Hyperviscosity syndrome secondary to a myeloma‐associated IgG
            <sub>1</sub>
            κ paraprotein strongly reactive against the HIV‐1 p24
            <i>gag</i>
            antigen

Jin, David; Nowakowski, Maja; Kramer, Martin; Essex, David W.

doi:10.1002/1096-8652(200007)64:3<210::aid-ajh13>3.0.co;2-#

Cited by 11 publications

(2 citation statements)

References 15 publications

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“…However, hyper-activation of B cells with high production of IgG could be the main mechanistic pathway of HVS in HIV-1 infection [ 7 ]. According to Jin et al, HVS was linked to the formation of myeloma-associated IgG1paraprotein against HIV-1 p24 antigen in HIV-1 patients [ 8 ].…”

Section: Hyperviscosity Syndrome and Viral Infectionsmentioning

confidence: 99%

Hyperviscosity syndrome in COVID-19 and related vaccines: exploring of uncertainties

et al. 2022

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Hyperviscosity syndrome (HVS) recently emerged as a complication of coronavirus disease 2019 (COVID-19) and COVID-19 vaccines. Therefore, the objectives of this critical review are to establish the association between COVID-19 and COVID-19 vaccines with the development of HVS. HVS may develop in various viral infections due to impairment of humoral and cellular immunity with elevation of immunoglobulins. COVID-19 can increase blood viscosity (BV) through modulation of fibrinogen, albumin, lipoproteins, and red blood cell (RBC) indices. HVS can cause cardiovascular and neurological complications in COVID-19 like myocardial infarction (MI) and stroke. HVS with or without abnormal RBCs function in COVID-19 participates in the reduction of tissue oxygenation with the development of cardio-metabolic complications and long COVID-19. Besides, HVS may develop in vaccine recipients with previous COVID-19 due to higher underlying Ig concentrations and rarely without previous COVID-19. Similarly, patients with metabolic syndrome are at the highest risk for propagation of HVS after COVID-19 vaccination. In conclusion, COVID-19 and related vaccines are linked with the development of HVS, mainly in patients with previous COVID-19 and underlying metabolic derangements. The possible mechanism of HVS in COVID-19 and related vaccines is increasing levels of fibrinogen and immunoglobulins. However, dehydration, oxidative stress, and inflammatory reactions are regarded as additional contributing factors in the pathogenesis of HVS in COVID-19. However, this critical review cannot determine the final causal relationship between COVID-19 and related vaccines and the development of HVS. Prospective and retrospective studies are warranted in this field.

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Section: Hyperviscosity Syndrome and Viral Infectionsmentioning

confidence: 99%

Hyperviscosity syndrome in COVID-19 and related vaccines: exploring of uncertainties

et al. 2022

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“…Bioinformatics tools to examine phage peptides have been used successfully to identify cognate antigens for cytomegalovirus (Kohler and others 1987) and HIV (Jin and others 2000). Sompuram and others (2008) applied the newly developed technology of epitope-mediated antigen prediction (E-MAP) to accurately identify antigen targets of multiple myeloma.…”

Section: Peptides and Bioinformatics In Identifying Ms Antigensmentioning

confidence: 99%

Viruses and Multiple Sclerosis

et al. 2011

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Multiple sclerosis (MS) is a chronic demyelinating disorder of unknown etiology, possibly caused by a virus or virus-triggered immunopathology. The virus might reactivate after years of latency and lyse oligodendrocytes, as in progressive multifocal leukoencephalopathy, or initiate immunopathological demyelination, as in animals infected with Theiler’s murine encephalomyelitis virus or coronaviruses. The argument for a viral cause of MS is supported by epidemiological analyses and studies of MS in identical twins, indicating that disease is acquired. However, the most important evidence is the presence of bands of oligoclonal IgG (OCBs) in MS brain and CSF that persist throughout the lifetime of the patient. OCBs are found almost exclusively in infectious CNS disorders, and antigenic targets of OCBs represent the agent that causes disease. Here, the authors review past attempts to identify an infectious agent in MS brain cells and discuss the promise of using recombinant antibodies generated from clonally expanded plasma cells in brain and CSF to identify disease-relevant antigens. They show how this strategy has been used successfully to analyze antigen specificity in subacute sclerosing panencephalitis, a chronic encephalitis caused by measles virus, and in neuromyelitis optica, a chronic autoimmune demyelinating disease produced by antibodies directed against the aquaporin-4 water channel.

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Multiple myeloma as the first manifestation of acquired immunodeficiency syndrome: a case report and review of the literature

Pouli¹,

Lemessiou

Rontogianni

et al. 2001

Ann Hematol

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Various hematologic malignancies and solid tumors are increasingly diagnosed in patients with human immunodeficiency virus (HIV) infection and may be the presenting manifestation of acquired immunodeficiency syndrome (AIDS). Multiple myeloma, however, has never been reported as the presenting manifestation of AIDS. We report on a 34-year-old man who presented with back pain, paresthesias, paraparesis, vertebral bony disease, and an associated soft tissue mass. Biopsy of the mass revealed immature plasmacytes with very faint cytoplasmic expression of kappa light chains. Bone marrow biopsy revealed 25% infiltration with poorly characterized malignant cells and 15% polyclonal plasma cells. Immunofixation of serum and urine was positive for IgG kappa and kappa light chains, respectively. A bone survey revealed lesions in the skull, left femur bone, and the pelvis. The diagnosis of an anaplastic myeloma was made. Because of the poorly characterized nature of the malignant cells and the difficulties in immunophenotyping, serologic evaluation for HIV was undertaken and was positive. The concept of myeloma as an opportunistic neoplasm defining AIDS was considered. We discuss this view and recommend that patients with multiple myeloma with poorly characterized myeloma cells as well as difficulties in immunophenotyping should undergo testing for HIV infection.

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Hyperviscosity syndrome secondary to a myeloma‐associated IgG ₁ κ paraprotein strongly reactive against the HIV‐1 p24 gag antigen

Cited by 11 publications

References 15 publications

Hyperviscosity syndrome in COVID-19 and related vaccines: exploring of uncertainties

Hyperviscosity syndrome in COVID-19 and related vaccines: exploring of uncertainties

Viruses and Multiple Sclerosis

Multiple myeloma as the first manifestation of acquired immunodeficiency syndrome: a case report and review of the literature

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Hyperviscosity syndrome secondary to a myeloma‐associated IgG 1 κ paraprotein strongly reactive against the HIV‐1 p24 gag antigen

Cited by 11 publications

References 15 publications

Hyperviscosity syndrome in COVID-19 and related vaccines: exploring of uncertainties

Hyperviscosity syndrome in COVID-19 and related vaccines: exploring of uncertainties

Viruses and Multiple Sclerosis

Multiple myeloma as the first manifestation of acquired immunodeficiency syndrome: a case report and review of the literature

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Product

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Hyperviscosity syndrome secondary to a myeloma‐associated IgG ₁ κ paraprotein strongly reactive against the HIV‐1 p24 gag antigen