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Russell W Read

Publications and source records attributed to Russell W Read.

At least 19 recordsLinked to original sources
PubMed2006

Distribution of complement anaphylatoxin receptors and membrane-bound regulators in normal human retina.

To characterize the distribution of membrane-bound components of the complement system in normal human retina, eyes from eight human donors with no history of ocular disease, ranging in age from 47 to 85 years were examined using immunohistochemistry to localize the C3a receptor (C3aR), C5a receptor (C5aR), CD46, CD55, and CD59 in cryosections prepared from donor posterior segments. The C3aR was identified in the nerve fiber layer in a sawtooth-patterned band. Vimentin, used as a Müller cell marker, produced a similar staining pattern. The C5aR was detected on specific rounded structures in the inner plexiform layer and occasionally in the nerve fiber layer. CD46 produced markedly specific staining of the basolateral surface of the retinal pigment epithelium. CD55 was localized to the nerve fiber layer. Staining for these proteins was consistent across all eyes studied. CD59 was expressed throughout the nerve fiber layer and labeled vessels that extended through the ganglion cell, inner plexiform, and inner nuclear layers, but this pattern was only confirmable in a single subject. Complement anaphylatoxin receptors and regulatory proteins are localized in different but internally consistent patterns in normal adult human retina, independent of the age of the donor. C3aR and C5aR localization only in the inner retina contrasts with previously reported findings in the central nervous system of wide spread diffuse staining. The complement regulators CD55 and CD59 were found primarily on the inner retina, while CD46 was present exclusively in a polarized fashion on the RPE.

Aged↗
PubMed2006

Uveitis: advances in understanding of pathogenesis and treatment.

Uveitis is a leading cause of blindness affecting individuals of all ages, genders, and races. Uveitis may be due to autoimmune, infectious, toxic, malignant, or traumatic processes. Some evidence supports an association between conditions previously presumed to be autoimmune and viral infectious agents. For autoimmune uveitis, therapy is nonspecific, typically beginning with corticosteroids. For nonresponsive disease or for corticosteroid sparing, recent reports on mycophenolate mofetil, infliximab, and interferon therapy show success for various forms of uveitis. Treatment of the complications of uveitis, especially cystoid macular edema, is difficult. Vitamin E appears to offer little benefit, whereas octreotide may be effective. Recent collaborative efforts at standardization in the field should enhance studies on these conditions.

Eye↗
PubMed2006

Evaluation of the effect on outcomes of the route of administration of corticosteroids in acute Vogt-Koyanagi-Harada disease.

PURPOSE: To compare the effect on outcomes of the route of administration of corticosteroids in acute Vogt-Koyanagi-Harada disease. DESIGN: Retrospective comparative interventional case series. METHODS SETTINGS: Nine international uveitis specialty clinics. STUDY POPULATION: Forty-eight patients presenting over a three-year period to a study center with acute Vogt-Koyanagi-Harada disease. INTERVENTION: Initial treatment with corticosteroid either orally (Oral only group) or intravenously followed by an oral taper (IV+Oral group). MAIN OUTCOME MEASURES: Change in visual acuity with treatment; development of ocular complications, including visually significant cataract, choroidal neovascularization, subretinal fibrosis, fundus pigment migration, nummular hypopigmented lesions, and diffuse fundus depigmentation; use of immunosuppressive therapy. RESULTS: The Oral only group comprised 15 patients (31%) and the IV+Oral group 33 patients (69%). Median follow-up was 15 months. There was no difference in duration of follow-up between groups (P = .234). There was no difference in the change in visual acuity between groups, adjusting for initial visual acuity (P = .402). There were no differences in the rates of development of visually significant cataract, fundus pigmentary changes, or in the rate of use of subsequent immunosuppressive therapy between treatment groups. No patients developed choroidal neovascularization or subretinal fibrosis over the study period. CONCLUSIONS: Route of administration of corticosteroid had no detectable effect on change in visual acuity nor on the development of visually significant complications over the study period. Prospective trials are necessary to address speed of resolution and definitively answer outcome questions.

