Neck and upper back pain among eye care professionals.

BACKGROUND: Ophthalmologists and optometrists have reported a higher prevalence of neck, hand/wrist and lower back pain than family medicine physicians. Work-related musculoskeletal disorders have not previously been studied in Saudi eye care professionals. AIMS: To determine the magnitude and determinants of neck and upper back pain among eye care professionals at a tertiary hospital in Saudi Arabia in 2013. METHODS: A cross-sectional study using a close-ended questionnaire to determine the frequency of neck and back pain and its association with age, sex, weight, comorbidities, duration of professional work, history of injury and physician sub-speciality. RESULTS: The response rate was 82% and 165 eye care professionals participated, 70% (113) of whom reported neck and back pain. The rate was similar in ophthalmologists and allied eye care professionals and among surgical and medical ophthalmologists. The prevalence rate of neck and upper back pain was not associated with number of years in the profession, comorbidities, self-reported weight or injury. Pain appeared to be associated with reported physical discomfort during professional activities (P < 0.01) but not with mental stress. Pain was thought to be work related by 50% of participants. A lower rate of neck and upper back pain was associated with regular exercise [odds ratio = 0.5 (95% confidence interval 0.2-0.9)]. CONCLUSIONS: Neck and back pain was reported by 70% of eye care professionals. The pain was graded as mild to moderate and improved when on holidays. Regular physical exercise appeared to prevent or reduce neck and upper back pain.

Expression of growth differentiation factor-5 and bone morphogenic protein-7 in intraocular osseous metaplasia.

BACKGROUND/AIMS: Intraocular bone is seen in a wide spectrum of ocular disorders. The pathogenetic mechanisms of bone formation in the eye are unclear. Growth differentiation factor-5 (GDF-5), bone morphogenic protein-7 (BMP-7), and transforming growth factor beta-1 (TGF beta1) are multifunctional cytokines that have important roles in bone formation. Immunohistochemistry was used to localise GDF-5, BMP-7, and TGF beta1 in the human eye to determine their role in intraocular bone formation. METHODS: Paraffin embedded sections from human eyes included fetal eyes (n = 5), normal adult eyes (n = 4), eyes with osseous metaplasia (n = 8), and eyes with focal fibrous metaplasia of the retinal pigment epithelium (RPE) without osseous metaplasia (n = 2). Immunohistochemistry was performed using indirect immunofluorescence with antibodies to GDF-5, BMP-7, and TGF beta1. The staining intensity was evaluated semiquantitatively in the RPE, retina, ciliary epithelium, and cornea; and analysed statistically. RESULTS: When compared with normal adult eyes, which showed no RPE immunoreactivity, the RPE metaplasia surrounding areas of osseous metaplasia showed mild GDF-5 and moderate BMP-7 (p = 0.004) intracytoplasmic immunoreactivity. In contrast, trace GDF-5 and mild BMP-7 staining was seen in zones of RPE fibrous metaplasia in areas not associated with osseous metaplasia. Mild intracytoplasmic TGF beta1 expression was seen in the RPE metaplasia surrounding the bone when compared with adult eyes. Both fetal and adult eyes showed trace to mild GDF-5 and BMP-7 labelling of the non-pigmented ciliary epithelium which was increased in the eyes with osseous metaplasia. In eyes with osseous metaplasia, a significant decrease in GDF-5 and BMP-7 labelling was noted in fetal keratocytes (p = 0.0159 for both antibodies) when compared to adult eyes. Also, a significant decrease in BMP-7 labelling was seen in keratocytes in eyes with osseous metaplasia (p = 0.0162). CONCLUSIONS: The increase in GDF-5, BMP-7, and TGF beta1 immunoreactivity in zones of RPE metaplasia in eyes with osseous metaplasia suggests that these proteins have an important role in intraocular ectopic bone formation.

Histopathological and immunohistochemical studies of lenticules after epikeratoplasty for keratoconus.

