Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the ocular abnormalities in cases of vitiligo, 100 patients were examined who underwent a series of investigations e.g., complete haemogram, urine analysis, blood biochemistry and chest x-ray and 70 cases were taken as control. Patients with systemic diseases such as diabetes mellitus, thyroid and auto-immune disorders were excluded. Detailed ocular examinations including recording of vision, slit-lamp biomicroscopy, gonioscopy, ophthalmoscopy and examination of fundus by 90 D lens were done. Of 100 vitiligo patients, 23% showed hypopigmented sports on the iris, 18% pigmentation on anterior chamber, 9% retinal pigment epithelium hypopigmentation, 5% uveitis, 11% had chorioretinal degeneration and 34% had no ocular findings. There lies a strong association of ocular disorder in patients with vitiligo.
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PMID:Clinical pattern of ocular manifestations in vitiligo. 1507

Uveitis is a common sequela to many ocular diseases. Primary treatment goals for uveitis should be to halt inflammation, prevent or control complications caused by inflammation, relieve pain, and preserve vision. Systemic and topical NSAIDs are essential components of the pharmaceutic armamentarium currently employed in the management of ocular inflammation by general practitioners and veterinary ophthalmologists worldwide. NSAIDs effectively prevent intraoperative miosis; control postoperative pain and inflammation after intraocular procedures, thus optimizing surgical outcome; control symptoms of allergic conjunctivitis;alleviate pain from various causes of uveitis; and circumvent some of the unwanted side effects that occur with corticosteroid treatment. Systemic NSAID therapy is necessary to treat posterior uveitis, because therapeutic concentrations cannot be attained in the retina and choroid with topical administration alone, and is warranted when diseases, such as diabetes mellitus or systemic infection, preclude the use of systemic corticosteroids. Risk factors have been identified with systemic and topical administration of NSAIDs. In general, ophthalmic NSAIDs may be used safely with other ophthalmic pharmaceutics; however, concurrent use of drugs known to affect the corneal epithelium adversely, such as gentamicin, may lead to increased corneal penetration of the NSAID. The concurrent use of NSAIDs with topical corticosteroids in the face of significant preexisting corneal inflammation has been identified as a risk factor in precipitating corneal erosions and melts in people and should be undertaken with caution[8]. Clinicians should remain vigilant in their screening of ophthalmic and systemic complications secondary to drug therapy and educate owners accordingly. If a sudden increase in patient ocular pain (as manifested by an increase in blepharospasm, photophobia, ocular discharge, or rubbing)is noted, owners should be instructed to contact their veterinarian promptly.
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PMID:Nonsteroidal anti-inflammatory drugs in veterinary ophthalmology. 1511 Sep 80

Type 1, or cellular, immune response is characterized by overproduction of IL-1, IL-2, IFN-gamma and TNF-alpha and is the underlying immune mechanism of some autoimmune disorders such as psoriasis, alopecia areata, rheumatoid arthritis, Crohn's disease, multiple sclerosis, insulin-dependent diabetes mellitus and experimental autoimmune uveitis. Type 2 immune response is seen in allergic and antibody-mediated autoimmune diseases and is characterized by IL-4, IL-6 and IL-10 overproduction. Linoleic acid is a precursor of prostaglandin E2 (PGE2) and its intake results in tissue production of PGE2, especially in the absence of other polyunsaturated fatty acids (PUFAS) which inhibit this conversion. PGE2 decreases the production of IL-1, IL-2, IFN-gamma and TNF-alpha and proliferation of TH1 cells and increases the production of IL-4, leading to suppression of the type 1 immune response. Taken together, linoleic acid, the major PUFA of maize oil, could have therapeutic efficacy against cellular autoimmune disorders. On the other hand, excessive intake of linoleic acid may aggravate type 2 autoimmune disorders.
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PMID:The beneficial and detrimental effects of linoleic acid on autoimmune disorders. 1511 15

Macular edema is the final common pathway of many intraocular and systemic insults. It may develop in a diffuse pattern where the macula appears generally thickened or it may acquire the characteristic petaloid appearance referred to as cystoid macular edema. Although macular edema may be associated with protean underlying conditions, it is most commonly seen following intraocular surgery, venous occlusive disease, diabetic retinopathy, and posterior segment inflammatory disease. As well as clinical suspicion, a wide range of investigations may lead to the diagnosis of macular edema. Fluorescein angiography and optical coherence tomography provide enhanced visualization of the geometry and distribution of macular edema. A variety of approaches to the treatment of macular edema have been attempted, with a variable degree of success. These options have included topical and systemic steroids, topical and oral non-steroidal anti-inflammatory agents and laser photocoagulation treatment. More recently other therapeutic modalities, including immunomodulators, intravitreal injection of triamcinolone, and pars plana vitrectomy have also been employed. Clinical trials are currently looking into the use of a steroid slow-release intravitreal device for the management of macular edema secondary to uveitis and diabetes. This article reviews the clinical entity of macular edema focusing on the current therapeutic strategies for its management.
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PMID:Macular edema. 1532 93

