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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the duration and pattern of cataract formation after pars plana vitrectomy, thirty-three eyes from 33 patients with complete data from March 1995 to January 2000 were collected in this study. The time and pattern of cataract formation was analyzed according to Lens Opacities Classification System III (LOCS III). The correlation between the mean cataract progression and follow-up time was determined by simple regression and correlation analysis. Diabetes mellitus and hypertension were the main causes of patients with vitreoretinopathy who underwent pars plana vitrectomy procedure. Twenty-one patients (63.6%) had diabetes mellitus and 11 patients (33.3%) had hypertension. Four eyes (13.8%) received intravitreal gas injection after pars plana vitrectomy. The correlation between cataract progression and follow-up time was clinically significant (p < 0.05). Thirty-one patients (94%) were nuclear cataract, the mean time of cataract formation being 9.1 months; 15 patients (46.9%) were cortical cataract, the mean time of formation being 8 months; and 24 patients (72.7%) were posterior subcapsular cataract, the mean time of formation being 13.3 months. Cataract formation after pars plana vitrectomy is not infrequent. Nuclear cataract is the most common type in this study. Vitreous microenvironmental changes, post-vitrectomy uveitis, intravitreal gas, and patient age may be the key points of cataract formation after surgery. The mechanism of longer-term effect of pars plana vitrectomy on lens status is still unknown and merits further study.
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PMID:Cataract formation after pars plana vitrectomy. 1141 62

This review addresses three related bone marrow failure diseases, the study of which has generated important insights in hematopoiesis, red cell biology, and immune-mediated blood cell injury. In Section I, Dr. Young summarizes the current knowledge of acquired aplastic anemia. In most patients, an autoimmune mechanism has been inferred from positive responses to nontransplant therapies and laboratory data. Cytotoxic T cell attack, with production of type I cytokines, leads to hematopoietic stem cell destruction and ultimately pancytopenia; this underlying mechanism is similar to other human disorders of lymphocyte-mediated, tissue-specific organ destruction (diabetes, multiple sclerosis, uveitis, colitis, etc.). The antigen that incites disease is unknown in aplastic anemia as in other autoimmune diseases; post-hepatitis aplasia is an obvious target for virus discovery. Aplastic anemia can be effectively treated by either stem cell transplantation or immunosuppression. Results of recent trials with antilymphocyte globulins and high dose cyclophosphamide are reviewed. Dr. Abkowitz discusses the diagnosis and clinical approach to patients with acquired pure red cell aplasia, both secondary and idiopathic, in Section II. The pathophysiology of various PRCA syndromes including immunologic inhibition of red cell differentiation, viral infection (especially human parvovirus B19), and myelodysplasia are discussed. An animal model of PRCA (secondary to infection with feline leukemia virus [FeLV], subgroup C) is presented. Understanding the mechanisms by which erythropoiesis is impaired provides for insights into the process of normal red cell differentiation, as well as a rational strategy for patient management. Among the acquired cytopenias paroxysmal nocturnal hemoglobinuria (PNH) is relatively rare; however, it can pose formidable management problems. Since its first recognition as a disease, PNH has been correctly classified as a hemolytic anemia; however, the frequent co-existence of other cytopenias has hinted strongly at a more complex pathogenesis. In Section III, Dr. Luzzatto examines recent progress in this area, with special emphasis on the somatic mutations in the PIG-A gene and resulting phenotypes. Animal models of PNH and the association of PNH with bone marrow failure are also reviewed. Expansion of PNH clones must reflect somatic cell selection, probably as part of an autoimmune process. Outstanding issues in treatment are illustrated through clinical cases of PNH. Biologic inferences from PNH may be relevant to our understanding of more common marrow failure syndromes like myelodysplasia.
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PMID:New Insights into the Pathophysiology of Acquired Cytopenias. 1170 33

Cystoid macular edema (CME) is a common problem after cataract extraction. It can occur after uncomplicated surgery in patients with otherwise healthy eyes, after complicated surgery, or after surgery in patients with ocular diseases such as uveitis or diabetic retinopathy. Usually vision loss from cystoid macular edema is temporary and responds to treatment with topical anti-inflammatory medications. However, some cases respond poorly to conservative treatment and may develop permanent visual loss. A review of the medical literature was performed for all articles published in English between August 1, 2001 and July 31, 2002 on the topic of cystoid macular edema after cataract surgery. The authors selected nine articles that were most relevant to the practicing ophthalmologist for inclusion in this review. Topics of interest included vitreous loss, retained lens fragments, diabetes, uveitis, retinitis pigmentosa, ocular hypotensive lipids, internal limiting membrane peeling, and intravitreal triamcinolone injection.
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PMID:Managing cystoid macular edema after cataract surgery. 1254 9