AIMS: To examine histopathological and immunohistochemical changes in lenticules and host of corneal buttons from patients who previously underwent epikeratoplasty for keratoconus. METHODS: 12 penetrating keratoplasty specimens from patients with keratoconus who had previously undergone epikeratoplasty, eight keratoconus, and seven normal corneas were examined. Immunostaining for Sp1, alpha1-proteinase inhibitor (alpha1-PI), and alpha2-macroglobulin (alpha2M) were performed. RESULTS: In nine of the 12 lenticules, the keratoconus-like disruptions were found in Bowman's layer. Peripheral and posterior keratocyte repopulation of the lenticules was observed in all cases. Keratocyte repopulation in the anterior and mid-stromal regions of the lenticules appeared related to the time since epikeratoplasty. Sp1 nuclear staining of the basal and wing epithelial cells was more intense in lenticules and keratoconus corneas than in normal corneas. Lenticular, host, and keratoconus keratocytes showed positive Sp1 staining, whereas staining was absent in normal corneas. Compared to normal corneas, alpha1-PI and alpha2M immunostaining was lower in the lenticules, host, and keratoconus specimens. CONCLUSIONS: The epithelial cells and keratocytes repopulated in the lenticules retain keratoconus-like biochemical abnormalities such as upregulation of Sp1 and downregulation of alpha1-PI and alpha2M. The authors speculate that both keratocytes and the corneal epithelium may participate in the development of keratoconus.

Endophthalmitis associated with the Ahmed glaucoma valve implant.

AIM: To investigate the rate, risk factors, clinical course, and treatment outcomes of endophthalmitis following glaucoma drainage implant (GDI) surgery. METHODS: A computerised relational database search was conducted to identify all patients who were implanted with Ahmed glaucoma valve (AGV) and developed endophthalmitis following surgery at the King Khaled Eye Specialist Hospital in Riyadh, Saudi Arabia, between 1 January 1994 and 30 November 2003. Only medical records of the patients who developed endophthalmitis were retrospectively reviewed. RESULTS: 542 eyes of 505 patients who were on active follow up were included in the study. Endophthalmitis developed in nine (1.7%) eyes; the rate was five times higher in children than in adults. Delayed endophthalmitis (developed 6 weeks after surgery) occurred in eight of nine eyes. Conjunctival erosion overlying the AGV tube was present in six of nine eyes. Common organisms isolated in the vitreous included Haemophilus influenzae and Streptococcus species. Multiple regression analysis revealed that younger age and conjunctival erosion over the tube were significant risk factors associated with endophthalmitis. CONCLUSION: Endophthalmitis is a rare complication of GDI surgery that appears to be more common in children. Conjunctival dehiscence over the GDI tube seems to represent a major risk factor for endophthalmitis. Prompt surgical revision of an exposed GDI tube is highly recommended.

Immunoreactivity against tau, amyloid precursor protein, and beta-amyloid in the human retina.

PURPOSE: Increased immunoreactivity (IR) of beta-amyloid and the amyloid-associated proteins tau and amyloid precursor protein (APP) in the brain have been linked to the pathogenesis of neurodegenerative disorders such as Alzheimer's disease. However, the expression of these proteins has not been investigated in the normal or diseased human retina. METHODS: Using immunohistochemical techniques, we examined the distribution and age-related changes of anti-tau-1, anti-tau-2, anti-APP, and anti-beta-amyloid IR in the human retina at various ages (n = 24), in retinitis pigmentosa (RP, n = 6), and in age-related macular degeneration (ARMD, n = 10). RESULTS: Tau-1 immunoreactivity was intense in the inner retinal layers and did not change with age or in RP. Eyes with ARMD showed less intense staining but exhibited a similar distribution. Tau-2 IR was faint and did not change with age but was mildly increased in the retinal pigment epithelium (RPE) of eyes with RP and in the retina of eyes with ARMD. APP IR was most prominent in the ganglion cell and nerve fiber layer, and it appeared to increase in ganglion cells of older persons and in RPE cells of eyes with RP and ARMD. Beta-amyloid IR was only detected focally in sub-RPE deposits in eyes from older persons. CONCLUSIONS: The proteins investigated in this study are present in the human retina. The staining pattern of tau is different from the brain, but it shows no age-related changes. The increased immunoreactivity of APP in retinal ganglion cells of older eyes and in RPE cells of eyes with RP and ARMD, as well as the patchy staining of beta-amyloid within sub-RPE deposits, might indicate a relationship of these proteins to retinal aging and possibly to retinal degeneration in RP.

