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PubMed2003

Phlebosclerotic colitis coincident with carcinoma in adenoma.

Phlebosclerosis of the colon is a rare disease characterized by a thickening of the wall of the colon with fibrosis, hyalinization and calcification to the affected veins. These symptoms result in a type of ischemic colitis known as phlebosclerotic colitis. A case of phlebosclerotic colitis coincident with carcinoma in adenoma is reported. A 74-year-old Japanese woman was admitted to hospital because of a mass in her right lower abdomen. Abdominal computed tomography examination revealed linear calcifications in the wall of the cecum and the ascending colon. Colonoscopy revealed dark purple mucosa with multiple ulcers in the cecum and the ascending colon. Biopsy specimens showed a marked hyalinous thickening of the wall of small blood vessels in the mucosa. Phlebosclerotic colitis was suspected because of negative results with amyloid stain. Alternative ileocolic angiography showed the serpentine of the peripheral nature blood vessels and pooling at the late venous phase. Microscopic examination of the surgically resected colon revealed mucosal and submucosal fibrosis, and a thickening of the venous wall with fibrosis, hyalinization and calcification from the mucosa to the serosa, which caused a marked luminal narrowing. A small polypoid lesion was also found in the affected region and was diagnosed histologically as carcinoma in adenoma. To our knowledge, this is the first reported case of phlebosclerotic colitis complicated by carcinoma.

Adenoma↗
PubMed1987

Deficiency of the effector mechanisms of the immune response and autoimmunity.

It has long been the conventional wisdom that most autoimmune responses represent a pathological aberration of the immune system and a great deal of effort has been devoted to investigating how such abnormal responses may be induced. It seems likely, however, particularly in the form of autoimmunity seen in diseases like systemic lupus erythematosus (LE) and associated with immune complex disease, that it is not the induction of the autoimmune response that is primarily abnormal, but its persistence, and that this abnormal persistence is a consequence of a failure of the proper functioning of the effector mechanisms of the immune response. The strongest reason for so believing is the striking incidence of these diseases in subjects with deficiencies of the early components of the classical complement pathway. Total, homozygous deficiencies are rare and account for only a small proportion of patients with systemic LE. However, partial, heterozygous deficiency of these components is much commoner and also carries an increased susceptibility to these diseases. An explanation for this association is given. In the presence of an adequately functioning complement system immune complexes remain soluble and of relatively small size. It is proposed that this is a result of the incorporation of C4 and C3 into the antigen-antibody lattice leading to a reduction in the effective valency of antigen and antibody. The Goldberg theory of immune precipitation predicts that a reduction in valency would inhibit precipitation and the formation of large complexes. In the absence of adequate complement function this mechanism will fail and large, potentially insoluble complexes with little C4 and C3 on them will be formed. These large immune complexes without sufficient C4 and C3 bound on them will also not be bound normally to erythrocyte CR1 and will therefore be transported in the (peripheral) plasma stream rather than in the (central) erythrocyte stream. It is proposed that this will result in the deposition of immune complexes in peripheral small blood vessels rather than in the sinusoids of the liver and spleen; and that this peripheral deposition gives rise to inflammation, with the release of autoantigens and the formation of further autoantibodies. The importance of CR1 in relation to these diseases is emphasized by the reduction in CR1 numbers that accompanies their active phase. This appears to be due to proteolysis of the receptor while the immune complex-bearing erythrocyte is sequestered in the reticuloendothelial system.

Antigen-Antibody Complex↗
PubMed1997

ICAM-1/LFA-1 expression in acute osteodestructive joint lesions in collagen-induced arthritis in rats.

Collagen-induced arthritis in rats is a widely used model of rheumatoid arthritis (RA). However, the joint immunohistopathology is less well characterized. The objective of this study was therefore to analyze whole ankle joints for markers known to mediate inflammatory mechanisms in RA. Indirect immunohistochemistry was performed on undecalcified cryostat sections for intercellular adhesion molecule-1 (ICAM-1, clone 1A 29) and leukocyte function-associated antigen-1 (LFA-1, clone WT.1) expression, for CD4+ lymphocytes (clone W3/25), B-cells (clone HIS 14), and macrophages (clone ED2). Acute, osteodestructive arthritis (n = 8) induced with bovine collagen Type II was verified by clinical and radiological measures. LFA-1 expression was found almost exclusively at sites associated with cartilage erosion or osteodestruction. ICAM-1 was similarly expressed in the vicinity of tissue degradation but also by blood vessels in peripheral areas of joint swelling. CD4+ lymphocytes and macrophages were more ubiquitous. B-cells were infrequent. In control animals (n = 4) ICAM-1 was expressed by synovial blood vessels. Macrophages were identified at the synovial lining. The results suggest that LFA-1 and ICAM-1 mediate important inflammatory events in this model. Similar findings in human RA synovium provide further arguments that collagen-induced arthritis in rats might be regarded as a comparable disease.

Animals↗