Disease relevance of Lymphatic Diseases

• The major core proteins (p25) of the isolates were antigenically identical and all three isolates were identical to prototype lymphadenopathy associated virus isolated in France [1].
• Two patients, after several weeks of zomepirac sodium use, experienced acute toxic eruption, fever, lymphadenopathy, arthralgias, angioedema of the hands, and eosinophilia [2].
• The diagnostic value of PBGD determinations was shown in a prospective study of a group of patients evaluated because of fever of unknown origin, anemia, or other constitutional symptoms with or without lymphadenopathy or a mediastinal mass [3].
• BACKGROUND: Imexon, a 2-cyanoaziridine, is therapeutic and reverses lymphadenopathy and splenomegaly in the LP-BM5 murine retrovirus-induced immunodeficiency disease (murine AIDS) [4].
• Staging HCC for metastases is insensitive and is based on conventional criteria (eg, pulmonary nodules, skeletal metastases, and lymphadenopathy) [5].

Psychiatry related information on Lymphatic Diseases

• We present the case of a 17-year-old woman with a history of bipolar disorder, who developed a clinical syndrome manifested by fever, lymphadenopathy, skin rash, diarrhea, and acute renal failure requiring dialysis after the use of lamotrigine [6].

High impact information on Lymphatic Diseases

• Hyperimmunoglobulinaemia D and periodic fever syndrome (HIDS; MIM 260920) is a rare, apparently monogenic, autosomal recessive disorder characterized by recurrent episodes of fever accompanied with lymphadenopathy, abdominal distress, joint involvement and skin lesions [7].
• Most patients also had increased appetite and weight, decreased lymphadenopathy and hepatosplenomegaly, decreased immunoglobulin levels, and increased numbers of CD4 cells [8].
• The asymptomatic and otherwise healthy T4 epitope-deficient brother of one of these patients also had lymphadenopathy in a distribution identical to that of his sister with SLE [9].
• Mice that are homozygous for either the lpr (lymphoproliferation) or gld (generalized lymphoproliferative disease) mutant genes develop a disease characterized by massive lymphadenopathy and autoantibody formation [10].
• Antibody to LAV p25 was found in the serum of 51 of 125 AIDS patients, 81 of 113 patients with lymphadenopathy syndrome, 0 of 70 workers at the Centers for Disease Control (some of whom had handled specimens from AIDS patients), and 0 of 189 random blood donors [11].

Chemical compound and disease context of Lymphatic Diseases

• Editorial: Lymphadenopathy induced by diphenylhydantoin [12].
• Prednisone in treatment of allergen-associated angio-immunoblastic lymphadenopathy [13].
• Regression of chronic generalised lymphadenopathy in a homosexual man after therapy with intravenous acyclovir [14].
• Letter: Levamisole in angio-immunoblastic lymphadenopathy [15].
• Sulindac causing a hypersensitivity reaction with peripheral and mediastinal lymphadenopathy [16].

Biological context of Lymphatic Diseases

• In January 1982, the Centers for Disease Control began a prospective study of unexplained generalized lymphadenopathy syndrome in 78 homosexual or bisexual men [17].
• These modifications preceded the lymphadenopathy, because early progenitors (colony-forming units-spleen [CFU-S] day 8) were already augmented in day-18 fetal livers of the lpr phenotype [18].
• lpr, a murine mutation of the Fas apoptosis receptor, causes lymphadenopathy and autoantibody production, with lymphadenopathy primarily due to a population of CD4-CD8-B220+ T cells [19].
• We find that in MRL-lpr/lpr mice bearing the CK2alpha transgene, the lymphoproliferative process is dramatically exacerbated, as these mice develop massive splenomegaly and lymphadenopathy by 12 wk of age in association with increased autoantibody production and accelerated renal disease [20].
• Along the same line, administration of either F23.1 or two different anti-F23.1 anti-idiotypic antibodies to MRL/Mp-lpr/lpr mothers elicited, in the offspring, the production of antibodies sharing a recurrent idiotype with F23.1 and resulted in long-term amelioration of autoimmunity and lymphadenopathy [21].

Anatomical context of Lymphatic Diseases

• Surprisingly, however, aging SEK1-deficient chimeric mice frequently develop lymphadenopathy and polyclonal B and T cell expansions [22].
• The elimination of lymphadenopathy was not due to a failure of thymic maturation since the thymus of H-2Db female lpr/lpr mice contained nearly normal numbers of mature thymocytes [23].
• None of these genes was expressed in 1 case of benign, localized Castleman's disease (CD), and only viral IL-6 and viral Cyclin-D were transcribed in 2 cases of benign lymphadenopathies with giant germinal center hyperplasia and increased vascularity [24].
• The presence of core antigens of retrovirus HTLV-III/LAV, referred to as "AIDS-related virus" (AV), has been sought in lymph node samples of patients with persistent generalized lymphadenopathy (PGL, 28 patients), prodromal AIDS (1 patient) and AIDS with Kaposi sarcoma (3 patients) [25].
• Development of splenomegaly and lymphadenopathy, caused primarily by increases in B cell immunoblasts, requires the presence of CD4+ T cells and is assumed to be mediated by lymphokines produced by these cells inasmuch as progression of disease is markedly inhibited by treatment of infected mice with cyclosporin A [26].

Gene context of Lymphatic Diseases

• Both IFN-gamma -/- and IL-4 -/- mice, however, developed significantly reduced lymphadenopathy and end-organ disease [27].
• Here we show that, in patients with lymphadenopathy, autocrine VEGF and alpha(4)beta(1) integrin are involved in the chemokine-dependent motility of CLL cells on and through endothelium-processes important for the invasion of lymphoreticular tissues, a major determinant of disease outcome [28].
• Lymphadenopathy and other disease manifestations were greatly reduced in Fyn-/- lpr mice concomitant to decreased DN cells (from 77 to 20%) [29].
• Increased levels of interleukin-6 (IL-6) in serum and spontaneous in vitro production of IL-6 by lymph node mononuclear cells of patients with angio-immunoblastic lymphadenopathy with dysproteinemia (AILD), and clinical effectiveness of cyclosporin A [30].
• In addition, the migration index of B-CLL cells in response to both of the CCR7 ligands correlated with the presence of clinical lymphadenopathy, thus indicating that the high expression of functional chemokine receptors justifies the widespread character of B-CLL, representing a clinical target for the control of tumor cell dissemination [31].

Analytical, diagnostic and therapeutic context of Lymphatic Diseases

• Patients who have bilateral hilar lymphadenopathy (BHL) alone need annual follow-up with chest X-ray, ECG, 24-h monitoring, exercise testing, lung function and possible thallium 201 scanning [32].
• Whole-body PET scanning was performed using 18F-fluorodeoxyglucose (FDG) in two patients with hilar lymphadenopathy in whom the clinical differential diagnosis was between sarcoidosis and lymphoma [33].
• Massive macrophage lipid accumulation presenting as hepatosplenomegaly and lymphadenopathy associated with long-term total parenteral nutrition therapy for short bowel syndrome [34].
• Genetic subgroups with distinct clinical features have been identified, such as the 11q deletion that is associated with marked lymphadenopathy and rapid disease progression, while the 17p deletion predicts treatment failure with alkylating agents as well as fludarabine and short survival times [35].
• A complete tumour response was seen in only one patient who presented with midline lymphadenopathy and remains disease-free 46 months after treatment [36].

References