Acute Disease↗
PubMed2005

Genetic deficiency of C3 as well as CNS-targeted expression of the complement inhibitor sCrry ameliorates experimental autoimmune uveoretinitis.

In this report, we describe the effect of complement deficiency and inhibition on experimental autoimmune uveoretinitis (EAU). C57BL/6 mice genetically deficient in C3 (C3-/-) or expressing a soluble complement activation inhibitor (soluble complement receptor related protein Y or sCrry) in a CNS-targeted fashion, (sCrry/GFAP) were induced for EAU via peripheral immunisation with a peptide of amino acids 1-20 of human interphotoreceptor retinoid binding protein in complete Freund's adjuvant with concurrent intraperitoneal pertussis toxin. The incidence and severity of EAU in the mutant mice was compared with that in simultaneously induced C57BL/6 wild type mice. The sCrry protein was detected in retinal extracts from transgenic but not wild type mice by western blot. C3-/- mice had a significant reduction in the incidence of EAU compared with wild type mice (incidence 44 versus 89%, respectively, p=0.0417) and a significant reduction in the severity of EAU (median disease score values 0 versus 1.3, respectively, p=0.0253). Similarly, sCrry mice had a significant reduction in the incidence of EAU compared with wild type mice (incidence 57 versus 100% respectively, p=0.0033) and a significant reduction in the severity of EAU (median disease score values 0.18 versus 1.85, respectively, p=0.0054). A genetic deficiency of C3 and production of a soluble complement inhibitor targeted to the CNS and eye are protective against EAU.

Animals↗
PubMed2005

Splendore-Hoeppli phenomenon in the conjunctiva: immunohistochemical analysis.

PURPOSE: To present two cases of conjunctival lesions exhibiting the Splendore-Hoeppli phenomenon, each with different immunohistochemical findings. DESIGN: Interventional case reports. METHODS: Two young males with conjunctival lesions underwent biopsy. Demographic data and timing of biopsy were extracted from the charts. The biopsy specimens were formalin fixed and paraffin embedded for light microscopy. Immunohistochemical staining using the peroxidase method was carried out on each for IgG, IgM, IgA, the C3 component of complement, and eosinophilic major basic protein. MAIN OUTCOME MEASURES: Presence of positive or negative staining for the various antigens. RESULTS: Both biopsy specimens exhibited the Splendore-Hoeppli phenomenon, a morphologically unique process consisting of an amorphous, eosinophilic material surrounded by epithelioid histiocytes, multinucleated giant cells, lymphocytes, and eosinophils. Two staining patterns were seen. One revealed predominately immunoglobulin deposition, whereas the other revealed primarily eosinophilic major basic protein. This is the first instance we are aware of in which eosinophilic major basic protein was the predominate finding in an ocular specimen. CONCLUSION: The composition of Splendore-Hoeppli phenomenon material varies and may be related to various factors, including timing of biopsy and prior treatment.

Adult↗
PubMed2005

Optic disk edema associated with sudden-onset anterior uveitis.

PURPOSE: To describe the clinical characteristics and course of optic disk edema (ODE) associated with isolated sudden-onset anterior uveitis. DESIGN: Interventional, noncomparative retrospective case series. METHODS: Review of patients with sudden-onset anterior uveitis and concomitant ODE seen in an academic uveitis referral center or a general ophthalmology clinic between August 2001 and November 2002. RESULTS: A total of eleven eyes of seven patients were included. Optic nerve function was intact in all. Cranial magnetic resonance imaging was normal in four of five and revealed an abnormality not felt to be responsible for the ODE in one. Resolution of anterior uveitis occurred over a mean of 36 days while ODE resolution lagged by a mean of 20 days. CONCLUSION: Resolution of ODE trailed that of the anterior uveitis by up to 6 weeks. No abnormalities responsible for ODE were found on cranial imaging.

Adolescent↗
PubMed2005

Evaluation of subconjunctival triamcinolone for nonnecrotizing anterior scleritis.