We have investigated the chemoattractant properties of self-antigens associated with autoimmune diseases and solid tumors. Many autoantigens induced leukocyte migration, especially by immature dendritic cells (iDC) by interacting with various chemoattractant Gi-protein-coupled receptors (GiPCR). Our initial observation that myositis-associated autoantigens, histidyl-tRNA synthetase and asparaginyl-tRNA synthetase, were chemotactic for CC chemokine receptor 5 (CCR5)- and CCR3-expressing leukocytes, while other nonautoantigenic aminoacyl-tRNA synthesases were not, suggested that only self-antigens capable of interacting with receptors on antigen-presenting cells were immunogenic. We next determined that self-antigens associated with autoimmune diseases, e.g., multiple sclerosis or experimental autoimmune encephalomyelitis, type I diabetes, scleroderma, systemic lupus erythematosus, autoimmune uveitis, or experimental autoimmune uveitis (EAU), were chemotactic for GiPCR expressed by iDC. The majority of autoantigens were DC chemoattractants at 10-100 ng/ml, but did not induce DC maturation until they reached 1000-fold higher concentrations. Interphotoreceptor retinoid-binding protein and retinal arrestin (S-antigen) are targets of autoantibodies in human uveitis and are chemotactic for CXC chemokine receptor 5 (CXCR5)- and/or CXCR3-expressing iDC. However, although S-antigen does not induce EAU in wild-type mice, it is nevertheless a chemoattractant for murine iDC. These unexpected observations suggested that the chemotactic activity of these tissue-specific self-antigens could be involved in promotion of tissue repair and restoration. Thus, the primary role of autoantigens may be to alert the immune system to danger signals from invaded and damaged tissues to facilitate repair, and autoimmune responses subsequently develop only in subjects with impaired immunoregulatory function.
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PMID:Autoantigens act as tissue-specific chemoattractants. 1591 48

This review reconsiders how the Th1/Th2 paradigm can be applied to Th1-mediated autoimmune disease. Although there is evidence that autoimmune diseases such as multiple sclerosis, type 1 insulin-dependent diabetes mellitus, and posterior uveitis are Th1 mediated and that in some cases reduction of the Th1 response or a Th2 type shift may alleviate disease, many apparent exceptions are now well documented. These exceptions center around the contradictory actions of the Th1 cytokine IFN-gamma and the evidence that Th2 lymphocytes can also cause disease. Recent information on the regulation of Th1 and Th2 lymphocytes in terms of the innate immune response and by other T cells helps to clarify the reasons for some of these discrepancies and enables the Th1/Th2 concept to be accepted as an integral part of the complex interactions occurring as autoimmune disease develops.
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PMID:Th1 and Th2 lymphocytes in autoimmune disease. 1595 31

Poly(ADP-ribosyl) ation is a reversible post-translational protein modification implicated in the regulation of a number of biological functions. Whereas an 18 member superfamily of poly(ADP-ribose) polymerase (PARP) enzymes synthesize poly(ADP-ribose) (PAR), a single protein, PAR glycohydrolase (PARG) is responsible for the catabolism of the polymer. PARP-1 accounts for more than 90% of the poly(ADP-ribosyl)ating capacity of the cells. PARP-1 activated by DNA breaks cleaves NAD(+) into nicotinamide and ADP-ribose and uses the latter to synthesize long branching PAR polymers covalently attached to acceptor proteins including histones, DNA repair enzymes, transcription factors and PARP-1. Whereas activation of PARP-1 by mild genotoxic stimuli may facilitate DNA repair and cell survival, irreparable DNA damage triggers apoptotic or necrotic cell death. In apoptosis, early PARP activation may assist the apoptotic cascade [e.g. by stabilizing p53, by mediating the translocation of apoptosis inducing factor (AIF) from the mitochondria to the nucleus or by inhibiting early activation of DNases]. In most severe oxidative stress situations, excessive DNA damage causes over activation of PARP-1, which incapacitates the apoptotic machinery and switches the mode of cell death from apoptosis to necrosis. Besides serving as a cytotoxic mediator, PARP-1 is also involved in transcriptional regulation, most notably in the NF kappaB and AP-1 driven expression of inflammatory mediators. Pharmacological inhibition or genetic ablation of PARP-1 provided remarkable protection from tissue injury in various oxidative stress-related disease models ranging from stroke, diabetes, diabetic endothelial dysfunction, myocardial ischemia-reperfusion, shock, Parkinson's disease, arthritis, colitis to dermatitis and uveitis. These beneficial effects are attributed to inhibition of the PARP-1 mediated suicidal pathway and to reduced expression of inflammatory cytokines and other mediators (e.g. inducible nitric oxide synthase).
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PMID:Structure and function of poly(ADP-ribose) polymerase-1: role in oxidative stress-related pathologies. 1602 17