Interferon (IFN)-gamma is an important immune regulator in normal immunity. When IFN gamma production is disturbed, various autoimmune diseases (ADs) can develop, in which we suggest that anti-IFN gamma could have a beneficial effect. Depending on the cell type in which IFN gamma synthesis is disturbed, different clinical manifestations may result. We have also proposed to remove tumor necrosis factor (TNF)-alpha, together with certain types of IFNs, to treat various ADs and AIDS, also an autoimmune condition. Anti-IFN gamma has been tested in several T-helper cell (Th1) ADs, including rheumatoid arthritis (RA), multiple sclerosis (MS), corneal transplant rejection, uveitis, Type I diabetes, schizophrenia (anti-IFN gamma and anti-TNF alpha), and various autoimmune skin diseases (alopecia areata, psoriasis vulgaris, vitiligo, pemphigus vulgaris and epidermolysis bullosa). A strong, sometimes striking, therapeutic response followed administration of anti-IFN gamma, indicating that it may be a promising therapy for Th1 ADs.
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PMID:Anti-interferon-gamma antibodies in the treatment of autoimmune diseases. 1266 71

Cystoid macular edema (CME) following cataract surgery has been recognized for over 50 years as an important cause of suboptimal post-operative vision. The incidence of CME varies widely, but is likely in the range of 1-2% using modern cataract extraction techniques. The diagnosis of CME can generally be made on clinical examination with evidence of perifoveal cystic spaces and can be confirmed with use of fluorescein angiography to document the classic petaloid pattern of leakage mainly into the outer retina. Leak from perifoveal vessels is induced by inflammatory mediators and results in intraretinal fluid accumulation and corresponding decrease in retinal function. The risk factors most associated with CME; rupture of posterior capsule, vitreous loss, iris incarceration, use of iris fixated lenses, active uveitis and diabetes, may all increase the potency of these mediators and exacerbate post-operative CME. The treatment of CME remains controversial but generally starts with conservative observation in isolated angiographic cases and progresses through topical non-steroidal anti-inflammatory agents (NSAIDs), topical steroids, peri-ocular steroids, systemic steroids and surgical intervention in refractory cases. Even more controversial is the role of NSAID prophylaxis peri-operatively in preventing clinical CME. Though the data is tantalizing in the short term, there is little to support the long-term benefit of such prophylaxis with respect to visual outcomes.
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PMID:Pseudophakic cystoid macular edema. 1275 47

A 78-year-old woman developed a severe fibrinous anterior chamber reaction 1 day after uneventful clear corneal incision cataract extraction with intraocular lens implantation. There was no history of uveitis or diabetes, and the fibrin responded immediately to topical steroids. The patient was followed closely to rule out endophthalmitis. The only risk factor identified was the use of systemic aminocaproic acid as prophylaxis for bleeding in chronic leukemia.
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PMID:Excessive fibrin after cataract surgery associated with aminocaproic acid use. 1295 20

Oral tolerance (OT) consists of the oral administration of antigens (Ag) that could alter the response of the immune system. This is a form of peripheral immune tolerance in which mature lymphocytes in the peripheral lymphoid tissues are rendered non functional or hyporesponsive by prior oral administration of Ag. It was first described in 1911 in animal models of anaphylaxis. This therapeutic approach requires the orally administration of Ag and the active participation of the gut-associated lymphoid tissue (GALT), a tissue comprising Peyer's patches, intraepitelial cells and villi containing epithelials cells which is a well organized immune network. The mechanisms by which OT is mediated included deletion or anergy and active cellular suppression. The primary factor determining which form of tolerance will be developed after oral administration of Ag is the Ag dosage. Thus, it is thought that low doses of Ag induce the generation of active suppression, via regulatory T cells in the GALT, which then migrate to the systemic immune system. These regulatory T cells produce down-regulatory cytokines such as IL4, IL10 and TGFbeta, a Th2 / Th3 cytokine pattern. Conversely, high dose of Ag favors anergy or clonal deletion. The phenomenon in which regulatory cells, as generated by oral tolerization, are primed in an Ag specific manner, but act in the respective microenvironment in a non-Ag specific manner is called bystander suppression. This phenomenon is of particular interest and explained the use of OT in T cell mediated autoimmune diseases such as rheumatoid arthritis (RA), multiple sclerosis (MS) and type I diabetes, some diseases in which the autoAg remains unknown or where there are reactivities to multiple autoAgs. There were several studies demonstrating the effectiveness of orally administered Ag in different animal models of autoimmune diseases, such as experimental allergic encephalomyelitis, collagen induced arthritis, diabetes, but also uveitis, myastenia gravis and transplantation. These mouse or rat models of autoimmune diseases gave the rationale for the therapeutic use of OT in human and this therapeutic approach has been tried in MS and RA, using oral myelin or oral collagen, respectively. In RA, 4 trials of oral type II collagen (CII) in RA have been published. Taken together, these studies suggested that oral CII in RA gave a trend toward clinical improvement, with significance in only 2 studies. Bacterial extract from Escherichia coli containing heat shock proteins has been tried in oral treatment for RA. Two placebo controlled trials and 2 comparative studies gave favorable results for this bacterial extract with no or mild adverse events. Although oral/mucosal tolerance has given successful results in animal models of autoimmune diseases, the enthusiasm for this therapeutic approach in human diseases must be tempered. The discrepancies between the effectiveness of OT in animal models and the results in human trials raise some questions, the identification of the subgroup of patients who might respond to this treatment and the source (or nature) of the administered Ag (homologous versus heterologous), for instance.
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PMID:Oral tolerance in the treatment of rheumatoid arthritis. 1456 Dec 5

