Biomedical subjects
Publications and source records attributed to M Friedlaender.
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A plethora of drugs is available for the treatment of ocular allergy. Traditional treatment includes antihistamine and antihistamine/vasoconstrictor combination eyedrops. These drugs are useful, safe, and readily available. Mast cell stabilizers are safe, effective, and an important component of antiallergic therapy. Nonsteroidal anti-inflammatory drugs also have antiallergic effects. In recent years, drugs with multiple mechanisms of action have proven to be effective antiallergics. These drugs often have mast cell stabilizing, antihistaminic, and anti-inflammatory properties. Corticosteroids are considered to be more potent than other antiallergic drugs, and modifications in their molecular structures have made certain corticosteroids suitable for the treatment of ocular allergy.
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A 66-year-old man presented with gastrointestinal symptoms and acute renal failure. He had paraproteinemia and tested positive for antinuclear antibodies. There was no evidence for autoimmune disorder or amyloidosis, and bone marrow biopsy was not consistent with multiple myeloma. Three months later he presented with diffuse lymphadenopathy and right lung mass, and lymph node histology revealed metastatic squamous cell carcinoma. This association of paraproteinemia and nonlymphatic neoplasia is unusual and still very rare. A review of the literature is presented.
Two patients who were systematically tortured and deprived of any oral intake presented with acute renal failure several days later. Unlike the classical crush syndrome, we describe a clinical entity wherein repeated direct muscle injury from blunt trauma, in addition to forced dehydration, led to myoglobinuria and renal failure. The literature is reviewed, and biochemical indices predicting severity of injury, pathophysiology, and management protocol are described. This pseudo-crush syndrome caused by rhabdomyorhexis in addition to rhabdomyolysis is an unusual entity, in part related to extreme sociopolitical factors.
Several growth factors have been found to play an important role in the recovery from acute renal failure (ARF). The effect of the continuous subcutaneous infusion of human recombinant insulin-like growth factor (IGF)-1 (125 micrograms daily by osmotic minipumps) in a rat model of mercuric chloride (HgCl2)-induced ARF was examined. HgCl2 (4 mg/kg) induced ARF with a mortality that was unaffected by IGF-1. However, IGF-1 significantly enhanced functional and histologic recovery in the survivors, as measured by serum creatinine and creatinine clearance and by histologic scoring. Solution hybridization RNAase protection assays showed that renal IGF-1 mRNA, IGF-1 receptor (IGF-1R) mRNA, and IGF-binding protein-1 (IGFBP-1) mRNA were unaffected by exogenous IGF-1, but this treatment significantly increased renal IGF-1 in ARF rats compared with normal rats and ARF rats not receiving IGF-1. After ARF renal mRNA for IGF-1 was decreased, IGF-1R was unchanged and IGFBP-1 was increased. Similar changes occurred in IGF-1-infused ARF rats. Thus, (1) IGF-1 enhances recovery from nephrotoxic ARF both functionally and histologically; (2) in nephrotoxic ARF, there is (a) a reduction in IGF-1 mRNA expression that is not prevented by IGF-1 infusion, and (b) an increase in renal IGFBP-1 mRNA. This may allow a significant increase in renal IGF-1 levels in IGF-1-infused ARF rats, despite the decrease in renal IGF-1 mRNA. A local increase in renal IGFBP-1 and IGF-1 may explain the accelerated recovery from ATN in this model. It was concluded that HgCl2-induced ARF is amenable to improvement by IGF-1 infusion and that the increase in renal IGFBP-1 mRNA may be an important modulator in the recovery of the kidney.
A multicenter, randomized, double-masked, parallel-group study compared the long-term efficacy and safety of lodoxamide 0.1% ophthalmic solution and placebo in 118 patients with vernal keratoconjunctivitis. The test drugs were instilled four times daily for 90 days. Lodoxamide 0.1% ophthalmic solution was significantly (P < .05) more effective than placebo in lowering severity scores for epithelial disease and corneal staining, evidence of the superior efficacy of lodoxamide 0.1% ophthalmic solution in reversing the corneal complications commonly associated with moderate to severe vernal keratoconjunctivitis. Additionally, lodoxamide 0.1% ophthalmic solution ameliorated the other key signs of vernal keratoconjunctivitis, including upper tarsal papillae, limbal signs (papillae, hyperemia, and Trantas' dots), and conjunctival discharge. The between-group differences in the relief of symptoms (itching, tearing, and photophobia) were clinically significant but not always statistically significant. Treatment-related adverse events were reported with similar frequency in both treatment groups, and none were serious.
