglobulinemia were associated with reduction in the transplacental transfer of these specific antibodies, IgG1, and IgG2 in this Gambian population.

Adult↗
PubMed1995

[Clinical course of a HIV-seropositive patient with thrombocytopenia and hypergammaglobulinemia who was initially screened by annual complete physical examination].

A 57-year-old man was admitted because of hypergammaglobulinemia which was initially pointed out by annual complete physical examination. No significant abnormal findings were observed except polyclonal hypergammaglobulinemia at that time (IgG; 2,662 mg/dl, IgA; 422 mg/dl). Seven months later, he has progressed to show thrombocytopenia. The laboratory data showing the reduction of peripheral CD 4-positive T cells (CD 4; 0.2 x 10(9)/l, CD 4/8 ratio; 0.19) and positive serum HIV antibody revealed that his hypergammaglobulinemia and thrombocytopenia were resulted from HIV infection. The peripheral platelet count decreased to 28 x 10(9)/l at minimal point, however, it recovered to 160 x 10(9)/l within 7 months without treatment. His good performance status has been still maintained over 4 years. His whole clinical course suggests that there is no significant correlation between peripheral platelet counts, serum gammaglobulin levels or the amounts of PAIgG in this case. This case proposes that we should also consider a possibility of HIV infection for the patients showing hypergammaglobulinemia.

HIV Seropositivity↗
PubMed2003

Hypergammaglobulinemia and autoantibody induction mechanisms in viral infections.

Polyclonal hypergammaglobulinemia is a characteristic of chronic inflammatory conditions, including persisting viral infections and autoimmune diseases. Here we have studied hypergammaglobulinemia in mice infected with lymphocytic choriomeningitis virus (LCMV), which induces nonspecific immunoglobulins as a result of switching natural IgM specificities to IgG. The process is dependent on help from CD4+ T cells that specifically recognize LCMV peptides presented by B cells on major histocompatibility complex class II molecules. Thus, hypergammaglobulinemia may arise when specific helper T cells recognize B cells that have processed viral antigens irrespective of the B cell receptor specificity. This nonspecific B cell activation may contribute to antibody-mediated autoimmunity.

Animals↗
PubMedDate not supplied

Hypergammaglobulinemia can be associated with a positive direct antiglobulin test, a nonreactive eluate, and no evidence of hemolysis.

To determine the cause of a positive direct antiglobulin test (DAT), blood banks routinely perform serologic tests on eluates prepared from DAT-positive red cells. Negative eluates traditionally have been suspected to be associated with drug reactions. This report confirms that the most frequent cause of a positive DAT and a nonreactive eluate is hypergammaglobulinemia. The results of 74 patient samples with positive DATs were analyzed retrospectively. Eluates prepared from the red cells of 54 patients (72.9%) reacted; eluates from 20 patients (27.1%) did not react. This latter group had identical serologic and clinical findings, suggesting that they made up a homogeneous group. In particular, the patients had a positive DAT, a negative indirect antiglobulin test, and a negative eluate; an increased serum concentration of IgG; and no evidence of hemolysis. In a subsequent study, DATs were performed prospectively on red cells from 44 consecutive patients with elevated serum IgG levels. The serum IgG concentration was highest in the three patients whose red cells had a positive DAT. The DAT also became positive in two patients treated with high-dose intravenous gammaglobulin (IV IgG). These studies indicate that a negative eluate from red cells with a positive DAT, a common serologic finding, is often caused by hypergammaglobulinemia. The authors postulate that IgG binds nonspecifically to the red cells because of the hypergammaglobulinemia.

Coombs Test↗
PubMed2006

Intraocular crystals in HIV-related hypergammaglobulinemia.

PURPOSE: To describe the occurrence of bilateral iris and retinal crystals in a patient with benign HIV-related gammopathy. DESIGN: Observational case report. METHODS: A 45-year-old HIV-positive male with a known, benign hypergammaglobulinemia was referred for routine ophthalmic assessment because of right ophthalmic zoster. RESULTS: Ophthalmoscopic examination revealed the presence of bilateral, multiple, refractile iris and macular crystals. No other signs of uveitis or stigmata of HIV were found. CONCLUSION: Intraocular crystals are a rare finding, usually seen in chronic uveitis with or without hypergammaglobulinemia. This finding has not been previously described in non-inflamed eyes, nor as an ocular manifestation of HIV. We hypothesize that HIV-related disruption of the blood-aqueous and blood-retinal barriers allows intraocular immunoglobulin deposition in patients with hypergammaglobulinemia.

Crystallization↗
PubMed1994

Mapping of a gene for hypergammaglobulinemia to the distal region on chromosome 4 in NZB mice and its contribution to systemic lupus erythematosus in (NZB x NZW)F1 mice.