Multiple mechanisms of tolerance are induced by oral antigen. Low doses favor active suppression, whereas higher doses favor clonal anergy/deletion. Oral antigen induces T-helper 2 [interleukin (IL)-4/IL-10] and Th3 [transforming growth factor (TGF)-beta] T cells plus CD4+CD25+ regulatory cells and latency-associated peptide+ T cells. Induction of oral tolerance is enhanced by IL-4, IL-10, anti-IL-12, TGF-beta, cholera toxin B subunit, Flt-3 ligand, and anti-CD40 ligand. Oral (and nasal) antigen administration suppresses animal models of autoimmune diseases including experimental autoimmune encephalitis, uveitis, thyroiditis, myasthenia, arthritis, and diabetes in the non-obese diabetic (NOD) mouse, plus non-autoimmune diseases such as asthma, atherosclerosis, graft rejection, allergy, colitis, stroke, and models of Alzheimer's disease. Oral tolerance has been tested in human autoimmune diseases including multiple sclerosis (MS), arthritis, uveitis, and diabetes and in allergy, contact sensitivity to dinitrochlorobenzene (DNCB), and nickel allergy. Although positive results have been observed in phase II trials, no effect was observed in phase III trials of CII in rheumatoid arthritis or oral myelin and glatiramer acetate (GA) in MS. Large placebo effects were observed, and new trials of oral GA are underway. Oral insulin has recently been shown to delay onset of diabetes in at-risk populations, and confirmatory trials of oral insulin are being planned. Mucosal tolerance is an attractive approach for treatment of autoimmune and inflammatory diseases because of lack of toxicity, ease of administration over time, and antigen-specific mechanisms of action. The successful application of oral tolerance for the treatment of human diseases will depend on dose, developing immune markers to assess immunologic effects, route (nasal versus oral), formulation, mucosal adjuvants, combination therapy, and early therapy.
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PMID:Oral tolerance. 1604 53

From 1991 to 2003, 20 patients with pasteurellosis were admitted to our unit, of whom 2 died. They presented with cellulitis (n = 14), arthritis (n = 6), pneumonia (n = 3), subcutaneous abscess (n = 3), bursitis (n = 2), meningitis, otitis, sinusitis and uveitis. Underlying diseases included diabetes (n = 6) and malignancy (n = 5). Diabetes could be a predisposing condition for pasteurellosis.
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PMID:Diabetes in patients with pasteurellosis. 1619 90

Diabetes mellitus influences the function and morphology of the eye lens. The cataract is the second most common complication of diabetes mellitus on the eye. A hundred patients with cataract were examined in the prospective study. The patients were divided into two groups. The first group consisted of 50 patients with cataract who had not suffered from a system or local disease. The second group consisted of 50 patients with cataract and diabetes mellitus that had lasted for at least five years. In both groups the patients underwent identical cataract extra capsular extraction with intraocular PMMA (polymethylmethacrylate) lens implantation in camera posterior. The objective of this study was to compare the two groups of patients in order to find out the most common intraoperative or postoperative complications in diabetics. The most common postoperative complications in patients suffering from diabetes were inflammatory reactions and bleeding: postoperative keratopathy, uveitis anterior serous and uveitis anterior fibrinous with posterior sinechia and opacity of the posterior lens capsule as results. Postoperative visual acuity was worse in the patients in group II on the seventh day and six months after operation. It was diabetic retinopathy and its progression that caused deterioration of visual acuity. Diabetic retinopathy and its progression, as well as maculopathy were found only in patients who were not treated with photocoagulation before the operation.
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PMID:Cataract surgery and postoperative complications in diabetic patients. 1619 78


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