Tau-2 immunoreactivity of corpora amylacea in the human retina and optic nerve.

PURPOSE: To characterize the constituents of corpora amylacea in the human retina and optic nerve. METHODS: Immunohistochemistry was performed on sections of retina, optic nerve, and brain tissue using antibodies against tau 1, tau-2, and amyloid precursor protein. RESULTS: Consistent anti-tau-2 immunoreactivity was noted in the corpora amylacea in the retina, optic nerve, and brain tissue, albeit with variations in pattern and intensity of staining. No immunoreactivity was observed with antibodies anti-tau 1 and anti-amyloid precursor protein. CONCLUSION: Our findings suggest the accumulation of possibly abnormal tau-2 within the corpora amylacea, which may be either astrocytic or axonal in origin.

Augmentation of intraocular inflammation by melanin.

The inflammatory response in endogenous uveitis or after anterior segment surgery was noted to be substantially greater in heavily pigmented eyes. Because varying amounts of melanin are released into the anterior chamber after intraocular inflammation, it was hypothesized that a proinflammatory effect of melanin might account for the enhanced inflammatory response in these eyes. To test this hypothesis, albino (BALB/c) or pigmented (C57BL/6) mice were challenged in the anterior chamber 2 weeks after a subcutaneous foot pad injection of horse serum or conalbumin dissolved in Freund's complete adjuvant. The degree of inflammation in the challenged eyes was determined by histologic examination 72 hr after the challenge. In all cases, the inflammatory infiltrate consisted mainly of polymorphonuclear leukocytes suggestive of an Arthus reaction. An anterior chamber challenge of horse serum-sensitized BALB/c or C57BL/6 mice with horse serum alone resulted in mild inflammation, which was augmented markedly by challenge with a combination of horse serum and melanin. The presence of melanin in the anterior chamber similarly increased the inflammatory response of conalbumin-sensitized mice to anterior chamber challenge with conalbumin. Melanin in the anterior chamber also significantly (P less than 0.05) augmented the inflammatory response of conalbumin-sensitized mice to a horse serum challenge, but it did not significantly augment the inflammatory response of horse serum-sensitized mice to a conalbumin challenge. The heterologous antigens induced minimal inflammation in the absence of melanin. Injection of melanin alone did not evoke an inflammatory response. Ocular challenge with melanin alone or in combination with antigen induced minimal inflammation in nonsensitized mice. However, preincubation of melanin with sera from horse serum-sensitized mice significantly increased its proinflammatory capacity when injected with horse serum into the anterior chamber of nonsensitized mice. In vitro binding studies using fluorescein isothiocyanate-conjugated mouse immunoglobulin G showed a high binding capacity of melanin for immunoglobulin G. It was concluded that the presence of free melanin in the anterior chamber can increase intraocular inflammation. Although the mechanism(s) by which melanin augments inflammation has not been defined, these data suggest that the binding of serum components (such as antibodies) to melanin may contribute to its proinflammatory effect.

Benign lymphoid hyperplasia of the conjunctiva in children.

Benign lymphoid hyperplasia of the conjunctiva occurs infrequently in children, and its presentation, clinical course, and appropriate management are not well established. We describe 2 children with nasal conjunctival masses that on pathological examination demonstrated benign lymphoid hyperplasia. Local irradiation of residual tissue was deferred, and the lesions remained stable for 1 year in one case and for 3 1/2 years in the other case. No systemic involvement had occurred. Although the natural history of extranodal lymphoid hyperplasia in children is poorly documented, most cases of nodal lymphoid hyperplasia in children are at very low risk of malignant transformation. Careful observation for local and systemic disease is indicated for ocular adnexal lymphoid hyperplasia in children until a more complete understanding of its natural history is available.

