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D A Jabs

Publications and source records attributed to D A Jabs.

At least 91 records · Page 5Linked to original sources
PubMed1991

Retinal detachments in patients with cytomegalovirus retinitis.

Retinal detachments are a recognized complication of cytomegalovirus retinitis. In a series of 145 patients with cytomegalovirus retinitis, 38 (26%) developed retinal detachments. The cumulative probability of a retinal detachment 1 year after the diagnosis of cytomegalovirus retinitis was 50%. Detachments were associated with increased size of the cytomegalovirus lesion and with lesions extending anteriorly up to the ora serrata. Treatment with an anticytomegalovirus drug appeared to delay the time to detachment. Median survival time after the diagnosis of retinal detachment was 9 months. In our study, vitrectomy with silicone oil as the initial surgical procedure was the most effective approach. Successful anatomic reattachment of the retina was achieved in 70% of patients undergoing this procedure. Despite the success of surgery, the visual outcome was disappointing, with only 20% of eyes achieving a final visual acuity of 5/200 or better.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Optic disc edema after bone marrow transplantation. Possible role of cyclosporine toxicity.

Bone marrow transplantation has become widely used in the treatment of aplastic anemia and leukemia. Cyclosporine is used as prophylaxis against graft-versus-host disease. The authors report on eight cases of optic disc edema in patients taking cyclosporine after allogenic bone marrow transplant. Thorough evaluation revealed a possible alternate cause in two cases. In all cases, the optic disc edema resolved after discontinuing or decreasing the cyclosporine. Although cyclosporine has not previously been associated with optic disc edema, it has been implicated as the cause of a variety of neurologic side effects. Bone marrow transplant patients taking cyclosporine should be followed for the development of optic disc edema.

Adolescent↗
PubMed1991

Autoimmune ocular disease in MRL/Mp-lpr/lpr mice is suppressed by anti-CD4 antibody.

MRL/Mp-lpr/lpr(MRL/lpr) mice spontaneously have a systemic autoimmune disease, characterized by vasculitis, lymphadenopathy, glomerulonephritis, and autoantibody formation. Among the many autoimmune lesions present are focal ocular inflammatory infiltrates, involving the choroid and sclera. These lesions appear to be related to the vasculitis seen in MRL/lpr mice and are mediated by L3T4-positive helper T-cells (CD4-positive T-cells). Systemic treatment of MRL/lpr mice with a monoclonal anti-L3T4 antibody (anti-CD4) resulted in a dramatic reduction of both the frequency and severity of the ocular disease, supporting the hypothesis that the CD4-positive T-cells play an essential role in the pathogenesis of the choroiditis and scleritis in this strain.

Animals↗
PubMed1991

Murine models of Sjögren's syndrome. Evolution of the lacrimal gland inflammatory lesions.

Lacrimal gland inflammation develops in a number of autoimmune mice, including the MRL/Mp-lpr/lpr (MRL/lpr), MRL/Mp(-)+/+ (MRL/+), and NZB x NZW F1 hybrid (NZB/W) strains. The authors studied the evolution of this process, MRL/lpr mice had inflammatory lesions at 4 weeks old. The lesions had enlarged by 2 months and were fully developed by 4 to 5 months of age. In MRL/+ mice, 4-week-old mice had no lesions, although some focal inflammation was detectable at 3 months old. Significant abnormalities were present at 6 months, and persisted and increased throughout life, with all mice having extensive lesions at 18 months or older. In NZB/W mice, the authors detected no lesions until 6 months of age, and these lesions were fully developed in 9 months. Immunocytochemical profiles, of the cell types infiltrating the lacrimal gland, showed differences not only between the strains, but also in each strain as inflammation progressed. All three types of mice had L3T4+ T cells as the major lymphocyte component, although MRL/+ had significantly more Lyt 2+ T cells than the other strains. NZB/W mice had significantly more B cells than the two MRL substrains. In both NZB/W and MRL/+ mice, there was a significant increase in the B cell population, and a decrease in the percentage of L3T4+ T cells. There was a significant decline in Lyt 2+ T suppressor/cytotoxic cells in both NZB/W and MRL/lpr mice. This last finding was consistent with the more rapid development of inflammation in these strains than in the MRL/+ mice, where Lyt 2+ T suppressor/cytotoxic cells persist. Together, these results indicate that the autoimmune response in murine models of Sjögren's syndrome is a dynamic, evolving process with strain-related changes in lymphocyte subsets.

