Fractal and stereological analyses of insulin-induced rat exocrine pancreas remodelling.

BACKGROUND: The effect of insulin on the endocrine pancreas has been the subject of extensive study, but quantitative morphometric investigations of the exocrine pancreas are scarce. This study was therefore undertaken to investigate the effect of acute and chronic insulin administration (two doses, 0.4 IU and 4 IU) on the morphology of rat pancreas acini. MATERIALS AND METHODS: Semi-fine sections stained with methylene blue and basic fuchsine or haematoxylin and eosin-stained 5-micrometer thick paraffin sections were used for fractal and stereological analysis of exocrine acini. Acute insulin treatment, independent of applied doses increased fractal dimension in line with decreased lacunarity of pancreas acini. Chronic low dose insulin decreased fractal dimension and increased lacunarity of pancreas acini, but a high dose had the opposite effect. The volume densities (Vv) of cytoplasm, granules and nucleus are affected differently: acute low dose and high chronic dose significantly decreased granules Vv, and in line increased cytoplasmic Vv, whereas other examined structures showed slight changes without statistical significance. RESULTS: The results obtained from this investigation indicate that insulin treatment induced structural remodelling of the exocrine pancreas suggesting a substantial role of insulin in its functioning. CONCLUSIONS: Additionally, we showed that fine architectural changes in acini could be detected by fractal analysis, suggesting this method as an alternative or addition to routine stereology.

New insights into male (in)fertility: the importance of NO.

Infertility is a global problem that is on the rise, especially during the last decade. Currently, infertility affects approximately 10-15% of the population worldwide. The frequency and origin of different forms of infertility varies. It has been shown that reactive oxygen and nitrogen species (ROS and RNS) are involved in the aetiology of infertility, especially male infertility. Various strategies have been designed to remove or decrease the production of ROS and RNS in spermatozoa, in particular during in vitro fertilization. However, in recent years it has been shown that spermatozoa naturally produce a variety of ROS/RNS, including superoxide anion radical (O2 (⋅-)), hydrogen peroxide and NO. These reactive species, in particular NO, are essential in regulating sperm capacitation and the acrosome reaction, two processes that need to be acquired by sperm in order to achieve fertilization potential. In addition, it has recently been shown that mitochondrial function is positively correlated with human sperm fertilization potential and quality and that NO and NO precursors increase sperm motility by increasing energy production in mitochondria. We will review the new link between sperm NO-driven redox regulation and infertility herein. A special emphasis will be placed on the potential implementation of new redox-active substances that modulate the content of NO in spermatozoa to increase fertility and promote conception.

Calcium-induced alteration of mitochondrial morphology and mitochondrial-endoplasmic reticulum contacts in rat brown adipocytes.

Mitochondria are key organelles maintaining cellular bioenergetics and integrity, and their regulation of [Ca2+]i homeostasis has been investigated in many cell types. We investigated the short-term Ca-SANDOZ® treatment on brown adipocyte mitochondria, using imaging and molecular biology techniques. Two-month-old male Wistar rats were divided into two groups: Ca-SANDOZ® drinking or tap water (control) drinking for three days. Alizarin Red S staining showed increased Ca2+ level in the brown adipocytes of treated rats, and potassium pyroantimonate staining localized electron-dense regions in the cytoplasm, mitochondria and around lipid droplets. Ca-SANDOZ® decreased mitochondrial number, but increased their size and mitochondrial cristae volume. Transmission electron microscopy revealed numerous enlarged and fusioned-like mitochondria in the Ca-SANDOZ® treated group compared to the control, and megamitochondria in some brown adipocytes. The Ca2+ diet affected mitochondrial fusion as mitofusin 1 (MFN1) and mitofusin 2 (MFN2) were increased, and mitochondrial fission as dynamin related protein 1 (DRP1) was decreased. Confocal microscopy showed a higher colocalization rate between functional mitochondria and endoplasmic reticulum (ER). The level of uncoupling protein-1 (UCP1) was elevated, which was confirmed by immunohistochemistry and Western blot analysis. These results suggest that Ca-SANDOZ® stimulates mitochondrial fusion, increases mitochondrial-ER contacts and the thermogenic capacity of brown adipocytes.