Serum autoantibodies to optic nerve head glycosaminoglycans in patients with glaucoma.

BACKGROUND: Serum autoantibodies that cross-react with glycosaminoglycans have been proposed to play a significant role in specific tissue injury in patients with systemic autoimmune diseases. OBJECTIVE: To investigate whether serum immunoreactivity to glycosaminoglycans is present in patients with glaucoma who have aberrant serum autoantibodies to DNA, RNA, nuclear proteins, or retinal proteins, as proteoglycans and their glycosaminoglycan side chains are important components of the optic nerve head and its vasculature. METHODS: We performed Western blotting using patient serum samples and human optic nerve head homogenates that were treated with or without specific glycosaminoglycan degrading enzymes. Monoclonal antibodies that recognize different determinants of glycosaminoglycans were used to identify specific substrate antigenicity. We compared the serum immunoreactivity to glycosaminoglycans in 60 age-matched patients with normal-pressure glaucoma, 36 patients with primary open-angle glaucoma, and 20 control subjects by enzyme-linked immunosorbent assay. In addition, immunohistochemistry was performed to compare the distribution patterns of glycosaminoglycans in the optic nerve head of postmortem eyes of age-matched patients with normal-pressure glaucoma, primary open-angle glaucoma, and control subjects. RESULTS: Western blotting demonstrated that serum samples from patients with glaucoma who have circulating autoantibodies can recognize optic nerve head proteoglycans, including chondroitin sulfate and heparan sulfate. The level of serum autoantibodies binding purified chondroitin sulfate and heparan sulfate glycosaminoglycans in an enzyme-linked immunosorbent assay was approximately 100% higher in patients with normal-pressure glaucoma than that in control subjects and approximately 50% higher than that in patients with primary open-angle glaucoma. We also observed increased immunostaining of glycosaminoglycans in the optic nerve head of eyes with glaucoma, particularly those with normal intraocular pressure, compared with control eyes. CONCLUSION: There are increased levels of autoantibodies recognizing glycosaminoglycans of the optic nerve head in the serum samples of some patients with glaucoma. CLINICAL RELEVANCE: These autoantibodies may increase the susceptibility of the optic nerve head to damage in these patients by changing the functional properties of the lamina cribrosa, its vasculature, or both.

Matrix metalloproteinases and tumor necrosis factor alpha in glaucomatous optic nerve head.

OBJECTIVE: To study expression and location of matrix metalloproteinases (MMPs) and tumor necrosis factor alpha (TNF-alpha) in glaucomatous optic nerve heads, which are known to be secreted in response to a variety of neuronal injury. METHODS: Four postmortem eyes from patients with primary open-angle glaucoma, 7 eyes from patients with normal-pressure glaucoma, and 4 eyes from age-matched normal donors were studied by immunohistochemistry. The sections of the optic nerve heads were examined after immunostaining with antibodies to MMPs (MMP-1, MMP-2, and MMP-3), TNF-alpha, or TNF-alpha receptor 1. RESULTS: The intensity of the immunostaining and the number of stained cells for MMPs, TNF-alpha, or TNF-alpha receptor 1 were greater in the glaucomatous optic nerve heads, particularly in eyes with normal-pressure glaucoma compared with age-matched controls. Positive immunostaining was observed in all regions of the glaucomatous optic nerve heads, but most prominently in the postlaminar region. Immunostaining was observed mainly in glial cells and their processes around the axons and blood vessels and in pial septae. CONCLUSION: There is increased immunostaining for MMPs, TNF-alpha and TNF-alpha receptor 1 in the glaucomatous optic nerve head, which suggests increased expression of these proteins in glaucoma and thereby implies a role in the tissue remodeling and degenerative changes seen in glaucomatous optic nerve heads. CLINICAL RELEVANCE: The MMPs and TNF-alpha may be components of astroglial activation that occurs in glaucomatous optic nerve heads. The biological alterations in the expression of these proteins may play a role in the progression of glaucomatous optic neuropathy.

