Biomedical subjects
Publications and source records attributed to E M Messmer.
Ocular leprosy is rarely seen in developed countries. We report the long-term follow-up of a patient with bilateral uveitis, glaucoma, and keratitis. Skin, iris and aqueous humor biopsies disclosed abundant Wade-Fite-positive organisms consistent with Mycobacterium leprae. Leprosy must be considered in the differential diagnosis of keratitis and uveitis.
OBJECTIVE: To analyze the referral patterns and diagnosis of uveitis during the past decade in a large tertiary eye center. DESIGN: The records of 1237 patients with uveitis referred to the Immunology Service of the Massachusetts Eye and Ear Infirmary from 1982 to 1992 were classified and analyzed. Data regarding sex, race, nationality, referral site, ages at presentation and onset of uveitis, ocular involvement, clinical characteristics, ocular condition, and systemic disease associations were obtained. RESULTS: The mean age at onset of uveitis was 37.2 years; the male-to-female ratio was 1:1.4. Most patients were white (85.8%), born in the United States (83.1%), and referred from within New England (84.7%). Anterior uveitis was most common (51.6%), followed by posterior uveitis (19.4%), panuveitis (16.0%), and intermediate uveitis (13.0%). Chronic (58.3%), nongranulomatous (77.7%), and noninfectious (83.1%) were the most frequent types of uveitis. The most common entities included idiopathic (34.9%), seronegative spondyloarthropathies (10.4%), sarcoidosis (9.6%), juvenile rheumatoid arthritis (5.6%), systemic lupus erythematosus (4.8%), Behçet's disease (2.5%), and the acquired immunodeficiency syndrome (2.4%). CONCLUSION: The appearance of new uveitic entities, such as the acute retinal necrosis syndrome, multifocal choroiditis and panuveitis, birdshot retinochoroidopathy, and acquired immunodeficiency syndrome-related uveitis, and the reemergence of the classic infectious causes of uveitis, tuberculosis and syphilis, have changed the way we approach the diagnosis and management of posterior and panuveitis at the Massachusetts Eye and Ear Infirmary.
UNLABELLED: Recently, good functional and anatomical results have been reported in treating full thickness macular holes. Only a few studies describe a removal of a membrane at the vitreoretinal interface after having removal of the vitreous and its cortex. To demonstrate the beneficial effects of removing this membrane at the vitreoretinal interface we present our functional and anatomical results in this retrospective study. PATIENTS: Altogether, 42 patients (27 women, 15 men) with an average age of 66.7 years and full thickness idiopathic macular holes stage II and III/IV (21 patients respectively) were retrospectively analysed. The minimum follow-up was 6 months. To reattach the macular, an intraocular gas tamponade was used in 36 patients (15% C2F6) and 6 patients were treated with an 20% SF6 gas tamponade. RESULTS: Six months after operation, patients in the main group (42 patients) showed visual improvement in 53% (22 patients): 26% (11 patients) showed no change in visual acuity before and after operation. A deterioration was present in 21% (9 patients). In the group of patients in which a membrane at the vitreoretinal interface had been removal 68% (22 patients) showed improved visual acuity. In all 26% (8 patients) showed no change and in one case a deterioration was noticed. After removal of a membrane at the vitreoretinal interface no further macular hole was seen in 80% (25 patients). In this group, 90% (28 patients) complained of metamorphosia before operation. In the group of patients in which were no membrane at the vitreoretinal interface had been removed (11 patients), 73% (8 patients) showed a deterioration in visual acuity, no patient showed improved visual acuity and 27% (3 patients) retained the same level of visual acuity. No macular hole was noticed 6 months postoperatively in 27% (3 patients) in this group. In all 36% (4 patients) in this group complained of metamorphopsia before operation. CONCLUSION: Removal of a membrane at the vitreoretinal interface in patients with idiopathic macular holes stage II in IV improves functional and anatomical results. Metamorphosia is reduced significantly after removal of that membrane. According to our studies, metamorphosia is an indicator for the presence of a membrane at the vitreoretinal interface. Our results suggest that there are different types of idiopathic macular holes with a different pathogenesis in those where a membrane at the vitreoretinal interface could not be removed and those where it is possible to remove it. Cases where removal of this structure should be attempted show better functional and anatomical results. Studies using adjuvants, e.g. autologous platelet concentrate or transforming growth factor beta 2, should take into account that two different types of idiopathic macular holes exist.
The incidence of a macular hole in the fellow eye of patients with macular hole stage I-IV according to Gass is observed in 3-14% of cases. The development of a macular hole over a period of 19-54 months is reported to occur in 1-22% of patients. Our clinical impression made us suspect a much higher number of changes at the vitreomacular interphase in the generally asymptomatic "second eye" already at first presentation in the hospital. We retrospectively examined 88 patients who presented with a macular hole between January and October 1994. We investigated the frequency of a macular hole or macular pucker in the fellow eye, taking into consideration that many common pathogenetic factors were described for these changes of the vitreoretinal interphase. We further examined the difference in number and appearance of macular pathology in the fellow eye between patients who had macular hole surgery in their "first eye" and patients whose "first eye" was observed. The group of patients whose "first eye" was operated on showed a macular hole stage I or stage II in 8% each in the "second eye", and a macular hole stage III/IV in 6% of cases. Patients whose "first eye" was observed were found to have only early macular holes in 18% of fellow eyes. Altogether, the fellow eye of patients with macular hole exhibited also a macular hole in 21% of patients and a macular pucker in 7% of patients. The incidence of pathological changes at the vitreomacular interface in 28% of the fellow eyes of patients with macular hole is higher than ever reported in the literature. The presence of early macular holes as well as early macular puckers supports clinically the thesis of common factors in the pathogenesis of these two disorders. As we only reviewed the incidence of pathological charges in this study, a much higher number of developing macular holes and macular puckers has to be expected in the fellow eye of patients with macular hole over a certain time period.
