Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined 11 brains of human immunodeficiency virus (HIV) seropositive cases who died from unnatural causes (10 intravenous drug abusers who died from heroin overdose and 1 homosexual dead from a gunshot injury); 10 brains of HIV seronegative heroin addicts who died from overdose and 1 seronegative drug abuser who died from gunshot injury served as controls. Complete postmortem examination did not show evidence of acquired immune deficiency syndrome (AIDS) or AIDS related complex. Terminal changes including nerve cell ischemia, edema and diffuse vascular congestion were observed in all cases. Perivascular pigment deposition with macrophages was a constant finding in drug addicts and was probably related to chronic intravenous injection. In contrast, cerebral vasculitis was significantly more frequent and marked in HIV seropositive cases and was often associated with lymphocytic meningitis. Granular ependymitis, myelin pallor with reactive astrocytosis and microglial proliferation were also more frequent and more severe in HIV seropositive cases. Immunocytochemistry was negative for HIV antigens. Our study further supports the view that early central nervous system changes occur in HIV infection.
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PMID:Early brain changes in HIV infection: neuropathological study of 11 HIV seropositive, non-AIDS cases. 153 41

A study of peripheral and central mechanisms of secondary immunodeficiency in atherosclerotic patients demonstrated altered structural layout of lymphocyte membranes due to cholesterol accumulation in the cells. This was associated with increased membrane viscosity, suppressed mitotic activity and lower cap formation rate as well as changed intracellular calcium redistribution. Thymic ischemia due to occlusion or stenosis of thymus-supplying vessels was shown to promote age-related transformation of thymic tissue. Experimental simulation of thymic ischemia resulted in an abrupt drop of serum thymic factor in the blood of animals and the development of an immunodeficient condition.
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PMID:[Secondary atherosclerotic immunodeficiency]. 272 80

Human immunodeficiency virus (HIV) infection can present with musculoskeletal syndromes including systemic vasculitis. We describe vasculitis resembling polyarteritis nodosa (PAN) in 2 HIV-infected individuals and review reported cases to emphasize clinical features. Our patients presented with digital gangrene and had vasculitis confirmed by angiography. In reports in the literature, patients have presented with digital ischemia and gangrene, peripheral neuropathy and constitutional symptoms. The diagnosis has been confirmed by angiography and by nerve and muscle biopsy. Treatment with systemic corticosteroids has afforded short term benefits to patients; however the effectiveness of alternative therapy and longterm prognosis remain unclear.
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PMID:Polyarteritis nodosa-like vasculitis in human immunodeficiency virus infection. 773 64

The cytokine tumor necrosis factor (TNF-alpha) is a pleotrophic polypeptide that plays a significant role in brain immune and inflammatory activities. TNF-alpha is produced in the brain in response to various pathological processes such as infectious agents [e.g., human immunodeficiency virus (HIV) and malaria], ischemia, and trauma. TNF-alpha mRNA is rapidly produced in response to brain ischemia within 1 h, reaches a peak at 6-12 h post ischemia, and subsides 1-2 days later. TNF-alpha mRNA expression corresponds in a temporal fashion to other cytokines such as interleukin (IL)-6, cytokine-induced neutrophil chemoattractant (KC), and IL-1 and precedes the infiltration of inflammatory cells into the injured zone. TNF-alpha is present early in neuronal cells in and around the ischemic tissue (penumbra), yet at later time points, the peptide is found in macrophages in the infarcted tissue. TNF-alpha has been demonstrated to cause expression of proadhesive molecules on the endothelium, which results in leukocyte accumulation, adherence, and migration from capillaries into the brain. Furthermore, TNF-alpha activates glial cells, thereby regulating tissue remodeling, gliosis, and scar formation. Thus, evidence is emerging in support of a role for TNF-alpha in injury induced by infectious, immune, toxic, traumatic, and ischemic stimuli. TNF-alpha promotes inflammation by stimulation of capillary endothelial cell proinflammatory responses and thereby provides leukocyte adhesion and infiltration into the ischemic brain. The evidence generated so far suggests that agents that suppress TNF-alpha's production or actions will reduce leukocyte infiltration into ischemic brain regions and thereby diminish the extent of tissue loss.
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PMID:Cytokines, inflammation, and brain injury: role of tumor necrosis factor-alpha. 788 Jul 18