IgM class hypergammaglobulinemia develops spontaneously in the early life of NZB mice. To determine the chromosomal location of the NZB gene(s) linked to this hypergammaglobulinemia and possible contribution to systemic lupus erythematosus (SLE)-like autoimmune disease observed in (NZB x NZW)F1 hybrid mice, we examined (NZB x NZW)F1 x NZW backcross mice, using a mapping technique based on polymorphism in simple nucleotide sequence repeats. In light of our previous data, we directed attention to chromosome 4. A single NZB locus or tightly linked group of loci on the distal region (70-90 cM distal from the centromere), theoretically mapped to 14.3 cM distal from marker locus D4Mit48, had the strongest association with IgM hypergammaglobulinemia. The backcross progeny heterozygous for this locus on chromosome 4, in association with heterozygosity of the MHC haplotype (H-2d from NZB/H-2z from NZW) on chromosome 17, showed significantly higher serum levels of IgG anti-DNA antibodies and more severe lupus nephritis than did the progeny heterozygous for either one of the two loci or homozygous for both loci on chromosomes 4 and 17. The NZB gene in the distal region of chromosome 4 is likely to be responsible for terminal maturation of B cells and, in concert with the effect of H-2 heterozygosity, may predispose to the full expression of SLE in (NZB x NZW)F1 mice.

Animals↗
PubMed1997

Case of malignant lymphoma associated with primary systemic plasmacytosis with polyclonal hypergammaglobulinemia.

Systemic plasmacytosis (SP), which has a histologic appearance similar to that of multicentric Castleman's disease (MCD), is also known as benign plasma cell proliferation with polyclonal hypergammaglobulinemia, cutaneous plasmacytosis, and/or generalized plasmacytic lymphadenopathy. The prognosis of SP reportedly has been good. A 59-year-old Japanese man was treated for multiple cutaneous lesions of his trunk as well as polyclonal hypergammaglobulinemia. A skin biopsy showed infiltration of lymphocytes and polyclonal plasma cells in the dermis. The patient developed enlarged superficial lymph nodes 5 years later, and T-cell lymphoma, diffuse mixed type, was diagnosed. At that time, his cutaneous plasmacytosis remained but the polyclonal hypergammaglobulinemia had resolved. Ours is the first reported case of SP to be complicated by the development of T-cell lymphoma.

Humans↗
PubMed1985

Sensory and autonomic polyneuropathy associated with hypergammaglobulinemia.

Sensory and autonomic polyneuropathy is a rare disease characterized by a sensory nerve disorder and postganglionic autonomic dysfunction. The etiology of this disease is unknown. We described a 51-year-old woman who had a chronic sensory dominant polyneuropathy and dysautonomia associated with hypergammaglobulinemia. In the previous reports of sensory and autonomic polyneuropathy, not much attention was given to coexisting hypergammaglobulinemia. By reviewing the literatures, hypergammaglobulinemia was frequently present in these case reports. This fact leads us to consider that an immunological mechanism may be playing a role in the pathogenesis of this disorder.

Autonomic Nervous System Diseases↗
PubMed2001

[Effect of highly active antiretroviral therapy (HAART) on hypergammaglobulinemia in HIV infected patients].

To investigate the mechanism of hypergammaglobulinemia in HIV infected patients, the effect of highly active antiretroviral therapy (HAART) on the hypergammaglobulinemia was analyzed. Involved in this study were 34 untreated, 21 HAART-effective (complete response) and 14 HAART-non-effective (partial response) patients. Serum levels of HIV-RNA and gammaglobulin and immunoglobulin (Ig) isotypes were measured. Mean HIV-RNA levels of untreated and partial response patients were 1.6 x 10(4) copies/ml and 0.4 x 10(4) copies/ml, respectively. HIV-RNA levels of all complete response patients were below 4.0 x 10(2) copies/ml. Mean gammaglobulin percentages of untreated, partial response and complete response patients were 24.4%, 21.8% and 17.9%, respectively (p < 0.01 in untreated vs complete response patients). Mean IgG levels in the three groups were 2,489 mg/dl, 1,947 mg/dl and 1,618 mg/dl, respectively (p < 0.001 in untreated vs complete response patients). IgA levels were high in some untreated patients and lower in complete response patients. IgE levels were increased in some untreated and partial response patients, but there was no significant difference among the three groups. These results suggested that the hypergammaglobulinemia found in HIV infected patients was associated with HIV replication. The activation mechanism might differ by Ig isotypes.

Adult↗
PubMed1997

Evaluation of renal acidification in HIV-infected patients with hypergammaglobulinemia.