Amelioration of light-induced retinal degeneration by a calcium overload blocker. Flunarizine.

Although free radical formation and lipid peroxidation have been implicated in photoreceptor degeneration following continuous light exposure, recent evidence led us to hypothesize that excessive stimulation of the photoreceptor cells in prolonged light exposure may cause intracellular calcium overload and consequent photoreceptor cell injury. To test this hypothesis, we studied the effects of flunarizine hydrochloride, a calcium overload blocker that inhibits the inositol 1,4,5-triphosphate-induced release of intracellular stores of calcium, in an established rat model of light-induced retinal degeneration. Light and electron microscopic examination of the flunarizine-treated retinas revealed remarkable preservation of the retinal pigment epithelium, rod inner and outer segments, nuclei, and synapses of the photoreceptor cells at all phases of the recovery period. This observation was further supported by morphometric evaluation of the outer nuclear layer thickness, which revealed a greater preservation of the photoreceptor nuclei in the drug-treated animals at 6 and 14 days after exposure. In addition, the rhodopsin levels in the flunarizine-treated retinas were also significantly higher than in the controls in all phases of recovery. The ability of flunarizine to ameliorate light-induced retinal degeneration in the rat supports our hypothesis that elevated intracellular calcium may indeed play a role in light-induced photoreceptor degeneration.

Apoptotic photoreceptor cell death after traumatic retinal detachment in humans.

OBJECTIVE: To determine the mechanism of photoreceptor cell death after traumatic retinal detachment in humans. DESIGN: Clinical records from 1975 to 1993 of 75 patients, whose eyes were enucleated after traumatic retinal detachment, were reviewed for age, sex, previous ocular or systemic medical history, interval from initial trauma to enucleation, visual acuity, and types of trauma. The patients were divided into five groups of 15 cases each, based on the interval from initial trauma to enucleation. The retinal tissue was examined for two markers of apoptosis: (1) nicked nuclear DNA in situ by the terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick end labeling (TUNEL) technique and (2) apoptotic bodies by light and electron microscopy. RESULTS: Of the 75 cases of ruptured globe and traumatic retinal detachment that were evaluated, 19 eyes (25.3%) showed TUNEL-positive labeling of photoreceptor cells. Nicked nuclear DNA was detected in photoreceptor cells of detached retinas as early as 8 hours after trauma. The detached retinas in seven of 15 eyes enucleated within 2 days after ocular trauma showed TUNEL-positive photoreceptor nuclei. The number of cases showing TUNEL-positive photoreceptor nuclei decreased as the interval between initial trauma and enucleation increased. The TUNEL-positive photoreceptor cells could still be seen in the detached retinas of two eyes enucleated 22 days after trauma. Light microscopy disclosed condensation and fragmentation of photoreceptor nuclei in the detached retinas. Electron microscopy showed structures resembling apoptotic bodies phagocytosed by neighboring cells in the TUNEL-positive retinas. CONCLUSIONS: Apoptosis is an important mechanism of photoreceptor cell degeneration in the early stage after traumatic retinal detachment in humans.

Effect of melanin on traumatic hyphema in rabbits.