Cytomegalovirus disease is an opportunistic infection that is seen in patients with inmunodeficiencies. The group most commonly affected are AIDS and transplanted patients. Only a few cases of cytomegalovirus disease in non-immunocompromised patients have been reported. In localized disease, the gastrointestinal tract is the most frequently affected. We report two cases of acute abdomen caused by cytomegalovirus enteritis and colitis (histopathological diagnosis) without any underlying immune disorder. The role that the cytomegalovirus infection might play in the development of the clinical manifestations in these two cases is discussed. Without an established immunodeficiency we must be careful to attribute to cytomegalovirus infection the direct responsibility of the lesions. In the reported cases, the existence of intestinal ischemia is more than just a clinical hypothesis and pathological examination is inconclusive. The absence of an immunocompromised state, the presentation as an acute abdomen and the clinical course forwards intestinal occlusion in the first case are not characteristic of cytomegalovirus enteritis and colitis. We conclude that the two reported cases are in fact an ischemic enteritis upon which cytomegalovirus enteritis and colitis was superimposed, an association that has not been reported before.
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PMID:[Cytomegalovirus enteritis and colitis in nonimmunodepressed patients, a primary disease or superinfection?]. 798 12

Two magnetization transfer (MT) contrast effects, a T2-like effect and the improved contrast observed when gadolinium is used with MT, are combined in a single sequence. Forty patients (22 males:18 females; mean age, 45 years (23-87)) with suspected intracranial pathology underwent MRI on a 1.5 Tesla system. Of 46 lesions; seven were ischemic, five infective, seven neoplastic, four hemorrhagic, four multiple sclerosis, seven human immunodeficiency virus (HIV) leukoencephalopathy, nine normal/miscellaneous, and three gliosis. A conventional spin-echo sequence (TR 900 TE 15) was used with on-resonance binomial MT pulses. The sequence was performed postgadolinium +/- MT. The signal intensity ratios +/- MT were: white matter, 0.62 +/- 0.03; gray matter, 0.75 +/- 0.04; ischemia, edema, and demyelination, 0.75 (0.57-0.86); and gadolinium/methemoglobin, 0.85 (0.81-0.98). Areas which exhibited MT had T2-like contrast and those that did not maintained expected contrast for the given parameters. The result was a combination of T2-like contrast, gadolinium enhancement, and dark cerebrospinal fluid (CSF) providing both increased sensitivity to lesions which exhibited both contrast features and improved delineation of periventricular lesions. Furthermore, the differential signal between T2-like contrast of edema and gadolinium enhancement in neoplastic or infective lesions was maintained.
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PMID:Clinical utility of a new contrast option from magnetization transfer contrast. 857 39

Acquired immunodeficiency syndrome (AIDS) caused by the human immunodeficiency virus (HIV) may turn out to be the largest lethal epidemic of infection ever. The estimated global number of HIV-infected adults in 1993 was 13 million, with projections of up to 40 million by the year 2000. Human immunodeficiency virus infections and AIDS are relevant to surgeons with respect to the surgical management of AIDS patients in general, the treatment of the increasingly long list of surgical complications specific to AIDS patients in particular, and the risks of patient-to-surgeon and surgeon-to-patient HIV transmission. Because of migration of individuals and populations throughout the world, even surgeons practicing in relatively unaffected regions should be familiar with the potential surgical implications of AIDS. Ethical considerations arise, as well. Are surgeons obliged to operate on HIV-positive or AIDS patients? Some surgeons adhere strictly to the Hippocratic Oath, whereas others reserve the right to be selective on whom they operate, except in emergencies. Other common ethical considerations in the AIDS patient are similar to those arising in the terminal cancer case: whether to operate or not; whether to provide advanced support such as total parenteral nutrition or hemodialysis. Answers are not simple and require close collaboration between the surgeon, the AIDS specialist, and involved members of other specialties. Emergency operations become necessary to treat AIDS independent disease such as acute cholecystitis and appendicitis or AIDS-related life-threatening conditions such as gastrointestinal bleeding, obstruction, perforation, or ischemia complicating Kaposi's sarcoma, lymphoma, and cytomegalovirus or disseminated nontuberculous mycobacterial infections. Delays and errors in diagnosis are frequent. Poor nutritional state with weight loss, low serum albumin, and leukocyte count prevails in most patients requiring emergency operations and account for a high mortality. By applying solid judgment and selecting management appropriately, the surgeon has the ability to prolong life and to improve the quality of life for these unfortunate patients, and to do so with extremely minimal risk to himself and his team.
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PMID:AIDS, emergency operations, and infection control. 887 99