Mutations of the Activation-Induced Cytidine Deaminase (AID) gene have been found in patients with autosomal recessive hyper-IgM (HIGM) syndrome type 2. We retrospectively analyzed clinical, immunologic and genetic characteristics of 29 patients from 22 families with AID deficiency. Patients' median age at diagnosis and at last evaluation was 4.9 years (range: 0 to 53) and 14.2 years (range: 2.7 to 63), respectively. Most patients had suffered from recurrent and severe infections, however, intravenous immunoglobulin (IVIG) replacement therapy resulted in a dramatic decrease in the number of infections. Lymphoid hyperplasia developed in 22 patients and persisted in 7 at last follow-up. It is striking to note that six patients developed autoimmune or inflammatory disorders including diabetes mellitus, polyarthritis, autoimmune hepatitis, hemolytic anemia, immune thrombocytopenia, Crohn's disease and chronic uveitis. Fifteen distinct AID mutations were found but there was no significant genotype-phenotype correlation. In conclusion, AID-deficient patients are prone to infections and lymphoid hyperplasia, which may be prevented by early-onset IVIG replacement, but also to autoimmune and inflammatory disorders.
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PMID:Clinical, immunologic and genetic analysis of 29 patients with autosomal recessive hyper-IgM syndrome due to Activation-Induced Cytidine Deaminase deficiency. 1496 93

Extensive clinical data (595 patients) were made use of to work out a clinical classification and to isolate 2 groups of patients, i.e. one with primary retinoschisis and the other with secondary retinoschisis. According to etiopathogenesis, primary retinoschisis is subdivided into the inherited (congenital) variation and the acquired one. Congenital retinoschisis comprises, in its turn, juvenile and linked with X-chromosome variants as well as retinoschisis observed in Goldman-Favre and Wagner syndromes. The group of acquired retinoschisis is made up of degenerative (senile) and myopic variants, which are triggered by the typical or cystic peripheral retinal degeneration. Secondary retinoschisis is observed in different eye diseases like trauma, diabetes, uveitis, angiomatosis etc. The central, peripheral and combined retinoschisis variations are distinguished according to localization; two variations are distinguished according to the disease clinical course, i.e. stationary with demarcation and complicated progressing without demarcation and with uneven borders. The study results show that retinoschisis of any variation begins at the extreme periphery; lamination of the flat type develops primarily in the lower-external quadrant and the one of the bullous type--in the upper-external quadrant.
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PMID:[Retinoschisis. 1. Diagnosis, classification, examination methods]. 1501 74

Type 1, or cellular, immune response is characterized by overproduction of TNF-alpha, IFN-gamma, IL-1, IL-2 and IL-8 and is the underlying immune mechanism of psoriasis, alopecia areata, rheumatoid arthritis, Crohn's disease, multiple sclerosis, insulin-dependent diabetes mellitus and experimental autoimmune uveitis (EAU). Type 2 immune response is seen in antibody-mediated autoimmune diseases. Based on the pharmacokinetic effects of cetirizine and allopurinol, this paper introduces these two safe and inexpensive drugs as novel potential agents against cell-mediated autoimmune disorders. Cetirizine, supposed to inhibit DNA binding activity of NF-kappa B, inhibits the expression of adhesion molecules on immunocytes and endothelial cells and the production of IL-8 and LTB4, two potent chemoattractants, by immune cells. It induces the release of PGE2, a suppressor of antigen presentation and MHC class II expression, from monocyte/macrophages and reduces the number of tryptase positive mast cells in inflammation sites. Tryptase is a chemoattractant, generates kinins from kininogen, activates mast cells, triggers maturation of dendritic cells and stimulates the release of IL-8 from endothelial cells and the production of Th1 lymphokines by mononuclear immunocytes. Allopurinol is a free radical scavenger, suppresses the production of TNF-alpha and downregulates the expression of ICAM-1 and P2X(7) receptors on monocyte/macrophages. ICAM-1 serves as a ligand for LFA-1 (on T lymphocytes), allowing proper antigen presentation. P2X(7) receptors are thought to be involved in IL-1beta release, mitogenic stimulation of T lymphocytes and the probable cytoplasmic communication between macrophages and lymphocytes at inflammation sites. Allopurinol was markedly more effective than prednisolone in treating experimental autoimmune uveitis and in combination with cyclosporine suppressed the inflammatory reaction of this condition more effectively than either agent alone. As allopurinol is a competitive inhibitor of xanthine oxidase and decreases serum levels of uric acid, which is protective against multiple sclerosis, it should preferably be coadministered with uric acid precursors in the treatment of this condition. Cetirizine and allopurinol may prove of benefit in the treatment of various cellular autoimmune disorders.
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PMID:Cetirizine and allopurinol as novel weapons against cellular autoimmune disorders. 1503 12


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