PURPOSE: Subconjunctival corticosteroid injection (SCI) for nonnecrotizing anterior scleritis remains controversial, partly because long-term follow-up is not available. This study documents the efficacy and adverse effects of SCI. DESIGN: Retrospective, noncomparative, interventional case series. PARTICIPANTS: Thirty-eight eyes of 35 patients with nonnecrotizing, noninfectious anterior scleritis resistant to prior systemic or local therapy. INTERVENTION: Subconjunctival triamcinolone acetonide injection. MAIN OUTCOME MEASURE: Persistence or resolution of signs and symptoms of anterior scleritis and development of complications. RESULTS: Thirty-six of 38 eyes had complete resolution of signs and symptoms within 6 weeks of SCI. Fifteen eyes had follow-up of > or =30 months. There were no instances of scleral melting or perforation; adverse events included subconjunctival hemorrhage (5 patients), transient ocular hypertension without evidence of glaucoma (4 patients), cataract (2 patients), and glaucoma (2 patients). Subconjunctival corticosteroid injection resulted in reduced dependence on systemic medications. CONCLUSION: Subconjunctival corticosteroid injection in eyes that failed other therapies is effective, reduces dependence on systemic medications, and did not result in scleral necrosis over a median follow-up period of 29 months.

Adolescent↗
PubMed2005

Acute aminoglycoside retinal toxicity in vivo and in vitro.

PURPOSE: Intentional and inadvertent intraocular administration of aminoglycosides is associated with cases of retinal toxicity. Clinical manifestations resemble a vaso-occlusive event and include edema, intraretinal hemorrhage, and nonperfusion detected by fluorescein angiogram. This study was conducted to measure the retinal function in avascular and isolated perfused retinas to separate vascular and neurologic effects of gentamicin. Enhanced understanding of the mechanism of gentamicin toxicity may lead to development of aminoglycosides that can be used to treat ophthalmic infections without retinal damage. METHODS: Whole animals and isolated rabbit and rat retina preparations were used to study the dose dependence and reversibility of toxicity on the ERG, with a 1- and a 10-mg/mL solution of gentamicin. The amplitude and implicit times of the a-, b-, and c-waves were measured before, during, and after exposure to the drug. RESULTS: In whole-animal ERG studies, intraocular administration of gentamicin eliminated the b-wave but left the a-wave intact. The c-wave was reduced in amplitude. Histopathologic evaluation demonstrated diffuse disruption of the nerve fiber layer and the inner plexiform layers. Isolated retinal studies showed that the b-wave was reduced in amplitude in the presence of low-dose gentamicin (1 mg/mL) and completely eliminated by high-dose gentamicin (10 mg/mL). This effect was reversible for short-term exposure to gentamicin. CONCLUSIONS: The results indicate that the initial loss of function due to exposure to aminoglycoside antibiotics is independent of the vascular supply. Elimination of the b-wave was dose dependent and reversible, indicating that a component of gentamicin toxicity is mediated through pathways other than vascular supply. Short-term effects are reversible, suggesting a receptor-mediated process.

Animals↗
PubMed2004

Clinical mini-review: systemic lupus erythematosus and the eye.

Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease, the exact etiology of which is unknown. It is characterized by the production of pathological autoantibodies which adhere to cellular surfaces or form immune complexes which deposit in tissue, leading to end-organ damage via inflammatory mechanisms including complement activation. SLE may manifest itself in any organ system. In the eye, keratoconjunctivitis sicca is the most common finding. Other ophthalmic sites of involvement include the cornea, conjunctiva, episclera, sclera, uveal tract, retina, vasculature, optic nerve, and orbit. Therapy varies based on the disease manifestation and severity.

Eye Diseases↗
PubMed2004

Magnetic resonance imaging of choroidal inflammation in Vogt-Koyanagi-Harada disease.

