The inflammatory, infectious and allergic diseases of the eye still remain an acute problem in practical ophthalmology due to their high prevalence, relapsing clinical course, a growing frequency rate of mycotic and acanthoamebic keratitis and a growing number of resistant causative agents of bacterial keratitis. 55.3% of corneal pathologies are related with the herpes simplex virus, 37.3%--with secondary bacterial infection, 33.2%--with primary bacterial infection, 6.7%--with mycotic infection and 5.6%--with acathoamebic infection. Algorithms of pharmacological therapy are suggested for a majority of inflammatory lesions of the eye, i.e. for herpetic keratitis, ulcerous keratitis caused by blue pus bacillus, gonococcus, staphylococcus, fungi, acanthomebas, as well as for adenoviral and Chlamidia conjunctivitis and allergy of the eye. The author points out that the treatment must be complex, including specific therapy--antiviral one (zovirax ointment, interferon locally, and zovirax or valtrex perorally), antibacterial one (okacin, tobrex, vitabact, fucithamic locally, quinine antibiotics perorally, aminoglycosides or cephalosporins subconjunctivally or intramuscularly) and antimycotic one (locally and perorally). Another part of the complex therapy is equally important--pathogenetic one (carnosine, taufon, vitacic, corneregel ointment), antiallergic one (spersallerg, allergophtal, alomide, lecrolin), antinflammatory one (naclof, maxidex, cyclolip) tears replacing one (natural tears, ophthagel) and immunomodeling one (affinoleicin, lycopid, tactivin).

Lodoxamid is an antiallergic drug, which stabilizes the mast cells' membrane blocking the release of the type I hypersensitivity reaction chemical mediators. A number of 25 patients with ocular allergic diseases (allergic conjunctivitis, vernal and atopic keratoconjunctivitis, giant papillary conjunctivitis), were included in this study. Lodoxamid, solution 0.1% (Alomide), was given 4 times daily for 6 weeks. The study's aim was to assess the lodoxamid's efficiency, on the ocular signs and symptoms. The study's results showed a significant improvement, or the disappearance of the ocular allergic disease. It is debated upon the lodoxamid's way and place of action, in blocking the type I hypersensitivity reaction. The lodoxamid's efficiency is due to its pharmacological features, by means of which it is effective on many links of the pathogenic chain: mast cells, eosinophils, lymphocytes, neutrophils, antigen presenting cells. Due to its action lodoxamid stabilizes the mast cell's membrane, and inhibits the release of histamine, prostaglandins, leukotrienes, triptase, interleukines -4, -8 and TNF-. During therapy with lodoxamid recruitment and activation of eosinophils is decreased, causing a significant reduction of the basic major protein, cationic eosinophilic protein, eosinophilic derived neurotoxin, eosinophilic peroxidase. Lodoxamid reduces the expression of ICAM-1 on the surface of the antigen presenting cells, and decreases the number of the TH2 cells, from the tears of the allergic patients.

A double-masked, randomized, placebo-controlled study was conducted to evaluate the effectiveness of lodoxamide tromethamine 0.1% eyedrops in preventing inflammatory cell accumulation in the tear fluid of patients with vernal conjunctivitis. A 1-week baseline period was followed by 4 weeks of treatment with either lodoxamide tromethamine 0.1% ophthalmic solution or placebo in 30 symptomatic subjects with vernal conjunctivitis. Cytological evaluation of tear fluid was performed before and after the treatment. In the lodoxamide-treated group, but not in the placebo-treated group, the number of neutrophils (P = 0.051) and eosinophils (P = 0.020) in the tears significantly decreased at the end of 4 weeks when compared with baseline (Wilcoxon-signed rank test). It was concluded that lodoxamide treatment was significantly more effective than the placebo in terms of reducing inflammatory cells in the tear fluid in vernal conjunctivitis. This objective inhibition of inflammatory cells may be associated with clinical relief.

Superior limbic keratoconjunctivitis (SLK) is a chronic and recalcitrant disease of the superior bulbar and tarsal conjunctiva, as well as the superior limbic aspect of the cornea. Both the etiology and the pathogenesis of this condition are poorly understood. Many treatment options have been advocated in the management of SLK, including: topical antibiotics, topical anti-inflammatory agents, topical vitamin A solutions, chemical cautery, thermal cautery, and surgical resection. Most recently, studies have suggested that lacrimal occlusion therapy may be beneficial in the treatment of SLK. A case is presented in which this method of treatment was used, with excellent results. The implications of this report suggest that the use of lacrimal occlusion in the management of SLK may be a viable treatment option before considering more radical and invasive therapy. In addition, this case helps to illustrate the significant link between SLK and thyroid disease.

New drug lodoxamine (alomide) opens new vistas in the treatment of allergic diseases of the eyes highly prevalent both in adults and children. This drug prevents release of mast cell mediators and delays eosinophil migration to conjunctival and corneal tissue, thus exerting a spectrum of antiallergic effects. Clinical studies carried out in 170 patients demonstrated a high efficacy of alomide in the treatment of subacute and chronic pollenosis conjunctivitis, spring keratoconjunctivitis, multiple and toxic allergic keratitis, and other allergic conjunctivities. Alomide can be used as a preventive drug in patients with allergies under high-risk conditions and in patients wearing contact lenses. It is effective in combined therapy of keratitis and keratouveitis. Alomide eye drops are well tolerated.

It has been proposed that the cardioprotective effects of myocardial ischaemic preconditioning may involve the release of mast cell mediators. The aim of the study was to determine whether mast cells are involved in the antiarrhythmic effect of ischaemic preconditioning in rat hearts. Preconditioning was achieved, both in anaesthetised rats and in rat isolated hearts, by a 3-min temporary occlusion of the left main coronary artery followed by 10 min of reperfusion before a 30-min permanent occlusion. Preconditioning had a marked antiarrhythmic effect, reducing the number of ventricular ectopic beats from 1,176 +/- 69 to 490 +/- 139 and the incidence of ventricular fibrillation from 40% to 0. Administration of the mast cell-stabilising drugs lodoxamide tromethamine and sodium cromoglycate (20 mg/kg/h i.v. 30 min before and throughout experimental protocol) did not modify the antiarrhythmic effect of preconditioning. Sodium cromoglycate, but not lodoxamide tromethamine, itself significantly reduced the number of ectopic beats that occurred over a 30-min period of ischaemia (from 760 +/- 181 to 153 +/- 33 in nonpreconditioned animals). Both drugs abolished the decrease in arterial blood pressure that occurred on coronary artery occlusion. The decrease in arterial blood pressure produced by the mast cell-degranulating compound 48/80 (50 microg/kg; i.v.) was attenuated to a similar degree by both drugs (decreases in pressure of 53 +/- 7, 31 +/- 1, and 25 +/- 3 mm Hg in control, sodium cromoglycate-treated, and lodoxamide tromethamine-treated animals, respectively). In rat isolated hearts, degranulation of mast cells with three consecutive doses of 50 microg of compound 48/80 had no antiarrhythmic effects and did not modify the antiarrhythmic effect of preconditioning. It is concluded that cardiac mast cells do not play a major role in the protection offered by ischaemic preconditioning on arrhythmogenesis in rat hearts.