Etiologies of Polyclonal Hypergammaglobulinemia: A scoping review

Beuvon, C.; Martin, M.; Baillou, Chloé; Roblot, P.; Puyade, Mathieu

doi:10.1016/j.ejim.2021.05.023

Cited by 10 publications

(4 citation statements)

References 9 publications

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“…High concentrations of specific or nonspecific antibodies result in HGG pictures in various pathological conditions, including several infectious diseases, 10 such as VL. In the manifestation of VL, HGG is related to polyclonal activation of B cells induced by antigens present in the cell membrane or even antigens excreted and secreted by the agent 11 .…”

Section: Introductionmentioning

confidence: 99%

Understanding hypergammaglobulinemia in experimental or natural visceral leishmaniasis

de Carvalho,

Hiramoto,

Meireles

et al. 2024

Parasite Immunology

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Nonspecific hypergammaglobulinemia (HGG) occurs in symptomatic human visceral leishmaniasis (VL) caused by L. L. infantum. This study assessed this finding in experimental infection in hamsters and natural infection in dogs. The serum concentration of proteins, albumin and globulins was determined through the biuret and bromocresol green reaction, where the HGG was better expressed through the albumin/globulin (A/G) ratio. HGG was associated with a higher concentration of specific anti‐glycan antibodies (BSA‐G)/promastigote soluble extract (PSE) and the presence of circulating immune complexes (IC) by dissociative enzyme‐linked immunoassay (ELISA). The study found monovalent IC in 37.9% (PSE) and 50% (BSA‐G) of sera from infected hamsters, with increased frequency as the disease progressed. HGG was found in >60% of the samples in dogs with VL, associated with higher levels of specific immunoglobulin (Ig)A and IgM, but not IgG, determined using the PSE and BSA‐G ELISA. HGG was associated with the presence of monovalent IC in 58.9% (PSE) and 63.4% (BSA‐G) positive dog samples. HGG may result not only from the nonspecific activation of B cells, with greater production of specific and nonspecific antibodies, but also due to lower IgG excretion due to the presence of soluble monovalent IC. HGG correlates to the progression of VL and may be a marker for manifested disease.

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Section: Introductionmentioning

confidence: 99%

Understanding hypergammaglobulinemia in experimental or natural visceral leishmaniasis

de Carvalho,

Hiramoto,

Meireles

et al. 2024

Parasite Immunology

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“…Polyclonal hypergammaglobulinemia (PHGG) results from the excessive production of immunoglobulins in response to diverse immunological challenges. In contrast to monoclonal hypergammaglobulinemia, whereby the monoclonal nature of immunoglobulin-producing cells is the central component of the pathophysiology (1), the etiologies of PHGG are manifold and not limited to hematological diseases, thus requiring clinicians to be well-versed with its diagnostic procedures and diverse differential diagnoses (2)(3)(4)(5)(6). While the diagnostic process of monoclonal hypergammaglobulinemia is relatively straightforward (7)(8)(9) it is often confounded when coincidentally encountered or consulted for PHGG, especially when some disease overlap is suspected.…”

Section: Introductionmentioning

confidence: 99%

Positive anti-nuclear antibody in patients with polyclonal hypergammaglobulinemia suggests the presence of multiple distinct comorbidities

Masuda,

Morita,

Kurokawa

2024

Intern. Med.