Animals↗
PubMed1991

Ocular inflammation in MRL/Mp-lpr/lpr mice.

A systemic autoimmune disease spontaneously developed in MRL/Mp-lpr/lpr (MRL/lpr) mice. The disease was characterized by vasculitis, lymphadenopathy, glomerulonephritis, and autoantibody formation. Among the many autoimmune lesions are focal ocular inflammatory infiltrates involving the choroid and sclera. Of 104 mice examined histologically, the sclera was most often involved, with 30% of mice 5 months of age or older having scleral lesions that were often centered around small arteries. The choroid was the second most frequently involved tissue, with focal inflammation developing in 16% of these mice. Immunohistologic analysis of the ocular infiltrates showed that most of the mononuclear cells seen were L3T4 + T cells (CD4+ helper T cells), suggesting that the process was largely T cell-mediated. Smaller numbers of B cells and Lyt 2+ T suppressor/cytotoxic cells were seen. No such lesions were seen in congenic MRL/Mp- +/+, (NZBxNZW) F1 hybrid mice, and control BALB/c mice; vasculitis did not develop in all of the mice. These results suggest that the ocular lesions in MRL/lpr mice may be a model for ocular involvement in patients who have systemic necrotizing vasculitis.

Animals↗
PubMed1990

Paraneoplastic pemphigus. An autoimmune mucocutaneous disease associated with neoplasia.

BACKGROUND AND METHODS: We describe five patients with underlying neoplasms in whom painful mucosal ulcerations and polymorphous skin lesions developed, usually with progression to blistering eruptions on the trunk and extremities. Histologic examination showed vacuolization of epidermal basal cells, keratinocyte necrosis, and acantholysis. Immunofluorescence testing revealed atypical pemphigus-like autoantibodies in perilesional epithelium and serum from all five patients. We studied the antigenic specificities of the autoantibodies by indirect immunofluorescence and immunoprecipitation, using extracts of 14C-labeled human keratinocytes. IgG purified from the serum of one patient was passively transferred to four neonatal mice to test for pathogenicity. RESULTS: Immunofluorescence testing showed that the autoantibodies bound to the surface of tissues containing desmosomes, including complex and simple epithelia, and myocardium. An identical and unique complex of four polypeptides with molecular weights of 250, 230, 210, and 190 was immunoprecipitated by all serum samples. The 250-kd polypeptide comigrated with desmoplakin I (a protein found in the desmosomes of all epithelia), and the 230-kd antigen comigrated with the antigen of bullous pemphigoid. Cutaneous blisters, a positive Nikolsky's sign, and epidermal and esophageal acantholysis developed in all mice into which the autoantibody was injected. Electron microscopy showed epidermal acantholysis similar to lesions of experimentally induced pemphigus vulgaris. CONCLUSION: These five patients with cancer had a novel acantholytic mucocutaneous disease characterized by autoantibodies that were pathogenic after passive transfer. The autoantibodies from these patients reacted with an antigen complex composed of desmoplakin I and the 230-kd antigen of bullous pemphigoid and two as yet unidentified epithelial antigens. We suggest the term "paraneoplastic pemphigus" for this disease.

Acantholysis↗
PubMed1990

Trabeculectomy with 5-fluorouracil for adult inflammatory glaucoma.

