Disease relevance of Purpura, Schoenlein-Henoch

• Selective deposition of immunoglobulin A1 in immunoglobulin A nephropathy, anaphylactoid purpura nephritis, and systemic lupus erythematosus [1].
• The other four patients with homozygous HLA A30 B18 DR7 had SLE, severe kidney disorders including mesangial or membranoproliferative glomerulonephritis, and/or Henoch Schoenlein purpura [2].
• The earliest cases did not seem to be associated with known diseases or syndromes; more recently, reports of C2 deficiency associated with systemic lupus erythematosus; anaphylactoid purpura, recurrent infections, and dermatomyositis have appeared [3].
• The former group consisted of IgA nephropathy (n = 45), lupus nephritis (6), membrano-proliferative glomerulonephritis (5), non-IgA mesangial proliferative glomerulonephritis (4), Henoch-Schoenlein purpura nephritis (4), membranous nephropathy (4), endocapillary proliferative glomerulonephritis (3), and minimal change nephrotic syndrome (2) [4].
• DATA SYNTHESIS: Nonthrombocytopenic purpura secondary to cutaneous vasculitis is a known, although rare, adverse effect of nifedipine [5].

High impact information on Purpura, Schoenlein-Henoch

• We also compared ICAM-1 levels in acute KD with those in anaphylactoid purpura (AP) and in measles [6].
• Anaphylactoid purpura and familial IgA nephropathy [7].
• Four patients developed nonthrombocytopenic purpura two to three weeks after initiation of quinidine therapy [8].
• Elevated levels of circulating immunostimulatory 90K in Henoch-Schoenlein purpura [9].
• Failure of cyclosporine A in controlling Schoenlein-Henoch purpura [10].

Chemical compound and disease context of Purpura, Schoenlein-Henoch

• Nonthrombocytopenic purpura associated sequentially with nifedipine and diltiazem [5].
• Early prednisone treatment and nephropathy in anaphylactoid purpura [11].
• Plasma levels of prostaglandin E2 in patients with anaphylactoid purpura, bacterial and viral infections were within the normal range [12].
• Henoch-Schoenlein purpura and angiotensin-converting enzyme inhibitors [13].
• Response of crescentic Henoch-Schoenlein purpura nephritis to corticosteroid and azathioprine therapy [14].

Biological context of Purpura, Schoenlein-Henoch

• Lack of association between the HLA-A10 (A25), B18 and C2o haplotype and anaphylactoid purpura (AP) [15].

Anatomical context of Purpura, Schoenlein-Henoch

• Histoimmunological discrepancies in primary IgA nephropathy and anaphylactoid purpura sustain relationships between mucosa and kidney [16].
• The immunoglobulins, complement components C3 and C4, lymphocyte subpopulations, and K-cell activity were studied in 13 children with anaphylactoid purpura and in 12 children of the same ages who acted as controls [17].
• We have also examined the secretion of IgA, IgM, and IgG by isolated human IMC, human bone marrow MNC from rib specimens, and PBMC from patients with CD, UC, SLE, or Henoch-Schoenlein purpura (HSP) [18].

Gene context of Purpura, Schoenlein-Henoch

• We determined the concentration of TGF-beta 1 in the sera of the patients with KD, anaphylactoid purpura (AP), and scarlet fever, using a sandwich enzyme linked immunosorbent assay [19].
• The occurrence of HLA-A, -B, and -C antigens was investigated in an unselected group of 26 consecutively admitted patients with Schoenlein-Henoch Purpura [20].
• We investigated whether TNF-alpha and IL-6 activities in serum from patients with KD differs from those in anaphylactoid purpura (AP) and measles [21].
• A case of anaphylactoid purpura with multiple blister formation: possible pathophysiological role of gelatinase (MMP-9) [22].
• 3. Sera from 16 of the 26 patients with Henoch-Schoenlein nephritis displayed increased IgG binding to the human glomerular extract compared with the normal control group (P < 0.001), whereas IgG binding was not significantly raised in the patients with Henoch-Schoenlein purpura without evidence of renal involvement [23].

Analytical, diagnostic and therapeutic context of Purpura, Schoenlein-Henoch

• We then looked for the presence of IgA-ANCA in Henoch-Schoenlein purpura (HSP): we found IgA-ANCA with immunoenzymatic assay but not with immunofluorescence in HSP, in primary IgA-GN and in membranous GN as well, thus suggesting the poor specificity of this type of ANCA [24].
• Plasma exchange as sole therapy was effective in patients with idiopathic anaphylactoid purpura and mixed cryoglobulinaemia, but not in one SLE patient with CIC [25].

References