Acute binocular visual loss, photophobia, headache, and pulsatile tinnitus developed in a 51-year-old woman. Ophthalmologic examination showed bilateral optic disc edema with peripapillary nerve fiber layer hemorrhages. Lumbar puncture disclosed a monocytic pleocytosis. A diagnosis of Vogt-Koyanagi-Harada disease was made. Magnetic resonance imaging showed striking enhancement and thickening of the posterior ocular wall. A macular star figure appeared several days after prednisone treatment was begun. Laboratory evaluation was entirely negative. Within weeks, the clinical manifestations had resolved except for retinal striae. This is the third report of the magnetic resonance imaging visualization of choroidal inflammation in Vogt-Koyanagi-Harada disease and shows the imaging abnormalities in finer detail than earlier reports.

Choroid↗
PubMed2003

Nucleotide-induced restoration of conjunctival chloride and fluid secretion in adenovirus type 5-infected pigmented rabbit eyes.

We evaluated the role of extracellular UTP and other nucleotides in the regulation of chloride (JCl) and fluid secretion (JCl) across the pigmented rabbit conjunctiva. Jv was determined in freshly excised conjunctival tissues mounted between two buffer reservoirs maintained in an enclosed environment at 37 degrees C. Short circuit current (Isc) and 36Cl flux were measured using modified Ussing-type chambers. Fluid flux measurements were made with a pair of capacitance probes. After observing the baseline for 15 to 30 min, fluid flux was measured in the presence of mucosally applied nucleotides (10 microM) for a period of 30 min. Mucosal application of 10 microM each of UTP, UDP, ATP, ADP, AMP, adenosine, and ATP-gamma-S transiently stimulated fluid secretion across the conjunctiva to a significant extent for 10 to 15 min. Other nucleotides did not show any significant effect. The stimulation of fluid secretion correlated well with the stimulation in Isc (r2 = 0.85). UTP (0.1-1000 microM) led to a maximal increase in fluid secretion by 11.72 +/- 0.48 microl/(h x cm2) with an EC50 value of 10.39 +/- 1.08 microM. ATP (0.1-1000 microM) caused a maximal increase in fluid secretion by 11.89 +/- 0.88 microl/(h x cm2) with an EC50 value of 17.23 +/- 2.63 microM. Adenovirus type 5 (Ad5) infection significantly decreased both net 36Cl secretion across the conjunctiva by approximately 56% and the rate of fluid secretion by approximately 56%. UTP (10 microM), but not 1 mM 8-bromo-cAMP, was able to elicit a normal stimulatory response in the Ad5-infected tissues. In conclusion, mucosal application of purinergic nucleotides may be therapeutically important in restoring ion and fluid secretion in the diseased conjunctiva.

Adenosine↗
PubMed2003

Histopathology of corneal melting associated with diclofenac use after refractive surgery.

PURPOSE: To describe the histopathology of the cornea in 3 cases of corneal melting associated with diclofenac therapy after refractive surgery procedures. SETTING: Clinic and pathology laboratory. METHODS: Three cases of corneal melting associated with diclofenac therapy (2 after laser in situ keratomileusis [LASIK] and 1 after mini-radial keratectomy enhancement of a LASIK undercorrection) were studied using patient and referring physician interviews, chart reviews, and histopathologic examination of the corneal tissue. RESULTS: In all 3 cases, the flaps were dislocated and the stromal corneal bed was exposed. Diclofenac, generic or brand name, was used in all cases; in 1 case, both generic and brand name were used. Dosing and duration varied, but in all 3 cases diclofenac was used at least 4 times a day for at least 3 days after LASIK. Topical steroids were also prescribed, but 1 patient did not use them. Preoperative medical conditions were present in 2 cases. Histologic analysis showed evidence of an inflammatory response in advanced cases and keratolysis and lack of inflammatory cells in the flaps that were amputated early. CONCLUSIONS: The use of generic or brand-name diclofenac with or without adjunctive topical steroids after LASIK can be associated with corneal melting when the LASIK flap is dislodged and the corneal stromal bed exposed. Caution is recommended with diclofenac use after LASIK in such cases.