We reviewed the records of 12 eyes of ten adult patients with inflammatory glaucoma who underwent trabeculectomy with the adjuvant use of 5-fluorouracil between January 1986 and January 1989. Intraocular pressure decreased from 36 +/- 10 mm Hg (range, 17 to 50 mm Hg) preoperatively to 11 +/- 4 mm Hg (range, 3 to 17 mm Hg) postoperatively after a median follow-up of 7.75 months (range, six to 38 months). All eyes achieved an intraocular pressure of less than 20 mm Hg, and ten of 12 required no intraocular pressure lowering medications. The mean (+/- S.D.) amount of 5-fluorouracil used was 33 +/- 10 mg (range, 20 to 55 mg). During the period of observation, five of 12 eyes had an episode of uveitis, but in no patient did this result in loss of intraocular pressure control. Preoperative and postoperative systemic and topical corticosteroid use was the same. Trabeculectomy with 5-fluorouracil is an effective treatment for selected cases of adult inflammatory glaucoma refractory to medical management.

Adult↗
PubMed1989

Cytomegalovirus retinitis and acquired immunodeficiency syndrome.

In a series of 157 patients with acquired immunodeficiency syndrome (AIDS), 46 (29%) developed cytomegalovirus (CMV) retinitis. In five patients, CMV retinitis was the initial AIDS-defining opportunistic infection (11% of patients with CMV retinitis and 3% of patients with AIDS). Retinal detachments developed in seven patients (15%) and in four were present before the institution of ganciclovir therapy. Bilateral CMV retinitis was present in 35% of patients at presentation and subsequently developed in nine (60%) of 15 patients while not being treated with ganciclovir. Conversely, none of 18 patients with unilateral disease developed bilateral disease while receiving ganciclovir. Of patients treated with ganciclovir for their CMV retinitis, 81% had a response to the drug, and 61% achieved a complete response, resulting in a nonprogressive and inactive scar. Patients who achieved a complete response with ganciclovir had a significantly longer survival than those who did not, suggesting greater immune compromise in those patients who failed to respond to ganciclovir.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Regression of cytomegalovirus retinitis with zidovudine. A clinicopathologic correlation.

A 55-year-old man with the acquired immunodeficiency syndrome had cytomegalovirus (CMV) retinitis develop in his left eye. The patient declined treatment with ganciclovir but elected to be treated with zidovudine. Two months later his CMV retinitis regressed, and it remained inactive for a total of 9 months. The most likely explanation was zidovudine-mediated improvement in the patient's immune function with subsequent suppression of the CMV retinitis in the left eye. The patient ultimately and preterminally had CMV retinitis develop in his right eye. He subsequently died and his eyes were examined at autopsy. Active CMV retinitis lesions were noted in the right eye while inactive scars were noted in the left eye. Immunoperoxidase staining and in situ hybridization studies demonstrated the presence of CMV in the right eye but not in the left eye. While ganciclovir remains the treatment of choice for CMV retinitis, zidovudine treatment may have a beneficial effect on CMV retinitis in some patients.

Acquired Immunodeficiency Syndrome↗
PubMed1989

The eye in bone marrow transplantation. III. Conjunctival graft-vs-host disease.

Of a series of 263 patients undergoing allogeneic bone marrow transplantation (BMT), 24 patients developed conjunctival involvement by graft-vs-host disease (GVHD). In each case, a distinct-appearing conjunctivitis developed that representing GVHD of the conjunctiva. In 19 cases (79%), conjunctival GVHD presented with pseudomembrane formation due to loss of the conjunctival epithelium; in 4 of these cases, the corneal epithelium was lost as well. Nineteen patients developed this feature in association with acute GVHD, and mortality among these patients was 89.5%. Kaplan-Meier analysis of survival demonstrated a decreased survival of patients with conjunctival involvement compared with all marrow transplant recipients and compared with all patients with GVHD. However, survival was similar to that seen in patients with severe systemic GVHD (overall stages II through IV). Five patients developed conjunctival GVHD in association with chronic GVHD, and all had severe chronic GVHD. four of these five with chronic GVHD subsequently died. Conjunctival involvement by GVHD represents a distinct clinical finding and is a marker for severe systemic involvement by GVHD. A clinical staging system for ocular involvement was formulated.