Immune-mediated mechanisms appear to play a primary role in the pathogenesis of polymyositis (PM) and dermatomyositis (DM). The serum of patients with active DM has high levels of circulating complement fragments C3b, C4b, and C5b-9 membranolytic attack complex (MAC) and demonstrates a very high C3 uptake in an vitro assay system. The MAC and the immune complex-specific C3bNEO fragment are deposited on the endomysial capillaries early in the disease and lead sequentially to loss of capillaries, muscle ischemia, muscle fiber necrosis, and perifascicular atrophy. In contrast, in PM the muscle fiber injury is initiated by sensitized CD8+ cytotoxic T cells that recognize heretofore unknown and probably endogenous muscle antigens in the context of major histocompatibility complex (MHC) class I expression. A restricted (oligoclonal) pattern of T-cell receptor with prominence of Va1, Vb6, and Vb15 genes is noted within the endomysial infiltrates suggesting that the T-cell response is antigen driven. In both PM and DM, intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 are upregulated in the endomysial endothelial cells and function as ligands for the leukocyte integrins leukocyte function-associated antigen (LFA)-1 and very late activating antigen (VLA)-4, allowing activated lymphocytes to adhere to the endothelial cells and migrate to the muscle fibers. Among viruses, only the retroviruses human immunodeficiency virus (HIV) and human T-cell lymphotropic virus (HTLV)-1 have been convincingly shown to trigger PM, which is mediated by nonviral-specific, cytotoxic CD8+ cells. The treatment of inflammatory myopathies remains empirical. Many patients respond to steroids to some degree and for some period of time. Azathioprine, methotrexate, cyclosporine, cyclophosphamide, and plasmapheresis can be of mild to moderate benefit. High-dose intravenous immunoglobulin (IVIg) is a promising therapeutic modality for some patients resistant to therapies. In a controlled study, IVIg was effective in DM not only in improving the clinical symptoms but also in reversing the underlying immunopathology. The role of IVIg in PM and IBM is under study in control trials.
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PMID:Immunopathogenesis of inflammatory myopathies. 896 19

There is substantial clinical evidence for the development of vascular disorders in human immunodeficiency virus (HIV)-infected individuals, particularly in the form of vasculitis. Transgenic mice carrying a replication-defective HIV-1 provirus with selective deletion of the gag, pol, and env genes developed extensive vasculopathy. Restricted expression of HIV nonstructural genes in smooth muscle cells was accompanied by the migration and proliferation of these cells in blood vessels of all sizes and at different body sites. The frequent infiltration observed in the hypertrophic vessel walls occurred predominantly in the adventitia and was composed of primarily T cells and occasionally plasma cells. The intimal thickening generated significant luminal narrowing in some vessels, and the restricted blood flow led to ischemia in the affected tissues. Interestingly, the endothelium did not appear to support HIV gene expression or be involved in the pathological process. This transgenic model provides an opportunity to dissect the mechanism underlying HIV-associated vasculopathy.
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PMID:Human immunodeficiency virus-associated vasculopathy in transgenic mice. 915 76

We treated foot ulcerations in diabetics with limb-threatening ischemia using percutaneous balloon dilatation (44) and popliteodistal vein grafts (94). After revascularization, we observed in 12% an increase in the infection which necessitated major amputation despite open bypass or successful dilatation. A diabetic local immunodeficiency leads to cellular and humoral alterations which may cause severe tissue damage although the perfusion has been improved.
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PMID:[Diabetic foot--uncontrollable infections despite successful revascularization]. 957 10


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