Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

All eye drops raise problems of local tolerance, but with variable frequencies. They can induce pain on instillation, allergic reactions, delayed healing, punctate keratitis, disturbances of lacrimal secretion, disturbances of accommodation (especially the parasympathomimetics) and local pigmentation after prolonged use. Corticosteroids are associated with 2 major risks: chronic glaucoma and cataract, initially reversible if treatment is stopped. There is still a major risk of corneal herpes with corticosteroids. It is important to be aware of these local problems as they are responsible for poor patient compliance. The systemic effects essentially concern the agonists and antagonists of the autonomic nervous system. beta-Blocker eye drops can cause bronchospasm, heart failure, syncope and psychiatric disorders, especially at high doses and with nonselective beta-blockers. These consequences are usually related to failure to comply with the prescribing precautions. alpha-Adrenergic agonists, which exert dose-dependent effects, can induce hypertensive crises or angina attacks. Apart from patients at risk (children under the age of 30 months and the elderly), parasympathomimetics cause few systemic adverse effects; anticholinesterases, which have curare-like properties, are contraindicated for 6 weeks before general anesthesia. In the very young and the very old, atropinic eye drops carry a risk of cardiovascular collapse and neuropsychiatric disturbances. Problems may also occur with other classes of drugs such as anti-infectives, antispectics, anti-inflammatories and contact lens products. Nevertheless, it is clear that this form of treatment is generally very well tolerated in relation to the volume of eye drops prescribed by ophthalmologists each day.
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PMID:Systemic and local tolerability of ophthalmic drug formulations. An update. 809 91

The DNA region encoding the complete herpes simplex virus type 1 (HSV-1) glycoprotein K (gK) was inserted into a baculovirus transfer vector, and recombinant viruses expressing gK were isolated. Four gK-related recombinant baculovirus-expressed peptides of 29, 35, 38, and 40 kDa were detected with polyclonal antibody to gK. The 35-, 38-, and 40-kDa species were susceptible to tunicamycin treatment, suggesting that they were glycosylated. The 38- and 40-kDa species corresponded to partially glycosylated precursor gK (pgK) and mature gK, respectively. The 29-kDa peptide probably represented a cleaved, unglycosylated peptide. The 35-kDa peptide probably represented a cleaved, glycosylated peptide that may be a precursor to pgK. Indirect immunofluorescence with polyclonal antibody to gK peptides indicated that the recombinant baculovirus-expressed gK was abundant on the surface of the insect cells in which it was expressed. Mice vaccinated with the baculovirus-expressed gK produced very low levels (< 1:10) of HSV-1 neutralizing antibody. Nonetheless, these mice were partially protected from lethal challenge with HSV-1 (75% survival). This protection was significant (P = 0.02). Despite some protection against death, gK-vaccinated mice showed no protection against the establishment of latency. Surprisingly, gK-vaccinated mice that were challenged ocularly with a stromal disease-producing strain of HSV-1 had significantly higher levels of ocular disease (herpes stromal keratitis) than did mock-vaccinated mice. In summary, this is the first report to show that vaccination with HSV-1 gK can provide protection against lethal HSV-1 challenge and that vaccination with an HSV-1 glycoprotein can significantly increase the severity of HSV-1-induced ocular disease.
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PMID:Characterization of baculovirus-expressed herpes simplex virus type 1 glycoprotein K. 813 20

We evaluated the epithelializing-promoting effect of a concentration of 0.005 mg/ml murine epidermal growth factor (mEGF), topically administered four times daily, on the herpes simplex virus 1 (HSV-1) corneal ulcers of the rabbit eye. The severity of the herpetic lesions was evaluated clinically, after the time course of the severity of epithelial keratitis, conjunctivitis, iritis, and stromal disease, for 14 days. A histological assessment was performed in the middle and at the end of the follow-up. The stromal keratitis of the mEGF-treated group was significantly more severe than the keratitis exhibited by the placebo-treated rabbits (Y = X3 X2*X4; p = 0.0001). There were no significant differences in the degree of conjunctivitis, epithelial keratitis, iritis, and virus shedding between these groups. No evidence of a toxic effect of mEGF or placebo was found in the mock infected rabbit eyes. More studies, using different herpes virus strains and a broad range of murine and human EGF concentrations, are mandatory to ascertain the general significance of these results. Meanwhile, caution is recommended when using mEGF in the presence of an occult or manifest herpetic eye disease.
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PMID:Aggravation of herpetic stromal keratitis after murine epidermal grown factor topical application. 815 89