Biopsy↗
PubMed1989

Ocular manifestations of acquired immune deficiency syndrome.

The ocular complications of acquired immune deficiency syndrome (AIDS) include: (1) a noninfectious microangiopathy, most often seen in the retina, consisting of cotton-wool spots with or without intraretinal hemorrhages and other microvascular abnormalities; (2) opportunistic ocular infections, primarily cytomegalovirus (CMV) retinitis; (3) conjunctival, eyelid, or orbital involvement by those neoplasms seen in patients with AIDS (i.e., Kaposi's sarcoma and lymphoma); and (4) neuro-ophthalmic lesions. In a series of 200 AIDS patients evaluated clinically, AIDS retinopathy was present in 66.5%. Sixty-four percent had cotton-wool spots, and 12% had intraretinal hemorrhages. Cytomegalovirus retinitis was diagnosed in 28% of AIDS patients. Neuro-ophthalmic lesions were found in 8% of all AIDS patients and were present in 33% of those patients with cryptococcal meningitis. Acquired immune deficiency syndrome retinopathy was present in 40% of 35 patients with the AIDS-related complex (ARC) and in 1.3% of 232 patients with asymptomatic human immunodeficiency virus (HIV) infection, evaluated photographically. These results suggest that the prevalence of AIDS retinopathy increases with increasing severity of HIV infection, and that CMV retinitis presents a significant vision-threatening problem in AIDS patients.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Vaso-occlusive retinopathy associated with antiphospholipid antibodies (lupus anticoagulant retinopathy).

The authors observed three cases (6 eyes) of vaso-occlusive retinopathy associated with the lupus anticoagulant and the related antiphospholipid antibody anticardiolipin. The disease occurred in patients who had no definable autoimmune disease such as systemic lupus erythematosus (SLE) and was characterized by severe bilateral retinal vascular occlusion. There was profound visual loss from intraretinal ischemia as well as vitreous hemorrhage from preretinal neovascularization. Results of laboratory testing showed a prolonged partial thromboplastin time (PTT) in two patients, and the presence of the lupus anticoagulant in all. Treatment with panretinal photocoagulation appeared to stabilize the neovascularization. The role of systemic anticoagulation and immunosuppressive therapy is uncertain.

Adult↗
PubMed1989

Characterization of the class I HLA 9.2-kb PVU II restriction fragment length polymorphism. Linkage to HLA-A and lack of disease association.

The strongest reported association between a class I HLA allele and disease is that of HLA-B27 with ankylosing spondylitis (AS). However, it has not been shown whether B27 is the gene that predisposes to the development of AS or if it is merely linked with the disease-susceptibility locus. Furthermore, if B27 itself is the disease-susceptibility gene, there may be epistatic loci that also contribute to the development of AS or modify its clinical manifestation. A class I HLA 9.2-kb Pvu II restriction fragment was recently identified, which, when present in a B27-positive individual, further increased the relative risk for developing AS (from 119 to 297). This study was therefore designed to confirm the association between AS and this restriction fragment length polymorphism (RFLP) and to map the location of this fragment in the genome. The data presented here suggest that the class I HLA 9.2-kb Pvu II RFLP represents a Pvu II polymorphism at the 5' end of the HLA-A locus that is tightly linked with both HLA-A3 and A9 alleles. However, there is no association between this RFLP and AS in a population of patients living in Baltimore.

Arthritis, Reactive↗
PubMed1989

Predictors of death from chronic graft-versus-host disease after bone marrow transplantation.

