Ocular immunology

In mammals, the toxicity of nickel is a function of the chemical form of nickel, dose, and route of exposure. Exposure to nickel by inhalation, injection, or cutaneous contact is more significant than oral exposure. Toxic effects of nickel to humans and laboratory mammals are documented for respiratory, cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, dermal, ocular, immunological, developmental, neurological, and reproductive systems (NAS 1975 Nielsen 1977 USEPA 1980, 1986 WHO 1991 USPHS 1993). 

Most toxicity studies of PBBs in animals have involved oral exposure, and numerous effects have been documented including hepatic, renal, dermal/ocular, immunological, neurological, and developmental. 

Koevary SB. Ocular immunology in health and disease. Boston Butterworth-Heinemann, 1999. 

SmoUn G, O Connor GR. Ocular immunology, ed. 2. Boston, Little, Brown, 1986. 

Keywords AC AID Autoimmunity Immune deviation Ocular immunology Ocular inflammation... 

Chronic-Duration Exposure and Cancer. Occupational exposure to metallic mercury vapors has been reported to result in adverse cardiovascular, gastrointestinal, renal, ocular, immunological, and reproductive health effects (Barregard et al. 1988, 1990 Bencko et al. 1990 Bidstrup et al. 1951 Buchet et al. 1980 Cardenas et al. 1993 Cordier et al. 1991 Danziger and Possick 1973 Ehrenberg et al. 1991 ... 

Richard D. Semba, Ocular Immunology Service, Suite 700, 550 North Broadway, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA e-mail rdsemba Jhmi.edu... 

D-penicillamine a well-recognized complication of the use of D-penicillamine is a myasthenic syndrome. Most reported cases of myasthenic syndrome are women and the ocular muscles appear to be particularly commonly affected at early stages of the abnormality. The onset of the myasthenic syndrome can range between a few months and many years, and is not always reversible. There is a clear immunological basis to this problem, because it is associated with raised anti-acetylcholine receptor antibodies circulating in the serum. Antibody levels fall when the drug is withdrawn, and this, in turn, is associated with clinical improvement. How the... 

No studies were located regarding immunological effects in humans or animals following dermal or ocular exposure to isophorone. 

Acute exposure to kerosene-based fuels, such as JP-8, has been associated with respiratory, cardiovascular, ocular, neurological, immunological, renal, and dermal effects. Those studies are briefly described below and are summarized in Table A-3. 

In the United States 70% of the population has immunologic evidence of prior HSV infection by the age of 15 to 20 years and 97% by the age of 60.The primary HSV infection is subclinical in 85% to 90% of cases. Of the two types of HSV, HSV-1 predominates, accounting for approximately 85% of adult cases and is responsible for infection above the waist. Type 1 and type 2 ocular infections are clinically indistinguishable, although type 2 infections tend to be more severe. 

Type Causes/Immunology Symptoms lid Signs Ocular Manifestations Management Miscellaneous... 

Zierhut M, Schlote T.Tomida I, Steimer R. Immunology of uveitis and ocular allergy. Acta Ophthalmol Scand Suppl 2000 230 22-25. 

With the growing sophistication of molecular immunology techniques, there is more hope for elucidation of complex mechanisms of ocular inflammation. 

In a study of compassionate use of intravenous cidofovir in AIDS patients with CMV retinitis, iritis developed in 21 of 51 individuals (7). The appearance of this inflammatory process did not fit the characteristics of the vitritis associated with immune reconstitution, or with HIV-induced vitritis. The high rate in this cohort (compared with a 5-7% incidence in randomized trials) was associated with severe CMV retinitis, and the authors suggested that breakdown of the blood-ocular barrier in these patients may promote higher intraocular concentrations of cidofovir and thus enhance local toxicity. Previous correlations of prior use of HIV protease inhibitors with iritis were not confirmed in this study, although patients with iritis had better immunological and virological status than those without the disease. 

Most people tolerate aspirin well, but not patients with asthma, of whom there is a subgroup in whom aspirin precipitates asthmatic attacks (61,62). This is a distinct clinical syndrome, called aspirin-induced asthma, which affects about 10% of adults with asthma (63). Aspirin-induced asthma is usually accompanied by naso-ocular symptoms and can be triggered not only by aspirin, but by several NSAIDs, a fact that makes immunological cross-reactivity most unlikely. The propensity of an NSAID to precipitate an attack of asthma is probably related to inhibition of COX (63). There is evidence that potent inhibitors of COX-1 (such as ibuprofen, indometacin, and naproxen) are more likely to precipitate bronchoconstriction than NSAIDs that inhibit COX-2 preferentially (such as meloxicam and nime-sulide) (64,65). A widely accepted hjrpothesis is that in patients with asthma and aspirin intolerance, NSAJD-induced COX inhibition results in increased products from the 5-lipoxygenase pathway, the leukotrienes, which are both potent bronchoconstrictors and also inducers of... 

Topical anesthetic abuse, mostly unintentional, remains a persistent cause of keratitis and epithelial defects, leading to continuing ocular pain, visual impairment, and at worst enucleation (SEDA-21,134) (SEDA-22,140) (327). Mechanisms include direct toxicity of the local anesthetic or preservative and immunological causes. 

For its protection, the retina is physiologically and immunologically segregated from the rest of the body by the blood retinal barrier formed by tight junctions between vascular endothelial cells and RPE cells. Only small molecules can cross this barrier, making it difficult for many drugs to reach ocular tissue. In addition, intraocular tissue is an immune privileged site. This protects the ocular tissue from the innocent bystander effect of inflammation. 

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