Herpes simplex virus type 1 (HSV-1) infection on the murine cornea induces an intense inflammatory response which can lead to blindness. This disease, known as herpes stromal keratitis, can be prevented by the timely passive transfer of monoclonal antibody specific for viral glycoprotein D (gD). Precisely how antibody treatment prevents excessive corneal inflammation is not known. In this study we investigated whether chemokine mRNA expression is inhibited by antibody treatment. Total cellular RNAs isolated from normal corneas and at various times after virus infection were analyzed via reverse transcription-PCR for mRNA coding for seven different chemokines. Constitutive levels of IP-10, KC, MIP-2, MCP-1, MIP-1 beta, and RANTES mRNA were detected in uninfected corneas of BALB/c mice. When the cornea was mechanically traumatized, message for all six chemokines was transiently elevated above constitutive levels. In contrast, HSV-1 infection resulted in prolonged enhanced chemokine message expression. The kinetics of mRNA accumulation was distinctive for each chemokine analyzed. MIP-1 alpha message, not detected constitutively, was not evident until day 7 postinfection. Administration of anti-HSV gD monoclonal antibody 1 day after infection was associated with reduced message for MIP-2, MCP-1, MIP-1 alpha, and MIP-1 beta. IP-10, KC, and RANTES messages were not altered. Collectively, our results suggest that anti-gD treatment may protect, at least in part, by inhibiting production of chemokines believed to promote inflammation.
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PMID:Protective antibody therapy is associated with reduced chemokine transcripts in herpes simplex virus type 1 corneal infection. 855 95

We examined the recurrence rate of herpetic uveitis (HU) in 13 patients (group A) treated prophylactically with long-term systemic acyclovir (600-800 mg/day) and compared it with that of 7 patients with no prophylactic therapy (group B). HU was diagnosed on the basis of a history of dendritic or disciform keratitis accompanied by iridocyclitis and iris atrophy. The study population consisted of 12 men and 8 women with a mean age at onset of uveitis of 52.9 years (range 19-78 years). All patients were followed for at least 8 months. The mean follow-up time of patients on long-term oral acyclovir was 26.0 months. In this group, only one patient experienced a single recurrent episode of uveitis while on 600-800 mg/day of acyclovir therapy; two additional patients had recurrence of HU within 16.2 months after the acyclovir dose was tapered below 600 mg/day. In striking contrast, 16 recurrences occurred in the 7 patients of group B (p < 0.05). Of these, the initial recurrence occurred within an average of 4.3 months following cessation of therapy. There was a significant difference (p < 0.05) in the mean recurrence-free interval between patients in group A (24.6 months) and those in group B (3.4 months). Herpetic uveitis is a serious ocular disease in which recurrence of inflammation results in severe ocular complications. The long-term use of oral acyclovir may be of benefit in the prevention of recurrences, and hence may reduce the blinding complications of this disease. Efforts at completing a randomized, placebo-controlled trial on this matter by the Herpes Epithelial Disease Study Group were unsuccessful due to insufficient patient recruitment.
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PMID:Recurrence rate of herpetic uveitis in patients on long-term oral acyclovir. 862 Aug 18

Recurrent ocular herpes is an insoluble problem for the clinician. As cellular immunity plays an important role in controlling herpes relapses, and other studies have shown the efficacy of HSV-specific transfer factor (TF) for the treatment of herpes patients, an open clinical trial was undertaken in 134 patients (71 keratitis, 29 kerato-uveitis, 34 uveitis) suffering from recurrent ocular herpetic infections. The mean duration of the treatment was 358 days, and the entire follow-up period 189,121 before, and 64,062 days after TF treatment. The cell-mediated immune response to the viral antigens, evaluated by the lymphocyte stimulation test (LST) and the leucocyte migration test (LMT) (P < 0.001), was significantly increased by the TF treatment. The total number of relapses was decreased significantly during/after TF treatment, dropping from 832 before, to 89 after treatment, whereas the cumulative relapse index (RI) dropped, during the same period, from 13.2 to 4.17 (P < 0.0001). No side effects were observed. It is concluded that patients with relapsing ocular herpes can benefit from treatment with HSV-specific TF.
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PMID:Efficacy of transfer factor in treating patients with recurrent ocular herpes infections. 899 59