Chronic graft-v-host disease (chronic GVHD) is a frequent cause of late morbidity and death after bone marrow transplantation (BMT). The actuarial survival after onset of chronic GVHD in 85 patients was 42% (95%Cl = 29%, 54%) at 10 years. Baseline characteristics present at the onset of chronic GVHD (before therapy) in 85 patients were reviewed to determine which were risk factors for death. In a multivariate proportional hazards analysis, three baseline factors emerged as independent predictors of death: progressive presentation (chronic GVHD following acute GVHD without resolution of acute GVHD; hazard ratio of 4.1, 95% Cl = 2.1 to 7.8), lichenoid changes on skin histology (hazard ratio of 2.2, 95% Cl = 1.1 to 4.3), and elevation of serum bilirubin greater than 1.2 mg/dL (hazard ratio = 2.1, 95% Cl = 1.1 to 4.1). Actuarial survival of 23 chronic GVHD patients with none of these risk factors was 70% at 6 years (95% Cl = 38%, 88%). Thirty-eight patients with one of these risk factors had a projected 6-year survival of 43% (95% Cl = 21%, 63%). The 29 patients with any combination of two or more of these factors had a projected 6-year survival of only 20% (95% Cl = 8%, 37%). Identification of baseline risk factors should facilitate design of trials of chronic GVHD therapies and assignment of high-risk patients to more aggressive innovative therapeutic regimens.

Actuarial Analysis↗
PubMed1988

Choroidopathy in systemic lupus erythematosus.

Choroidopathy in association with systemic lupus erythematosus (SLE) is a clinically unusual manifestation, previously described in only six patients, to our knowledge. We have followed up six patients with SLE and choroidopathy manifested by multifocal, serous elevations of the retinal pigment epithelium and sensory retina. In four patients, macular involvement was present, and they suffered visual loss. Two eyes of two patients progressed to large, bullous, exudative retinal detachments. In the three patients in whom control of the systemic disease was achieved, the serous detachments resolved. The pathogenesis is most likely related to choroidal vascular disease with resultant pigment epithelial damage and serous fluid leakage beneath the retina.

Adult↗
PubMed1988

Murine models of Sjögren's syndrome. Immunohistologic analysis of different strains.

Lacrimal gland inflammation develops in several strains of autoimmune mice, including MRL/Mp-lpr/lpr (MRL/lpr), MRL/Mp-+/+ (MRL/+), and NZBxNZW F1 hybrids (NZB/W). These mice all develop an autoimmune disease characterized by glomerulonephritis and autoantibody formation, but each strain has unique clinical features and immunologic abnormalities. Previous studies have suggested that the intrinsic immunologic defect in MRL/lpr mice may be at the level of T cells, while in NZB/W mice it appears to be B cell-mediated. Immunohistologic analysis of the lacrimal gland lesions was performed on all three strains. Although T cells predominated (MRL/lpr 85%, MLR/+ 78%, and NZB/W 57%), differences in the immunohistologic profiles did exist. NZB/W mice had a significantly higher percentage of B cells (33% vs. 10% for MRL/lpr and 13% for MRL/+) and a correspondingly lower percentage of T cells. MRL/lpr mice differed from MRL/+ mice in that they exhibited a significantly higher percentage of helper T cells (63% vs. 49%) and a lower percentage of suppressor/cytotoxic T cells (14% vs. 30%). Class II antigen expression could be detected on the mononuclear cells at inflammatory sites within the lacrimal glands of all three strains, suggesting T cell activation and an active autoimmune immunologic event occurring in the lacrimal gland.

Animals↗
PubMed1987

Reactive lymphocytes in lacrimal gland and vasculitic renal lesions of autoimmune MRL/lpr mice express L3T4.

The lacrimal gland inflammatory lesions and renal vasculitic lesions of autoimmune MRL/lpr mice were analyzed for the lymphocyte subsets present. The majority of cells were Thy-1.2+ T cells (mean, 85%) of the L3T4+ helper T phenotype (mean, 64 and 58%, respectively). Lesser numbers of Lyt-2+ suppressor/cytotoxic T cells, B cells, and macrophages were present. The finding that the majority of lymphocytes in both the lacrimal gland inflammatory lesions and renal vasculitis of MRL/lpr mice expressed L3T4 suggests that these cells may be capable of responding to antigen presentation and that an active immunologic response occurs at these sites.

Animals↗