OBJECTIVE: To investigate the role of melanin in influencing the clearance of traumatic hyphema and in the incidence of rebleeds following the hyphemas. METHODS: Hyphemas were induced in 30 eyes of New Zealand white albino rabbits using an Nd:YAG laser. A total of 3.75 mg of synthetic melanin suspended in 0.1 mL of balanced salt solution was introduced into the anterior chambers of 16 animals. A total of 0.1 mL of balanced salt solution was injected into 14 control eyes. Hyphema levels were measured by a masked observer (V.D.B.) daily for 15 days. Pairs of animals were sacrificed at 1, 3, 5, 10, and 15 days and the eyes studied histologically. RESULTS: Hyphemas were consistently produced in all eyes with mean+/-SD levels of 1.44+/-0.22 mm and 1.57+/-0.24 mm in the melanin-treated and control eyes, respectively. The clearance of hyphemas in the melanin-treated eyes was significantly prolonged throughout the study (P<.001). The rate of rebleed in the melanin-treated group was 18.8% and in the control group was 7.1% (P<.01). Histologically, both groups showed variable degrees of blood in the anterior chambers and trabecular meshwork. In addition, the melanin-treated eyes showed free melanin, melanin-laden macrophages, and an inflammatory response in the anterior chamber and trabecular meshwork that was greater than that in the control eyes. Melanin-treated eyes with rebleeds showed organized hemorrhage with neovascularization. CONCLUSIONS: The presence of melanin results in a significantly prolonged course of hyphemas and may influence the rate of rebleeds. Occlusion of the trabecular meshwork with melanin-laden macrophages and inflammation may be the mechanisms responsible for these effects. CLINICAL RELEVANCE: The release of melanin into the anterior chamber during ocular trauma may be partly responsible for the susceptibility of darker-pigmented individuals to more serious complications following a traumatic hyphema.

Transscleral iontophoresis of dexamethasone.

Transscleral iontophoresis has been suggested to be a potentially useful noninvasive technique in intravitreal introduction of ionizable drugs, such as cefazolin sodium, ticarcillin disodium, and gentamicin sulfate. To investigate the usefulness of this technique in the administration of corticosteroids, we performed transscleral iontophoresis of dexamethasone sodium phosphate (300 mg/mL, 20 mmol/L edetic acid [EDTA]) into rabbits at a current of 1.6 mA for 25 minutes. Eyes were enucleated at different time intervals and frozen in liquid nitrogen. The frozen vitreous bodies and adherent sensory retina were collected and sonicated, and dexamethasone levels were measured using high-pressure liquid chromatography. In addition, to study the facilitation of drug transport by cryotherapy, a second group of rabbits were given a single application of cryotherapy (-78 degrees C, 45 seconds) 3, 7, and 14 days before iontophoresis in the same region. Without cryotherapy, the initial level of dexamethasone in the vitreous body-sensory retina after iontophoresis was 139.3 +/- 51.5 mg/L (mean +/- SE) (n = 6) with a half-life of less than 2 hours. In the cryotreated group, the levels of dexamethasone immediately after iontophoresis 3, 7, and 14 days after cryotherapy were 61.5 +/- 31.7 (n = 6), 88.4 +/- 55.1 (n = 6), and 112.2 +/- 32.5 (n = 6) mg/L, respectively, indicating that levels were lower compared with the group without cryotherapy. Our results suggest that a high dose of dexamethasone can be delivered by using this noninvasive technique and that cryotherapy before iontophoresis does not increase drug levels in the vitreous body.

Protective effects of flunarizine on ischemic injury in the rat retina.

Intracellular calcium overload has been implicated to be a major factor in triggering cell death after ischemic neuronal injury. We investigated the effects of flunarizine hydrochloride, a calcium-overload blocker, on pressure-induced retinal ischemia in a rat model. Retinal ischemia was induced in intraocular pressure to 110 mm Hg for 45 minutes. Two regimens of treatment with flunarizine were examined: (1) prophylactic treatment, in which flunarizine was administered before ischemia and in the early phase of reperfusion; and (2) postischemic treatment, in which flunarizine was administered only in the early phase of reperfusion. Injury was evaluated morphologically and morphometrically by measuring the thickness of the inner retinal layers on plastic-embedded retinal sections and by counting the retinal ganglion cells on retinal flat preparations. By morphologic and morphometric criteria, a significant but partial protection of the inner retinal layers was noted in the groups given either regimen. This protective effect of flunarizine suggests that elevated intracellular calcium concentration may play an important role in ischemic retinal injury.

Ocular manifestations of Whipple disease: an atypical presentation.

