Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum interleukin 6 (IL-6) and tumour necrosis factor (TNF) were measured in children with dysentery during an epidemic caused by Shigella dysenteriae 1. IL-6 and TNF were also measured in fresh stool filtrates from children with acute gastroenteritis. The median serum IL-6 concentration was raised significantly in the children with complications (haemolytic uraemic syndrome, leukemoid reaction, thrombocytopenia, thrombocytosis, and severe colitis lasting more than one week) during the first week (n = 18, 9-7728 pg/ml; median 107) and in the second week (n = 13, 5-312 pg/ml; median 77), compared with convalescent sera (n = 10, < 3-85 pg/ml; median 39; p < 0.02 and < 0.05 respectively). The median IL-6 concentration during the first week was significantly higher in the group with complicated disease than in those with no complications (n = 8, < 3-37 pg/ml; median 5; p < 0.001). Although serum TNF concentrations were significantly raised in the complicated group during the first and second weeks of the illness and in the uncomplicated group compared with convalescence, there was no significant difference in the TNF concentrations between the complicated and uncomplicated groups. IL-6 was detectable in stool filtrates from eight of 13 children with S dysenteriae 1 infection and four of eight children with S flexneri infection. It was not detectable in Cryptosporidia, rotavirus, or adenovirus infections, those with pathogen-negative acute diarrhoea or controls. Seven of 13 children with S dysenteriae 1 and three of nine children with S flexneri infections had TNF detectable in stools. None of the children with Salmonella, Cryptosporidia, rotavirus of children with pathogen-negative diarrhoea and controls had detectable TNF in stool filtrates. It is postulated that the local and generalised vasculitis observed in shigellosis may be related to a direct effect of Shiga toxin on endothelial cells or caused by cytokine production stimulated by endotoxin, or both.
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PMID:Concentrations of interleukin 6 and tumour necrosis factor in serum and stools of children with Shigella dysenteriae 1 infection. 830 92

Plasma concentrations of soluble vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (sE-selectin) and intercellular adhesion molecule-1 (sICAM-1) were measured by enzyme-linked immunosorbent assay in four groups of children. Group 1 consisted of 20 patients with acute diarrhoea-associated haemolytic uraemic syndrome (D+HUS), the aetiology of HUS being verocytotoxin-producing Escherichia coli infection in each case. Controls consisted of 11 patients who had previously had D+HUS (group 2), 12 with chronic renal failure (group 3) and 8 healthy controls (group 4). When compared with healthy controls, the acute D+HUS group had higher sVCAM-1 (median 1,875 ng/ml, range 1,200-6,450 ng/ml vs. 1,200 ng/ml, range 975-2,125 ng/ml), von Willebrand factor antigen, (1.9 U/ml, range 0.85-5.1 U/ml vs. 0.55 U/ml, range 0.3-1.57 U/ml), white cell count (WBC, 14.5 x 10(9)/l, range 7.8-43.1 10(9)/l vs. 8.9 10(9)/l, range 5.7-10.8 10(9)/l) and neutrophil count (PMN, 10.1 x 10(9)/l, range 4.3-26.5 10(9)/l vs. 4.3 10(9)/l, range 3.7-6.6 10(9)/l), all P < 0.005, and sICAM-1 was reduced (230 ng/ml, range 130-340 ng/ml vs. 400 ng/ml, range 260-690 ng/ml), P < 0.05. Within the acute D+HUS group there was a significant correlation between sICAM-1 and PMN (r = 0.56, P < 0.01). There was no correlation between any adhesion molecule and plasma creatinine or von Willebrand factor. Comparing the acute HUS group with children with chronic renal failure, WBC (P < 0.001), PMN (P < 0.01) and sVCAM-1 (P < 0.01) were significantly elevated, but there was no difference between the von Willebrand factor (P = 0.08) or the sICAM-1 (P > 0.1). sVCAM-1 is elevated and sICAM-1 decreased in acute D+HUS. This pattern of altered adhesion molecule concentration is unlike that in adults with vasculitis and suggests that different endothelial regulatory factors are at play.
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PMID:Soluble circulating cell adhesion molecules in haemolytic uraemic syndrome. 858 13

The antiphospholipid antibody syndrome (APS) is characterized by arterial or venous thromboses and recurrent foetal loss. It occurs as primary disease, but also in the context of systemic lupus erythematosus (SLE). Whereas primary APS induces a thrombotic microangiopathy without significant inflammatory reaction, secondary APS in SLE is usually associated with vasculitis. Here we report a patient with APS who presented with acute diarrhoea and then developed a HELLP-like syndrome characterized by a spontaneous abortion, multifocal hepatic necroses and thrombocytopenia. Thereafter an acute flare of SLE with arthralgias, pleuritis, skin rash and glomerulitis occurred. Clinical amelioration was only achieved by combining curettage, anticoagulation and immunosuppression, a treatment taking into account the pathogenesis of HELLP-like disease, APS and SLE. To our knowledge this is the first reported case of APS associated with combined acute manifestations of these three syndromes triggered by a presumable intestinal infection.
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PMID:Foetal loss, liver necrosis and acute lupus erythematosus in a patient with antiphospholipid antibody syndrome. 1153 Oct 1

Selective immunoglobulin A deficiency (IgAD) is a primary immunodeficiency disease characterized by low levels (< 7 mg/dl) of serum immunoglobulin (Ig) A and normal serum levels of IgG and IgM. Patients with IgAD have increased risk for recurrent respiratory and gastrointestinal infections, autoimmune disease, asthma and allergy. A 26-year-old woman was admitted with sudden onset of painful cutaneous lesions on her lower extremities, pyrexia and arthromyalgia. Her medical history was remarkable for recurrent respiratory tract infections, self-limited episodes of acute diarrhea, atopy, splenomegaly and a 4-year history of a lung granulomatous lesion. Laboratory and imaging tests ruled out severe life-threatening infection, connective tissue disease and neoplasm. Serum protein electrophoresis showed a low IgA serum level (6.67 mg/dl), with normal serum levels of IgG and IgM, conducting to a diagnosis of selective IgAD. A skin biopsy showed necrotizing vasculitis without any sign of internal organ disease. We report a patient with IgAD and granulomatous involvement of lungs, spleen and medium-sized arteries of the skin. Although IgAD results from a failure of B-cell differentiation, we propose that deregulated immune response with production of cross-reactive antibodies and hyperstimulation of T cells and macrophages could contribute to this widespread granulomatous reaction.
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PMID:Necrotizing vasculitis with a polyarteritis nodosa-like pattern and selective immunoglobulin A deficiency: case report and review of the literature. 1849 27