Ocular Hypotonia and Transient Decrease of Vision as a Consequence of Exposure to a Common Toad Poison.

The common toad produces venom (bufotoxin) that is produced in the parotid gland of the toad as well as in the skin. This toxic compound is a potent inhibitor of Na+/K+-ATPase activity. Physiological effects of bufotoxin are similar to those of digitalis and cause increased heart rate and muscle contractions. Ocular toxicity was described. A 67-year-old female patient was admitted to the emergency service because of sudden vision loss and a burning sensation in both eyes after she had been exposed to the poison of a toad. Slit lamp examination showed conjunctival hyperaemia and signs of ocular hypotonia. Topical antibiotic treatment was administered, and after 24 hours, corneal oedema and ocular hypotonia were in remission. Inhibition of Na+/K+-ATPase is a well-known effect of the toad venom. Na+/K+-ATPase is a part of corneal endothelial cells, ciliary body, and iris, and its inhibition caused by exposure to bufadienolides induces corneal dysfunction, decreased vision, and ocular hypotonia. Effects of bufadienolides on the decrease of ocular pressure appear to be very strong, with quick action. This rarely described effect of the bufotoxin can be used as a basis for further research of toad venom and its pharmacological potential. Purpose. To present a case of a 67-year-old female patient who experienced a sudden decrease in vision after exposure to the poison from a common toad (Bufo bufo).

Structure-Function Relationship of Changes in Visual Field Indices with Quadrant and Average Retinal Nerve Fiber Layer Thickness in the Eyes with Exfoliation.

The progressive nature of glaucoma suggests it should be possible to detect structural changes such as retinal nerve fiber layer (RNFL) thickness loss before the condition becomes clinically apparent with visual field (VF) impairment. Therefore, the aim was to analyze RNFL thickness and VF changes in study groups with unilateral exfoliation syndrome (XFS), bilateral XFS and bilateral exfoliative glaucoma (XFG), and compare it with controls. The study included 114 subjects (228 eyes) divided into 4 groups according to the presence of exfoliation: 30 subjects with unilateral XFS (30 with clinically visible XFS and 30 fellow eyes), 24 subjects (48 eyes) with bilateral XFS, 28 (56 eyes) subjects with bilateral XFG, and control group (32 subjects). All subjects underwent VF and RNFL measurements after ophthalmologic examination. Both eyes of unilateral XFS (clinically -visible and fellow eye) showed positive correlation between Mean Defect (MD) and square root of Loss of Variance (sLV) and between MD and inferior quadrant RNFL thickness. In bilateral XFS and XFG, there was negative correlation between MD and inferior quadrant RNFL thickness. Inferior, superior and nasal quadrant RNFL thickness was lower in XFG group than in other groups. In bilateral XFS group, the inferior quadrant RNFL thickness was lower as compared with unilateral XFS group (in both eyes). The mean RNFL thickness negatively correlated with MD in bilateral XFS and XFG groups. In conclusion, structural changes before VF impairment have an important role in early detection of glaucoma in subjects at risk.

CORRELATION BETWEEN MACULAR CHANGES IN EXFOLIATION SYNDROME AND EXFOLIATIVE GLAUCOMA.

The aim of the study was to evaluate macular thickness and macular volume in unilateral and bilateral exfoliation syndrome and to compare them with exfoliative glaucoma and control eyes using optical coherence tomography. This prospective study included 114 subjects (228 eyes) divided into 4 groups according to the presence of exfoliation: 30 patients with unilateral syndrome, 24 patients with bilateral syndrome, 28 patients with bilateral glaucoma and control group without glaucoma or exfoliation syndrome (32 subjects). All subjects were older than 50 years. Patients with visual acuity under 0.6 according to Snellen were excluded, as well as those with refraction errors, i.e. hypermetropia over +3 spherical diopters, myopia over -5 spherical diopters, astigmatism over 2 cylindrical diopters, patients with affections that might affect the macula or the optic nerve, such as diabetic retinopathy, macular degeneration, macular edema, epiretinal membrane, vascular occlusions, neuropathies, and patients having undergone eye surgery except for pseudophakic patients with visual acuity within the set limits. Study results confirmed the hypothesis on the existence of structural changes of macular parameters before the functional ones, thus representing an early sign of glaucomatous damage in risk groups such as unilateral and bilateral exfoliation syndrome. If the glaucoma had already manifested (exfoliative glaucoma in this study) with changes in optic disc and visual field, structural changes confirmed the clinical findings and warned of the disease severity.