153 patients suffering from recurrent pathologies, i.e. viral infections (keratitis, keratouveitis, genital and labial herpes) uveitis, cystitis, and candidiasis were treated with in vitro produced transfer factor (TF) specific for HSV-1/2, CMV and Candida albicans. The cell-mediated immunity of seropositive patients to HSV-1/2 and/or CMV viruses was assessed using the leucocyte migration inhibition test (LMT) and lymphocyte stimulation test (LST) in presence of the corresponding antigens, and the frequency of positive tests before, during and after TF administration was studied. The data were stratified per type of test, antigen and the recipients' pathology, and statistically evaluated. For the LMT, a total of 960 tests were carried out for each antigen dilution, 3 different antigen dilutions were used per test. 240/960 tests (25.4%) were found positive during non-treatment or treatment with unspecific TF, whereas 147/346 tests (42.5%) were found positive when the antigen corresponding to the specificity of the TF administered to the patient was used (P < 0.001). When the data were stratified following pathology, a significant increased incidence of positive tests during specific treatment was also observed (0.0001 < P < 0.05). In the LST (1174 tests), a significant increase of thymidine uptake was observed in the absence of antigen (control cultures), during treatment with both specific and unspecific TF, but also in the presence of antigen and/or autologous serum during specific TF administration (P < 0.0001). TF administration also significantly increased the soluble HLA class I antigens level in 40 patients studied to this effect.
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PMID:In vitro studies during long-term oral administration of specific transfer factor. 899 78

Herpes simplex virus type 1 infection of corneas can lead to blinding inflammation in the corneal stroma, which is referred to clinically as herpes stromal keratitis. In our mouse model of this prevalent human disease, a heavy polymorphonuclear neutrophil (PMN) infiltration of the infected cornea leads to progressive tissue destruction. This inflammatory process can be abrogated by in vivo depletion of CD4 T lymphocytes and by neutralization of the cytokines IL-2 and IFN-gamma. The goal of this study was to define the mechanisms by which IL-2 mediates the corneal inflammation. Systemic neutralization of IL-2 after the onset of corneal disease resulted in a rapid regression of inflammation and complete resolution in 50% of the treated mice. The disease remission was associated with loss of IFN-gamma expression in the cornea, as determined by immunohistochemistry, and a significant reduction of IFN-gamma mRNA, as measured by a semiquantitative reverse transcription-PCR analysis. Within 48 h after anti-IL-2 mAb administration, the PMN chemotactic gradient in the infected corneas was abolished, and those PMN that were already present in the central cornea exhibited clear signs of apoptotic cell death. Our results demonstrate that IL-2 mediates corneal inflammation by 1) regulating local IFN-gamma production in an autocrine or a paracrine fashion, 2) establishing a PMN chemotactic gradient, and 3) maintaining PMN viability in the cornea. These results suggest that IL-2 might be targeted for therapeutic intervention in this blinding disease.
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PMID:Proinflammatory functions of IL-2 in herpes simplex virus corneal infection. 901 70

Herpes stromal keratitis (HSK) is a blinding infectious disease that results from an array of immunopathogenic processes, including herpes simplex virus 1 (HSV-1)-specific T helper 1 (Th1) and Th2 cells, cytotoxic T cells and antibodies. As discussed here by Wayne Streilein and colleagues, strategies designed to prevent and treat this syndrome must be aware of the fact that the disease is multifactorial in its cause and pathogenesis.
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PMID:Immunity causing blindness: five different paths to herpes stromal keratitis. 929 61

This study investigated the effect of tetrandrine (TDR) on experimental herpes simplex keratitis (HSK) in mice. BALB/c mice were divided as follows: Group 1, untreated; Group 2, acyclovir (ACV)-treated from day 0 postinfection; Group 3, ACV-treated from day 7; Group 4, TDR-treated from day 0; and Group 5, TDR-treated from day 7. All mice were infected in the right cornea with herpes simplex virus (HSV) type I. TDR 30 mg/kg and ACV 120 mg/kg were administered intraperitoneally daily. The mice were observed for 14 days postinfection. Clinical inflammatory reactions and ocular histopathology were analyzed. The herpes specific antibody response and the delayed type hypersensitivity (DTH) response were studied. Of the 22 untreated mice, 16 developed HSK (incidence, 72.7%). TDR given from day 7 reduced the HSK incidence to 8.5% (p < 0.01); the incidence of HSK was 45.4% in mice treated with TDR from day 0 (p > 0.05). Systemic ACV given from day 0 inhibited HSK development (p < 0.01); ACV given from day 7 resulted in an HSK incidence of 50% (p > 0.05). The specific anti-HSV antibody response in the serum of mice treated with TDR or ACV either from day 0 or day 7 was significantly less than that of untreated mice (p < 0.01 and p < 0.05, respectively), and TDR treatment suppressed DTH responses to HSV (p < 0.05). Systemic TDR administered after HSV inoculation of the cornea significantly modulates murine HSK development at least partly by modifying the host immune/inflammatory response to the virus.
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PMID:Tetrandrine potently inhibits herpes simplex virus type-1-induced keratitis in BALB/c mice. 932 62


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