Adult↗
PubMed2003

Intraocular pressure in a Somali population living in the United States.

PURPOSE: Intraocular pressure is a risk factor for the development of glaucomatous optic neuropathy. With few exceptions, higher mean intraocular pressure and greater prevalences of glaucoma have been reported for individuals of African origin. This study was performed to compare the mean intraocular pressure of a group of ethnic East Africans living in the United States with that of Caucasians living in the same community. PATIENTS AND METHODS: Retrospective comparison of Somali patients 30 years of age or greater with age- and gender-matched Caucasian control subjects. All patients were seen in the same clinic in Seattle, Washington, between July 1996 and March 1998. Patients were excluded for conditions or medications affecting intraocular pressure and for a diagnosis of glaucoma. Mean intraocular pressure of the two populations was compared using an independent sample two-tailed t test. RESULTS: Following exclusions and defined age limits, 57 Somali patients and 57 Caucasian control subjects were included in the final analysis. Mean age of Somalis was 48.5 +/- 12.2 years versus 48.1 +/- 11.3 years for control subjects (P = 0.84). The mean intraocular pressure of Somalis was 13.76 +/- 3.63 mm Hg versus 13.94 +/- 2.78 mm Hg for control subjects (P = 0.77). CONCLUSION: Some populations of African origin may not have higher mean intraocular pressures compared with non-African populations. Consideration of ethnic and racial origins more specific than "African" should be given when evaluating intraocular pressure in individual patients.

Adult↗
PubMed2003

Pathogenic role of retinal microglia in experimental uveoretinitis.

PURPOSE: To devise methods for unequivocal identification of activated retinal microglia in experimental autoimmune uveoretinitis (EAU) and to investigate their role in the development of EAU. METHODS: A group of Lewis rats underwent optic nerve axotomy with the application of N-4-(4-didecylaminostyryl)-N methylpyridinium iodide (4Di-10ASP) at the axotomy site. On days 3, 14, and 38 after axotomy, the rats were killed, the eyes were enucleated, and the retinas were stained for OX42. Another group of such axotomized rats were immunized with S-antigen peptide and were killed on days 7 through 12 after the injection with peptide. The enucleated eyes were stained for OX42 and examined by confocal microscope. After axotomy, bone marrow (Y-->X) chimeric rats were injected with S-antigen peptide and were killed on days 10 and 12 after injection. The retinas were evaluated by PCR with Y-specific primers. Finally, a group of axotomized rats was injected with the S-antigen peptide and killed on days 6, 8, 9, and 10 after injection. Their enucleated eyes were examined for microglial expression of TNFalpha and for generation of peroxynitrite. RESULTS: In the axotomized, non-EAU eyes, 4Di-10ASP-labeled ganglion cells were detectable on days 3 and 14, and 4Di-10ASP-containing OX42-positive cells (microglia) were found in the nerve fiber and other inner retinal layers on days 14 and 38. The S-antigen peptide-injected rats showed migration of the microglia (4Di-10ASP-positive and OX42-positive) to the photoreceptor cell layer on day 9, and these cells increased in number at this site on day 10. No macrophages (OX42-positive and 4Di-10ASP-negative) were present at this early stage of EAU, but such cells appeared in the retina on days 11 and 12. PCR of the chimeric EAU retinas showed an absence of the Y chromosome-amplified product on day 10, but the presence of this product was detected on day 12. The expression of TNFalpha and generation of peroxynitrite were noted in the migrated microglia at the photoreceptor cell layer on days 9 and 10 of EAU. CONCLUSIONS: In the early phase of EAU, the microglia migrate to the photoreceptor cell layer where they generate TNFalpha and peroxynitrite. Such microglial migration and activation take place before infiltration of the macrophages. These findings indicate a novel pathogenic mechanism of EAU, in which retinal microglia may initiate retinitis with subsequent recruitment of circulation-derived phagocytes, leading to the amplification of uveoretinitis.

Animals↗
PubMed2002

A prospective evaluation of subconjunctival injection of triamcinolone acetonide for resistant anterior scleritis.