Initial Clinical Experience with Ahmed Valve Implantation in Refractory Pediatric Glaucoma

The purpose is to report on the safety and efficacy of Ahmed Glaucoma Valve (AGV, New World Medical, Inc., Rancho Cucamonga, CA, USA) implantation for the management of refractory pediatric glaucoma observed during one-year follow up period. A retrospective chart review was conducted on 10 eyes, all younger than 11 years, with pediatric glaucoma that underwent AGV implantation for medicamentously uncontrolled intraocular pressure (IOP) between 2010 and 2014. Outcome measures were control of IOP below 23 mm Hg (with or without antiglaucoma medications) and changes in visual acuity. Complications were recorded. After AGV implantation, IOP values ranged from 18 mm Hg to 23 mm Hg (except for one eye with postoperative hypotonia due to suprachoroid hemorrhage, where the postoperative IOP value was 4 mm Hg). The number of antiglaucoma medications was reduced, i.e. four patients had two medications, one patient had one medication, and the others did not need antiglaucoma medication on the last follow-up visit. One eye had suprachoroid hemorrhage, one eye had long-term persistent uveitic membrane, and two eyes had tube-cornea touch. In conclusion, AGV implantation appears to be a viable option for the management of refractory pediatric glaucoma and shows success in IOP control. However, there was a relatively high complication rate limiting the overall success rate.

[Croatian guidelines for gastric cancer prevention by eradication of Helicobacter pylori infection]. / Hrvatski postupnik za prevenciju zelucanog raka eradikacijom infekcije Helicobacterom pylori.

Gastric cancer is the fourth most common type of cancer and the second leading cause of cancer-related death in the world. Although gastric cancer has a multifactorial etiology, infection with Helicobacter pylori is highly associated with gastric carcinogenesis. Carcinogenesis is also influenced by some environmental factors and host genetic diversity, which engenders differential host inflammatory responses that can influence clinical outcome. Chronic gastritis induced by H. pylori is the strongest known risk factor for adenocarcinoma of the distal stomach, but the effects of bacterial eradication on carcinogenesis have remained unclear up to now. Although eradication of H. pylori infection appears to reduce the risk of gastric cancer, several recent controlled interventional trials by H. pylori eradication to prevent gastric cancer have yielded disappointing results. To clarify this problem in a high-risk population, the investigators conducted a prospective, randomized, double-blind, placebo-controlled, population-based studies. The results of previous studies highlight the importance of longer and careful follow-up after eradication therapy. It seems that eradication treatment is effective in preventing gastric cancer if it is given before preneoplastic conditions/lesions, gastric atrophy, metaplasia, and dysplasia, have had time to develop. Furthermore, the significant efficacy of treatment observed in younger patients suggests the need to eradicate H. pylori as early as possible. This consensus aimed to propose guidelines for the diagnosis, management and control of individuals with chronic gastritis, atrophy, intestinal metaplasia, or dysplasia.

[The urea breath test]. / Izdisajni test ureje.

Helicobacter pylori is infective cause of peptic ulcer and a risk factor for gastric carcinoma. The discovery of the bacterial ed to importance of finding a new reliable and inexpensive diagnostic method for detection of infection before and after eradication therapy. Urea breath test is isotope based test. It has become the most specific and sensitive method in detection of Helicobacter pylori infection, therefore many other isotope based tests become popular in diagnostic of gastrointestinal diseases. Because of its simplicity and no need in using endoscopy in the procedure it is very popular in primary diagnosis and in controlling eradication. It is successfully used in diagnostics of Helicobacter pylori and bacteria eradication success testing, where it is one of most reliable diagnostic methods.

[The rapid urease test]. / Brzi ureazni test.

Today there are many methods in diagnostics of Helicobacter pylori infection. They are divided in two major groups based on using of endoscopy (invasive and non-invasive methods). Helicobacter pylori bacteria are specific because of having very big amounts of urease enzyme that divides urea on NH3 and CO2 which enables environment suitable for survival. Rapid ureas test is based on detecting of the enzyme activity. Because of its simplicity and high sensitivity and specificity it belongs to methods that are used in every day practice in endoscopic laboratories.

[Gastric ulcer and Helicobacter pylori infection]. / Zelucani ulkus i infekcija Helicobacterom pylori.

Helicobacter pylori infection and the use of non-steroidal anti-inflammatory drugs (NSAID) are considered to be the two major risk factors implicated in the development of gastric ulcer. Helicobacter pylori infection related chronic gastritis is known to be the underlying condition which may lead to gastric ulcer. Development of gastric ulcer as the consequence of underlying chronic gastritis is caused by many factors. Treating Helicobacter pylori infection entails the healing of gastric ulcer, it concomitantly prevents recurrences and complications of gastric ulcer, primarily bleeding, and changes the natural course of gastric ulcer disease. Continuation of antisecretory maintenance treatment beyond ulcus healing and eradication of Helicobacter pylori infection is only indicated in risk groups. Patients with gastric ulcer caused by NSAID use are managed with antisecretory therapy.

[Duodenal ulcer and Helicobacter pylori infection]. / Ulkus na dvanaesniku i infekcija Helicobacterom pylori.

