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Eosinophilic enteritis

Clofazimine [kloe FA zi meen] is a phenazine dye that binds to DNA and inhibits template function. Its redox properties may lead to the generation of cytotoxic oxygen radicals that are also toxic to the bacteria. Clofazimine is bactericidal to M- leprae and has some activity against M- avium intracellulare complex. On oral absorption, it accumulates in tissues, allowing for intermittent therapy, but it does not enter the CNS. Patients may develop a red-brown discoloration of the skin. Eosinophilic enteritis has been reported as an untoward effect. The drug also has some anti-inflammatory activity, thus erythema nodosum leprosum does not develop. [Pg.347]

Eosinophilic enteritis has been attributed to interferon alfa (244). [Pg.1807]

A. caninum, Uncinaria stenocephaia). Occasionally A, caninum larva may migrate to the human intestine causing eosinophilic enteritis this may happen when larva is ingested rather than through skin invasion. It is the second most common human helminthic infection (after ascariasis). Worldwide distribution, mostly in areas with moist, warm climate. Both N. americanus and A. duodenale are found in Africa, Asia, and the Americas. N. americanus predominates in the Americas and Australia, while only A, duodenale is found in the Middle East, North Africa, and southern Europe. [Pg.504]

Almost all patients with eosinophilic gastroenteritis have a peripheral eosinophilia. A history of allergy can be obtained in half of the patients. The stomach can be solely involved, but more commonly the small bowel also participates in the disease process. If patients only have eosinophilic gastritis, they present with epigastric pain, nausea and vomiting or hematemesis and/or melena, while patients with eosinophilic enteritis will have diarrhea, malabsorption or a protein-losing enteropathy. [Pg.122]

Mason et al. (1977) report a case of eosinophilic enteritis in a 29-year-old woman after 3 years of clofazimine therapy at 600 mg daily. At laparotomy there was nodular thickening of the upper ileum with black-brown pigmentation of the ileal wall, mesentery, and mesenteric lymph nodes. Ileal biopsy showed eosinophilic enteritis. [Pg.547]

Mandal BK, Stevenson J (1970) Haemolytic crisis produced by nalidixic acid. Lancet 1 614 Mason GH, Ellis-Pegler RB, Arthur JF (1977) Clofazimine and eosinophilic enteritis. Lepr Rev 48 175... [Pg.554]

Similar US findings have been reported also in a case of eosinophilic enteritis presenting as acute abdomen (Seelen et al. 1992). [Pg.96]

Gastrointestinal - eosinophilic gastroenteritis A 54-year-old male treated with pegylated IFNa-2a for chronic hepatitis C infection showed abdominal distension and diarrhoea 28 weeks after initiation of therapy. Elevation of the eosinophil count in blood and ascites and eosinophil infiltration observed in gastrointestinal histopathology led to a diagnosis of eosinophilic enteritis but therapy was not initiated due to spontaneous improvement in both the eosinophil count and abdominal symptoms. This appears to be the first case report of eosinophilic enteritis induced by IFN therapy [45 ]. [Pg.565]

ELISA Enzyme-linked immunosorbent assay EMS Eosinophilia-myalgia syndrome ENS Enteric nervous system EO Eosinophil... [Pg.282]

Figure 4.8. Hypothesis for the local generation of mast-cell-stimulating peptides by the action of neutrophil-derived enzymes on albumin. Initial stimulation of the mast cell by any of a variety of agents causes the release of preformed histamine (H) neutrophil and eosinophil chemotactic factors (NCF, ECF) and enzymes and the de novo synthesis of prostaglandins (PG) and leukotrienes (LT). These agents increase vascular permeability and vessel diameter. As a result, albumin and later neutrophils (PMN) enter the tissue space where the latter undergo phagocytosis and the secretion of proteolytic enzymes to the extracellular space where they act on albumin to generate NRP (neurotensin-related peptide) and HRP (histamine-releasing peptide). These newly formed peptides then act as a second stimulus to the mast cell. In addition NRP and HRP may affect other immunocompetent celt such as monocytes, macrophages or eosinophils. Figure 4.8. Hypothesis for the local generation of mast-cell-stimulating peptides by the action of neutrophil-derived enzymes on albumin. Initial stimulation of the mast cell by any of a variety of agents causes the release of preformed histamine (H) neutrophil and eosinophil chemotactic factors (NCF, ECF) and enzymes and the de novo synthesis of prostaglandins (PG) and leukotrienes (LT). These agents increase vascular permeability and vessel diameter. As a result, albumin and later neutrophils (PMN) enter the tissue space where the latter undergo phagocytosis and the secretion of proteolytic enzymes to the extracellular space where they act on albumin to generate NRP (neurotensin-related peptide) and HRP (histamine-releasing peptide). These newly formed peptides then act as a second stimulus to the mast cell. In addition NRP and HRP may affect other immunocompetent celt such as monocytes, macrophages or eosinophils.
The full name of these cells is neutrophilic polymorphonuclear leukocytes, but the terms neutrophil and, less-commonly now, polymorph are generally used to describe this cell (Fig. 1.1a). In fact, most preparations of neutrophils contain about 95-97% neutrophils, the remainder being largely eosinophils, because the commonly-used separation techniques do not efficiently separate these cell types. Neutrophils are the most abundant white cell in the blood, accounting for 40-65% of white blood cells, and are found at concentrations usually in the range 3-5 x 106 cells/ml blood. This number can increase dramatically (up to tenfold) in cases of infection. They have a relatively short half-life in the circulation (estimated at about 8-20 h), but this may be extended to up to several days if the cells leave the circulation and enter tissues - although it is difficult to measure the lifespan of a tissue neutrophil. Because of the large numbers of neutrophils in the circulation and their relatively short lifespan, vast numbers of neutrophils enter and... [Pg.4]

Inflammation is a local protective response to infection or injury whereby cells and proteins in the blood enter to remove the pathogens and repair the damaged tissue. Edema, redness, pain, and heat are the four cardinal symptoms of inflammation. Extent of reactions is determined by inflammatory mechanisms mediated by serum protein or cellular systems. Serum protein systems include complement, coagulation, fibrinolysis, and kinin cellular systems include PMN cells, mast cells, platelets, eosinophils, lymphocytes, macrophages, and reticuloendothelial system. Insufficient responses result in immunodeficiency leading to cancer and infections excessive responses are the cause of a number of chronic diseases like diabetes, cardiovascular disease, rheumatoid arthritis, multiple sclerosis, and Alzheimer s disease (Tracey, 2002). [Pg.105]


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See also in sourсe #XX -- [ Pg.95 ]




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Enteral

Enteric

Entering

Eosinophile

Eosinophilic

Eosinophils

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