Sjögren's syndrome is an autoimmune disease characterized by lymphocytic infiltration of the salivary/lacrimal glands, autoantibody production, and polyclonal hyperglobulinemia. In view of the efficacy and relative safety of hydroxychloroquine in other autoimmune disorders, the potential benefit of hydroxychloroquine (200 mg per day for 12 months) in 10 patients with Sjögren's syndrome was evaluated. Changes in levels of total immunoglobulin, antibody against Sjögren's syndrome-associated antigen B, rheumatoid factor, and in vitro production of immunoglobulin in the serum were evaluated. For comparison, 10 patients matched according to age and sex, who did not receive hydroxychloroquine were studied. In the hydroxychloroquine-treated group, the following observations were made: (1) significantly decreased total immunoglobulin G (IgG) and IgA levels with little change in IgM levels; (2) significant decrease in IgA-rheumatoid factor with a smaller decrease in IgM-rheumatoid factor; (3) decreased IgG anti-Sjögren's syndrome-associated antigen B autoantibody; and (4) decreased erythrocyte sedimentation rate and increased hemoglobin level. Further, a specific idiotype present on their rheumatoid factor (defined by monoclonal antibody 17-109) was significantly decreased, with disappearance of detectable circulating paraprotein in two hydroxychloroquine-treated patients. Finally, rheumatoid factor production in vitro by lymphocytes from hydroxychloroquine-treated patients using a T cell-dependent mitogen was significantly decreased. These results suggest that hydroxychloroquine modulates lymphoproliferation in patients with Sjögren's syndrome and may prevent progression to extraglandular sites of neoplastic transformation.
The right eyes of guinea pigs were injected with 1.5 mg sterile ovalbumin. Two months later, one drop of ovalbumin (approximately 0.6 mg) was applied to the conjunctiva of both eyes. All challenged eyes developed an immediate hypersensitivity reaction within 5 min. The reaction subsided within 2 hrs. Prechallenge antibody titers, as determined by passive hemagglutination, passive cutaneous anaphylaxis, and by an ELISA test were low. Titers rose rapidly after two conjunctival applications at weekly intervals. The hypersensitivity reaction was elicited each time antigen was applied to the conjunctiva of the intravitreally sensitized guinea pigs. Control guinea pigs received weekly conjunctival application of ovalbumin, without prior intravitreal sensitization. Most animals developed an immediate hypersensitivity reaction following the fourth application of the antigen. There was no detectable hemagglutinating or ELISA (IgG1, IgG2) antibody at the time the conjunctival reaction was first elicited. These experiments demonstrated that high circulating IgG1 or IgG2 antibody is apparently not necessary to initiate an immediate hypersensitivity reaction in the guinea pig conjunctiva. The authors also demonstrated that weekly topical application of ovalbumin sensitized guinea pigs for immediate hypersensitivity.
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Human buffy-coat interferon and a leukocyte subtype (LeIF-A) obtained by gene cloning in Escherichia coli were equally effective in ameliorating the course of herpetic keratitis in rabbits when applied topically at a daily dose of 0.5 X 10(6) units per eye for six days commencing one day before infection. When given intramuscularly at the same dose, there was no alteration in the course of the disease. Topical treatments with LeIF-A were equally effective in suppressing epithelial damage seven days after infection, regardless of whether treatment commenced one day before infection or two days after infection. However, treatment from the day before infection also caused a significant decrease in epithelial defect two days after infection.
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In an experimental model of Pseudomonas keratitis caused by a gentamicin-resistant strain of Ps aeruginosa, the results of treatment with gentamicin alone and a gentamicin-steroid combination were evaluated. Treatment with steroids did not reduce the amount of corneal inflammation when compared to eyes treated with gentamicin alone. Eyes treated with the gentamicin-steroid combination were, however, infected with a statistically significant greater number of organisms at the end of a 3-day treatment period. Corticosteroids probably should not be used in the treatment of Pseudomonas keratitis during the early period when the antibiotic sensitivities of the organism are not known.
The entire corneal epithelium of each of 16 rabbits was removed bilaterally. Tretinoin (vitamin A acid) ointment was applied topically twice daily to the eyes of one half of the experimental animals, and the ointment base alone was applied to the eyes of the other half (the controls). On days 1, 2, and 3 after the removal of the epithelium, the healing of the denuded corneas of the animals receiving tretinoin was significantly (P = .01, .01, and .05, respectively) more advanced than the healing of the corneas of the control animals.
We produced chronic experimental herpetic keratitis by dropping PH-strain herpes simplex virus on scarified rabbit corneas and then injecting the rabbits subconjunctivally with low doses of corticosteroid (namely, triamcinolone acetonide suspension). Vitamin-A-treated rabbits developed milder, more rapidly healing epithelial lesions than untreated rabbits. Whereas most of the untreated rabbits developed moderate or severe stromal disease, most of the vitamin-A-treated rabbits developed only mild stromal disease or none at all.
Corneas of 20 rabbits were treated with idoxuridine or a bland ointment before and after their inoculation with Staphylococcus aureus. The rabbit corneas treated with idoxuridine had a significantly more severe keratitis and yielded significantly greater numbers of S. aureus on culture than the rabbit corneas treated with the bland ointment.
To study the effect of locally administered indoxole (with polysorbate 80) on the inflammatory and immunologic responses, we made unilateral intracorneal injections of rabbit eyes with bovine gamma globulin (BGG). The indoxole was injected subconjunctivally one day before, and 1, 2, 3, and 5 days after the BGG injection. The homolateral lymph nodes, uveal tracts, and corneas of rabbits killed on postinjection days 6 and 12 were tested for antibody-forming cells (AFC) by a modification of the Jerne plaque technique. On day 6 the indoxole-treated eyes were more inflamed and had a greater number of AFC in the tested tissues than the control eyes, but in neither of these respects was there any essential difference between the treated and control eyes on day 12. The possible mechanisms by which indoxole achieved its effect were explored.