PURPOSE: Prospective evaluation of the efficacy and safety of subconjunctival triamcinolone injections for resistant, nonnecrotizing, anterior scleritis. DESIGN: Prospective, noncomparative, interventional case series. PARTICIPANTS: Twelve eyes of 10 consecutive patients seen in the Doheny Eye Institute between August 1999 and December 2000 with diffuse, nonnecrotizing anterior scleritis that was resistant to systemic antiinflammatory therapy. Eyes with a history of steroid response were excluded. INTERVENTION: Subconjunctival injection of triamcinolone acetonide to the areas of maximal inflammation. MAIN OUTCOME MEASURES: Scleritis activity, adverse treatment effects, and number of systemic medications required at the end of the follow-up period. RESULTS: Within 1 to 14 days after injection, complete resolution of signs and symptoms was achieved in 11 eyes and partial resolution in 1 eye. Two patients had one recurrence each, 2.5 and 11 months after injection. Six of 10 patients were able to discontinue all systemic therapy (prednisone +/- immunosuppressive drugs); the remaining 4 needed continued oral therapy for systemic indications. Transient ocular hypertension and subconjunctival hemorrhage occurred in one eye each. Median follow-up period was 15 months. No eye developed necrotizing scleritis. CONCLUSIONS: Subconjunctival injection of triamcinolone acetonide is a safe and effective treatment for resistant, nonnecrotizing anterior scleritis. It provides rapid effect, is well tolerated, and may spare patients the significant complications and side effects of systemic corticosteroid and immunosuppressive therapy.

Adult↗
PubMed2002

Massive mycobacterial choroiditis during highly active antiretroviral therapy: another immune-recovery uveitis?

PURPOSE: To describe the ocular presentation of disseminated mycobacterial disease occurring during immune-recovery in a patient with acquired immune deficiency syndrome (AIDS). STUDY DESIGN: Case report and literature review. PARTICIPANTS: A 41-year-old AIDS patient with a prior diagnosis of cytomegalovirus retinitis. METHODS: The patient developed progressive, bilateral multifocal choroiditis with panuveitis 2 months after beginning and responding to highly active antiretroviral therapy. His left eye became blind and painful and was enucleated. Pathologic examination revealed massive choroiditis with well-formed, discrete granulomas and multiple intracellular and extracellular acid-fast organisms within the choroidal granulomas. Culture and polymerase chain reaction of vitreous specimens revealed Mycobacterium avium complex (MAC). RESULTS: Empiric, and later sensitivity-guided, local and systemic antibiotic therapy was used to treat the remaining right eye, but it continued to deteriorate. Despite medical therapy, three vitrectomies and repeated intravitreal injections of amikacin, a total retinal detachment ensued. One week after the third vitrectomy, the patient died from mesenteric artery thrombosis in the setting of disseminated mycobacterial disease. CONCLUSIONS: This is the first report of ocular inflammation as the presenting finding in the recently recognized syndrome of immune-recovery MAC disease. Pathogenesis of this entity is related to an enhanced immune response to a prior, subclinical, disseminated infection. The formation of discrete granulomas, normally absent in MAC infections in AIDS, reflects this mechanism.

AIDS-Related Opportunistic Infections↗
PubMed2002

Vogt-Koyanagi-Harada disease.

Vogt-Koyanagi-Harada disease is a chronic, granulomatous systemic autoimmune disease with manifestations in the ocular, central nervous, auditory, and integumentary systems. The target of attack seems to be antigens associated with melanocytes. Patients are usually of Asian, Middle Eastern, Asian Indian, Native American, or Hispanic ethnicity, and complain of neurologic symptoms quickly followed by decreased vision caused by a choroiditis, frequently with exudative retinal detachments. Corticosteroids are the mainstay of therapy, but other immunosuppressive therapy may be required. Complications, including cataract, glaucoma, choroidal neovascular membrane formation, and subretinal fibrosis, may limit final visual acuity.

Humans↗