Academic literature on the topic 'Hyperglobulinemia'

Hyperglobulinemia is a common manifestation of plasma cell disease, and it is sometimes caused by autoimmune diseases (AIDs). We report an uncommon presentation of hyperglobulinemia, with a high amount of plasma cells in bone marrow, pancytopenia, hematemesis, and splenomegaly in an 18-year-old woman. Some examinations were performed to determine the diagnosis, including serum protein electrophoresis, immunofixation electrophoresis, the free light chain assay, abdominal enhanced computed tomography (CT) and CT venography, and positron-emission tomography-CT. The patient was finally diagnosed with AID. Considerable improvement in her symptoms was observed after immunosuppressive therapy. Findings in this case highlight that not only differentiation of hyperglobulinemia caused by monoclonal or polyclonal immunoglobulin, but also AIDs, need to be considered to exclude non-Hodgkin’s lymphoma and plasma cell disease.

Surgical removal of macroscopically detectable metacestode tissue followed by postoperative chemotherapy according to established human protocols resulted in complete clinical remission and immediate normalization of hyperglobulinemia in a dog with alveolar echinococcosis (AE). The disease is caused by the metacestode stage of the cestode, Echinococcus multilocularis. In endemic areas, AE should be included in the differential diagnosis of polycystic liver masses, especially if concomitant hyperglobulinemia is present. However, the importance of AE is not only the disease of the single dog itself but also the potential risk of infection for humans in an endemic area.

Les anomalies phénotypiques et fonctionnelles des lymphocytes B (LB) sont typiques d'une infection au VIH et se traduisent principalement par une activation polyclonale, une perte de la mémoire immunitaire ainsi qu'une réponse humorale déficiente et des phénomènes auto-immunitaires souvent précurseurs de lymphomes B. Ces anomalies se retrouvent principalement chez les patients lors de la phase chronique de la maladie et semblent être reliées en partie au niveau de la charge virale ainsi qu'à un compartiment de lymphocytes T CD4+ altéré. Cependant, quoique controversé, des éléments d’activation polyclonale ont également été observés chez les non-progresseurs à long terme (LTNPs) qui présentent une charge virale faible et un compartiment T CD4+ semblable aux individus séronégatifs. Ainsi, les objectifs principaux de cette étude sont 1) d’établir une chronologie des anomalies du compartiment des cellules B chez des individus infectés par le VIH qui ont une progression différente de la maladie (PHI normaux, rapides, sains et LTNP). 2) corréler les niveaux sériques du stimulateur de lymphocytes B (BLyS), un facteur de croissance des cellules B, avec les phénotypes observés chez ces mêmes patients. L’hyperglobulinémie, les niveaux sériques de BLyS et d’auto-anticorps ont été mesuré longitudinalement chez une cohorte d’individus en primo-infection (PHI) avec des progressions différentes de la maladie (rapides et normaux), LTNP et sujets sains. Nos résultats démontrent que l’activation polyclonale des LB survient indépendamment de la vitesse de progression et persiste chez les LTNP ou malgré une thérapie antirétrovirale efficace chez les progresseurs rapides. Des niveaux élevés de BLyS dans le sérum des progresseurs rapides corrèlent avec des fréquences altérées de monocytes et cellules dendritiques, suggérant un rôle de celles-ci dans l’atteinte du compartiment des cellules B.
B lymphocyte abnormalities are an important consequence of HIV infection, where both polyclonal activation and loss of B cell memory and humoral immunity have been described, and often evolve towards rheumatic-like autoimmunity and lymphoma. Although these abnormalities are prevalent in chronically infected patients, polyclonal B cell activation is also reported in patients with primary HIV-infection (PHI), who already present signs of defective humoral immunity. Although controversial, elements of B cell dysregulation have been reported in long term non progressor (LTNP) patients, even though they bear low viral loads and present a relatively "normal" CD4+ T cell compartment, suggesting that other factors are involved. Therefore, the main objectives of this study are to 1) establish a timeline for specific B cell abnormalities in HIV-infected patients with different rates of disease progression (PHI normal and fast progressors, LTNP), and controls 2) to correlate serum levels of the B lymphocyte stimulator (BLyS) a B cell growth factor, among these patients and controls. Thus we have longitudinally assessed hyperglobulinemia, auto-antibody and soluble BLyS levels in the serum of subjects undergoing primary HIV infection (PHI) with different rates of disease progression; rapid and normal progressors, long term non-progressors (LTNPs), and healthy donors. Here, we report that B cell polyclonal activation occurs independently of the rate of disease progression, with hypergammaglobulinemia persisting beyond successful therapy in rapid progressors and despite non-progressing clinical disease in LTNPs. High levels of BLyS in the serum of PHI rapid progressors correlate with altered blood monocyte and dendritic cell frequencies suggesting their contribution in triggering B cell dysregulations.