Distal renal tubular acidosis has been reported in several diseases associated with hypergammaglobulinemia, particularly Sjögren's syndrome. Since HIV infection is now a common cause of hypergammaglobulinemia, we evaluated renal acidification under basal and dynamic conditions in 8 asymptomatic HIV-seropositive subjects. Basal acid-base status was normal in all except 1 patient who had respiratory acidosis subsequent to recent pneumonia. Acid-loading tests showed normal acid excretion except for 1 patient who had low acid excretion attributed to non-ingestion of the ammonium chloride capsules. Bicarbonate-loading tests showed normal distal acidification indexes in 7 patients. The only patient with a low acidification defect was diagnosed 2 weeks later as having tuberculosis. Our results suggest that hypergammaglobulinemia per se is not a sufficient condition to induce renal tubular acidosis.

Acidosis, Renal Tubular↗
PubMed1990

Meningioma with hypergammaglobulinemia. Case report.

The case of a 14-year-old boy presenting with hypergammaglobulinemia (immunoglobulin (Ig)G and IgA) and a cerebellopontine angle tumor is reported. The tumor was histologically confirmed as meningioma infiltrated with plasma cells, lymphocytes, and histiocytes. Immunohistochemical studies showed that the infiltrating plasma cells were stained by antibodies to IgG and IgA. After total tumor removal, the hypergammaglobulinemia immediately resolved. A plausible interpretation of this sequence of events is that the inflammatory cell reaction to the meningioma caused the immunological response followed by an unusual hypergammaglobulinemia.

Adolescent↗
PubMed1979

[Study of the acidification capacity of the urine in polyclonal hypergammaglobulinemia (author's transl)].

The renal capacity of acidification of urine was studied in 21 patients with hypergammaglobulinemia (polyclonal gammapathies) secondary to several conditions. The reabsorption threshold of bicarbonate was determined by Rodriguez-Soriano's technique; the acid and ammonium production was measured using Wrong and Davies' technique. Values for the bicarbonate threshold ranged from 18.5 to 29 mmol/liter of plasma bicarbonate with a mean value of 25 +/- 2.29; they were not significantly different from the control values. Urinary pH ranged from 4.6 to 5.8; ammonium excretion ranged from 18.4 to 114.5 microEq/min (mean value 63.01 +/- 25.36). Acidity values ranged from 13 to 65.05 microEq/min (mean value 33.61 +/- 19.36). Thhre was no statistical difference between these values and those obtained from the controls. We found no evidence that the acidification function of urine was limited in patients with hypergammaglobulinemia secondary to several conditions as compared with normal subjects. In the two cases in which this function was altered there was no reason why it should be attributed to hypergammaglobulinemia.

Adolescent↗
PubMed1984

Helper T-cell lymphoma with marked plasmacytosis and polyclonal hypergammaglobulinemia. A case report.

A case of malignant lymphoma with a helper activity of neoplastic cells is reported. On admission, a significant number of plasma cells of polyclonal nature were seen in the peripheral blood, and polyclonal hypergammaglobulinemia was seen. The biopsied lymph node showed poorly differentiated lymphocytic lymphoma with marked proliferation of plasma cells. At the terminal stage, the patient became leukemic in contrast with the disappearance of plasma cells from the peripheral blood. Although the leukemic cells failed to form sheep erythrocyte rosettes, they were considered to be of T-cell origin morphologically. Cytochemically, they had a "dot"-like pattern of alpha-naphthyl acetate esterase and acid phosphatase activity. Ultrastructurally, they had highly convoluted nuclei, and cytoplasmic clustered dense bodies. They showed marked helper activity on pokeweed mitogen-induced B-cell differentiation in vitro. This case may provide a novel view concerning the cause of hypergammaglobulinemia induced by lymphoproliferative disorders.

Azure Stains↗
PubMed1988

Polyclonal B-cell lymphocytosis and hypergammaglobulinemia in patients with Gaucher disease.

Sera from 23 individuals with Gaucher disease (GD) were analyzed for hypergammaglobulinemia and oligoclonal and monoclonal gammopathies. Serum IgG level was elevated in 15/23 (65%) patients, and a diffuse hypergammaglobulinemia was present in 10/23 (43%) patients. An oligoclonal gammopathy was noted in six patients, and a monoclonal gammopathy in two. Lymphocyte subset analysis was also carried out in eight individuals with GD. Four of five individuals showed increased surface Ig-positive lymphocytes, while 7/7 were positive for either increased CD19- and/or CD20-positive lymphocytes. An eighth patient was found to have a B-cell leukemia. Statistical analysis of kappa and lambda histograms were suggestive of a monoclonal excess. However, restriction enzyme analysis of four individuals with GD and increased B cells failed to show any evidence of Ig gene rearrangements. Serum Ig abnormalities and perhaps B-cell lymphocytosis appear to be common in the GD patient population and are not associated with circulating monoclonal lymphocytes.

Adult↗