During intraocular silicon oil tamponade, recurrent vitreoretinal membranes can become clinically relevant and may need surgical excision. We investigated 40 PVR and 10 diabetic membranes which had formed during intraocular tamponade with highly purified silicone oil (5000 cs). The membranes were investigated by light and electron microscopy with respect to silicone oil-specific alterations. The participating cells were differentiated immunohistochemically. Mechanisms of intercellular growth regulation were analyzed by the use of antibodies against cell adhesion molecules and growth factor receptors (PDGFr-B). Most of the membranes showed typical signs of the underlying disease process. However, seven PVR and four diabetic membranes had specific interstitial and intracellular vacuoles which were considered to be silicone oil droplets. The phagocytosing cells were macrophages, partially embedded within vitreous residues. T-lymphocytes can be drawn to the area of macrophage activity by the expression of ICAM-1 and LFA-1. The residual parts of the membranes are typical vitreoretinal membranes. The receptors for PDGF, fibronectin and laminin were negative, but the receptors for collagen and vitronectin were positive within these membranes. The silicone oil-specific macrophage reaction might be supported by emulsified silicone oil droplets, which might get phagocytosed at a certain size. The secondary inflammatory reactions can further enhance silicone oil emulsification and start a vicious circle. Nevertheless, the underlying disease process seems to be much more important in stimulating recurrent membrane formation than silicone oil-specific cell reactions.
The onset of necrotizing scleritis (NS) and peripheral ulcerative keratitis (PUK) in the clinical course of rheumatoid arthritis (RA) may reflect the presence of systemic, potentially lethal vasculitis. In an effort to better characterize this subset of patients with severe RA-associated corneal and/or scleral inflammation and to analyze the efficacy of therapy, we reviewed our experience in the medical and surgical management of 16 tertiary referral cases (25 eyes) unresponsive to aggressive conventional therapy with topical and systemic steroids as well as with systemic nonsteroidal drugs. Cytotoxic immunosuppressive therapy was instituted in all patients with NS and/or PUK. Cyclophosphamide and methotrexate were the most successful agents used. Cytotoxic immunosuppressive drugs in conjunction with early aggressive surgical treatment halted the relentlessly progressive inflammation and preserved the integrity of the globe in 92% of eyes. Visual acuity could be stabilized or improved in 83% of patients with NS and in 68% of patients with PUK.
Natural killer (NK) cells and acquired cell-mediated immunity effector cells (delayed type hypersensitivity (DTH) and cytotoxic T lymphocytes (CTL)) have been reported to play a vital role in the defence of the host against tumour and viral infections in locations other than the eye. A vigorous cellular inflammatory response to viral infections of the cornea, however, with the attendant damage to the corneal clarity, has obvious evolutionary disadvantages, and a substantial body of evidence indicates that in animals (e.g. mice) which are highly susceptible to inflammatory destruction of the cornea following corneal encounter with herpes simplex virus, it is the animal's immunological/inflammatory response which is responsible for the corneal damage. We examined the role of natural killer cells in the development of herpes stromal keratitis (HSK) in NK-deficient (C57BL/6J-bgj (beige)) mice and their NK-competent (C57BL/6J (black) relatives. The beige (NK-deficient) mice were just as resistant to HSK as were the black mice. We also studied the effects of NK cell depletion of BALB/c Igh-1 disparate congenic mice. C.AL-20 (Igh-1d) mice are ordinarily highly susceptible to necrotising HSK. In vivo NK-cell depletion in these mice significantly decreased the incidence and severity of HSK in these animals (p < 0.0005). Corneas from untreated C.AL-20 mice contained T cells, macrophages and NK cells. The corneal infiltrate from NK-depleted C.AL-20 mice consisted of T cells and macrophages but no NK cells. These data indicate that NK cells are participants in the development of HSK in the murine model of this disease.
The onset of peripheral ulcerative keratitis in the course of a connective tissue disorder, such as rheumatoid arthritis, relapsing polychondritis, or systemic lupus erythematosus, may reflect the presence of potentially lethal systemic vasculitis. Moreover, peripheral ulcerative keratitis may be the first sign of systemic necrotizing vasculitis in patients with Wegener's granulomatosis, polyarteritis nodosa, microscopic polyangiitis, or Churg-Strauss syndrome. Although the exact pathogenesis of this severe corneal inflammation and destruction is not well understood, evidence points to a dysfunction in immunoregulation with immune complexes formed in response to autoantigens or to some unknown microbial antigen depositing in scleral and limbal vessels. These events lead to changes that are mainly responsible for the resulting tissue damage. In pauci-immune vasculitides positive for antineutrophil cytoplasmic antibodies, cell-mediated cytotoxicity may play an important role in the pathogenesis of peripheral ulcerative keratitis. Untreated systemic conditions such as those mentioned above may carry a grave prognosis for the eye and may also be life-threatening. Immunosuppressive therapy with corticosteroids and cytotoxic agents is, we believe, mandatory in the treatment of these multisystem disorders associated with vasculitic peripheral ulcerative keratitis.