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Objective Polyclonal hypergammaglobulinemia (PHGG) is a classic problem in internal medicine; however, its conditions and diagnostic procedures have not been well studied. We therefore conducted a retrospective study to characterize the PHGG disease spectrum. Methods We included all patients who underwent serum protein electrophoresis (SPEP) at a hematology tertiary referral center during a five-year period. For these patients, globulin clonality was determined and clinical data were extracted from the records. Results Out of 209 consecutive cases of hypergammaglobulinemia demonstrated by SPEP, 79 cases of PHGG were identified. A total of 46 diagnoses were associated with PHGG. Patients with PHGG were younger (median 71.0 years old (yo) vs. 65 years; P = 0.002) and had lower gamma-globulin levels (median, 26.5 g/L vs 24.8 g/L; P = 0.03) than those with monoclonal hypergammaglobulinemia. Interestingly, out of 79 patients with PHGG, 15 were associated with more than one diagnosis, and a female predominance was observed in this specific subset of patients. PHGG cases with multiple diseases showed higher gammaglobulin levels than those with monoclonal hypergammaglobulinemia, in a disease-dependent manner. Additionally, positive antinuclear antibodies (ANAs) had a discriminative ability with an area under the curve of 0.81 (95% confidence interval, 0.65-0.96) and were highly sensitive to multimorbidity in PHGG (sensitivity, 92.3%). Conclusion These results establish a previously underappreciated unique immunological state of multimorbidity in PHGG and indicate that the gamma-globulin levels and ANAs could serve as markers for the clinical assessment of comorbidities in PHGG.

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“…The specificity and affinity of different IgG subclasses to antigens and their effector molecules vary enormously [11]. For instance, IgG1 is the primary subclass responsible for reactions to protein antigens and is a powerful mediator of FcγR and complement‐mediated activities [12]. IgG2 mainly binds to FcγRIIAH131, and also to FcγRIIAR131 and FcγRIIIAV158 with a low affinity and the IgG2 subclass is responsible for almost all IgG responses to polysaccharide antigens [13].…”

Section: Introductionmentioning

confidence: 99%

Serological characteristics and clinical implications of IgG subclasses in visceral leishmaniasis

Han,

Li,

Wei

et al. 2023

Tropical Med Int Health

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ObjectivesVisceral leishmaniasis (VL) represents the most severe form of Leishmaniasis infection, often resulting in fatality without timely treatment. Previous studies have found that immunosuppression increases the risk of VL disease progression and mortality, and the total immunoglobulin G (IgG) levels in peripheral blood vary before and after treatment. However, the distinct levels and roles of IgG subclasses in VL have not been documented yet. This study aims to elucidate the characteristics and clinical significance of IgG subclasses in VL.MethodsA total of 43 cases newly‐diagnosed with VL were enrolled in the cohort. We measured the levels of IgG subclasses before and after standard treatment and conducted assessments of bone marrow features. In addition, we analysed other haematological indices and examined the variations in IgG subclasses, as well as their correlation with clinical and laboratory factors.ResultsThe levels of total IgG, IgG1, and the ratios of both IgG1/IgG and IgG1/IgG2 decreased significantly after treatment, whereas the ratios of IgG2/ IgG showed an obvious increase. The VL patients without hyperglobulinemia displayed significant lower IgG1/IgG2 ratios, but higher IgG2/IgG ratios compared with those with hyperglobulinemia. In addition, VL patients with positive bone marrow amastigotes had significant higher IgG1/IgG and IgG1/IgG2 ratios, but lower IgG2/IgG ratios. IgG subclasses were correlated with abnormal blood test results, particularly immunological elements including IgM and Complement 4 (C4).ConclusionsIgG1 and IgG2 exhibited contrasting changes after treatment in VL patients. The features of bone marrow and laboratory tests indicated that IgG1 and IgG2 serve different roles in the progression of VL. The ratios of IgG subclasses may be more precise indicators to evaluate immune reaction in VL than traditional total IgG.

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Etiologies of Polyclonal Hypergammaglobulinemia: A scoping review

Cited by 10 publications

References 9 publications

Understanding hypergammaglobulinemia in experimental or natural visceral leishmaniasis

Understanding hypergammaglobulinemia in experimental or natural visceral leishmaniasis

Positive anti-nuclear antibody in patients with polyclonal hypergammaglobulinemia suggests the presence of multiple distinct comorbidities

Serological characteristics and clinical implications of IgG subclasses in visceral leishmaniasis

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