A 62-year-old man developed bilateral granulomatous iridocyclitis after uncomplicated cataract surgery. On ophthalmic examination, we found moderate inflammation in the anterior chamber and vitreous, with granular crystalline deposits on the iris, intraocular lens, and capsular bag. Biopsy of the lens capsule and vitreous revealed periodic acid-Schiff-positive, diastase-resistant bacilli consistent with Tropheryma whippelii. Electron microscopy and polymerase chain reaction confirmed the diagnosis of Whipple disease. A jejunal biopsy specimen also revealed T whippelii. Treatment with trimethoprim-sulfamethoxazole, cefixime, rifampin, and doxycycline resulted in improvement of systemic symptoms, but intraocular inflammation persisted. Intraocular inflammation was eventually reduced with the intravenous administration of ceftriaxone sodium.

Heterogeneity in macular corneal dystrophy.

Macular corneal dystrophy is an autosomal recessive disorder in which abnormal deposits in the corneal stroma have been identified. We examined the corneal buttons of 12 patients, who had clinical features of macular dystrophy, by histochemical staining, transmission electron microscopy, and immunohistochemical techniques. All corneas exhibited positive staining with Muller Mowry's colloidal iron. Using monoclonal antibodies 1/20/5-D-4, J-10, J-19, and J-36 that recognize specific sites on the sulfated keratan sulfate molecule, we stained corneal sections by an avidin-biotin-peroxidase complex method and identified two groups of macular corneal dystrophy. One group consisting of four corneas reacted positively with all four antibodies, and the other group consisting of eight corneas did not react with any of the antibodies used. These results confirmed those recently presented by Yang et al that there may be subgroups of macular dystrophy that can be identified by immunohistochemical methods. Also, serum levels of sulfated keratan sulfate were determined in seven patients. One patient who displayed a normal level of serum keratan sulfate had positive corneal immunoreactivity. Of the six patients who lacked serum keratan sulfate, four showed negative and two had positive corneal immunostaining, suggesting at least three subgroups in the disease. An attempt was made to correlate the clinical features, histochemical-staining characteristics, and ultrastructural morphology with the immunoreactivity to keratan sulfate antibodies, but no correlations could be made.

Bilateral orbital emphysema from compressed air injury.

PURPOSE: To describe a patient who developed bilateral subconjunctival and orbital emphysema after an automobile tire explosion. METHOD: Case report. RESULTS: A 60-year-old man sustained bilateral ocular injury after a tire explosion. Ophthalmic examination disclosed bilateral subconjunctival air, with no visible conjunctival laceration. Computed tomography showed orbital emphysema, with no evidence of orbital fracture. Follow-up examination 2 weeks after the injury disclosed resolution of the subconjunctival air. Best-corrected visual acuity in the right eye was decreased after the explosion but improved to the baseline level of 20/40 2 weeks after the injury. CONCLUSION: Subconjunctival and orbital emphysema can occur from high-pressure air injury in the absence of an obvious entry site.

An immunohistochemical study of gelsolin immunoreactivity in corneal amyloidosis.

A variant of the actin-modulating protein gelsolin has recently been identified as a component of the amyloid deposits in familial amyloidosis, Finnish type (Meretoja's syndrome), and has been demonstrated immunohistochemically in amyloid deposits in the cornea, and in the skin, kidney, heart, thyroid gland, salivary gland, and rectum of patients with this disease. With the use of immunohistochemistry involving an antibody against gelsolin, we examined a corneal specimen from a patient with Meretoja's syndrome and 14 corneal specimens with lattice dystrophy type I, atypical lattice dystrophy, polymorphic amyloid degeneration, primary familial amyloidosis, or secondary corneal amyloidosis. Our results showed the presence of a gelsolin-related protein either within or around corneal amyloid deposits in nine of the 15 specimens and markedly increased anti-gelsolin immunoreactivity of the corneal keratocytes in 13 of the 15 diseased corneas. These data indicated that the accumulation of gelsolin may be seen in various forms of amyloidosis and may not be confined to Meretoja's syndrome.