The research accomplishment of Australian investigators Marshall and Warren, published in 1983, has entirely changed our understanding of ulcer genesis and proposed a new strategy in diagnostics and therapy of peptic ulcer disease. The key etiopathogenetic role of Helicobacter pylori has been recognised. Marshall confirmed on himself that Helicobacter pylori, as an infectious agent, fulfilled all Koch's postulates. The bacterial infection caused the mucosal inflammatory changes in his stomach which were rapidly resolved by antibiotics. During later clinical and experimental investigations the association of Helicobacter pylori and peptic ulcer has also been proved. Etiopathogenetic influence of Helicobacter pylori infection on duodenal ulcer development is nowadays very well known. Diagnostic guidelines, the modes of treatment and clinical management of these patients are mostly precisely defined. In this article, besides the general review of modern knowledge about Helicobacter pylori infection concerning epidemiology, etiopathogenesis, diagnostics and duodenal ulcer therapy, we are going to present also our results in the management of the large group of patients with duodenal peptic ulcer or ulcer scars.

[Gastroesophageal reflux disease and Helicobacter pylori infection]. / Gastroezofagealna refluksna bolest i infekcija Helicobacterom pylori.

Gastroesophageal reflux disease (GERD) is one of the common diseases of the upper gastrointestinal system. It is present in the whole world population, especially frequent in the developed countries. It evolves from pathological reflux which exposes the esophagus to the gastric contents which must overcome esophageal defense system. Many factors have been found to be involved in the pathogenesis of GERD; the most important one is the relaxation of the lower esophageal sphincter. Intensity of the disease is proportional to the amount of gastric contents refluxing from the stomach and the duration of esophageal exposure to this contents. GERD is currently in the spotlight because of its special significance in the development of very specific disease in the lower part of the esophagus--Barrett's esophagus, as well as esophageal adenocarcinoma which has lately been increasing in prevalence. Today, unrecognized and inadequately cured GERD is known to be a high risk factor for adenocarcinoma of the esophagus. In recent years the relation between GERD and Helicobacter pylori infection has been the topic of investigation by many prominent researchers. Therapy of GERD is based on inhibition of acid secretion. There are many different therapeutic agents available, however, proton pump inhibitors (PPI) are considered to be the most effective in the treatment of this disease.

[Helicobacter pylori and malignant diseases of the stomach]. / Helicobacter pylori i maligne bolesti zeluca.

The association between Helicobacter pylori infection and gastric malignancies, cancer and MALT lymphoma, has been suggested through several lines of evidence during the last decade. Although unresolved issues still cast doubts on the real weight of these association, in the sequence of events that leads to gastric cancer or lymphoma, Helicobacter pylori appears to play a prominent role in the very initial steps as causative agent of chronic gastritis. The subsequent events in the sequence--atrophy, intestinal metaplasia, dysplasia and cancer are multifactorial involving environmental agents, host response and characteristics of the bacterial strain itself. Recognition of the causal role of Helicobacter pylori infection in the cancer induction theoretically presents tools for its prevention. The ongoing studies will show in the future whether eradication or prevention of infection are followed by a reduction in risk of cancer. Lymphomas arising from gastric mucosa-associated lymphoid tissue (MALT) may be a clonal evolution starting from the infection. In low-grade gastric MALT lymphoma cure of the infection induces complete remission in the majority of patients. Longer follow-up investigations are necessary to determine if remissions indicate a cure of the disease.

[Helicobacter pylori--overview of therapy]. / Helicobacter pylori--pregled terapijskih mogucnosti.

The clinical significance of Helicobacter pylori infection in the etiopathogenesis of many gastroduodenal disorders, especially peptic ulcer disease and current awareness of the benefits of its eradication has entirely changed the current treatment of these diseases. Eradication was already defined as the disappearance of Helicobacter pylori from the gastric mucosa (finding negativization) confirmed at least 4 weeks (or later) after completed antibiotic eradication therapy. The regimen has to be simple, cheap and tolerable so that the patient could carry it out completely and as easy as possible (good compliance is required). The success of Helicobacter pylori eradication, evaluated by the strict "intention-to-treat" criteria, has to be higher than 80%. Current modern therapy should be triple and not longer than 7 days. One of three proton pump inhibitors is recommended as the antisecretory component (omeprazole, pantoprazole or lansoprazole). Two of three following antibiotis is added to this therapy: metronidazole/tinidazole, clarithromycin or amoxicillin. Treatment failure and growing number of antimicrobial resistant Helicobacter pylori strains require new ways of therapy and more effective drugs. Our results of 7-, 10- and 14-day therapy consisting of omeprazole, amoxicillin and metronidazole are poorer than those of drug combination including clarithromycin instead of amoxicillin. The results of Clinical Hospital "Merkur" showed that combination of amoxicillin, metronidazole and pantoprazole was more effective than the same combination with omeprazole, and the opposite was true for metronidazole and azithromycin combined with omeprazole and pantoprazole, respectively. The results of other medical centers prescribing the same eradication protocols were completely different. The differences are probably caused by poor patient compliance.