Endothelial cell apoptosis in brown adipose tissue of rats induced by hyperinsulinaemia: the possible role of TNF-α.

The aim of the present study was to investigate whether hyperinsulinaemia, which frequently precedes insulin resistance syndrome (obesity, diabetes), induces apoptosis of endothelial cells (ECs) in brown adipose tissue (BAT) and causes BAT atrophy and also, to investigate the possible mechanisms underlying ECs death. In order to induce hyperinsulinaemia, adult male rats of Wistar strain were treated with high dose of insulin (4 U/kg, intraperitonealy) for one or three days. Examinations at ultrastructural level showed apoptotic changes of ECs, allowing us to point out that changes mainly but not exclusively, occur in nuclei. Besides different stages of condensation and alterations of the chromatin, nuclear fragmentation was also observed. Higher number of ECs apoptotic nuclei in the BAT of hyperinsulinaemic rats was also confirmed by propidium iodide staining. Immunohistochemical localization of tumor necrosis factor-alpha (TNF-α) revealed increased expression in ECs of BAT of hyperinsulinaemic animals, indicating its possible role in insulin-induced apoptotic changes. These results suggest that BAT atrophy in hyperinsulinaemia is a result of endothelial and adipocyte apoptosis combined, rather than any of functional components alone.

Expression pattern of thermogenesis-related factors in interscapular brown adipose tissue of alloxan-treated rats: beneficial effect of L-arginine.

Metabolic abnormalities underlying diabetes can be abrogated by L-arginine. Here we examined the molecular basis of disturbed interscapular brown adipose tissue (IBAT) thermogenesis and the possible role of nitric oxide (NO) in the IBAT of diabetic rats. To induce diabetes, adult Mill Hill hybrid hooded male rats were given a single alloxan dose (120 mg/kg). Both non-diabetic and diabetic groups were further divided into three subgroups receiving: (i) L-arginine.HCl (2.25%) or (ii) N(omega)-nitro-L-arginine methyl ester (L-NAME.HCl, 0.01%) for 12 days in drinking water and (iii) untreated controls. Treatment of the diabetic animals started after diabetes induction (glucose level 12 mmol/L). Diabetes led to a decrease in the mRNA levels of uncoupling protein 1 (UCP1), peroxisomal proliferator activator receptor gamma (PPARgamma) and endothelial NO synthase (eNOS) as revealed by RT-PCR. The diabetic rats had reduced eNOS and inducible NOS (iNOS) protein contents accompanied by low tissue vascularization, a parameter directly related to tissue thermogenic state. Downregulation of glutathione peroxidase (GSH-Px) and catalase (CAT) transcripts were also observed in diabetes. In contrast, the expression level of PPARgamma coactivator-1alpha (PGC-1alpha) mRNA was elevated. Supplementation with L-arginine not only restored diabetes-induced changes in the expressions of these molecules important for IBAT regulation, but also increased the vascularity. Interestingly, L-NAME induced similar patterns of changes in vascularity and PGC-1alpha mRNA level as did l-arginine. In summary, our results provide insight into the molecular basis underlying diabetes-induced metabolic and functional disturbances in the IBAT and suggest a beneficial role for the L-arginine-NO production pathway.

Nitric oxide regulates mitochondrial re-modelling in interscapular brown adipose tissue: ultrastructural and morphometric-stereologic studies.

As a complex, cell-specific process that includes both division and clear functional differentiation of mitochondria, mitochondriogenesis is regulated by numerous endocrine and autocrine factors. In the present ultrastructural study, in vivo effects of L-arginine-nitric oxide (NO)-producing pathway on mitochondriogenesis in interscapular brown adipose tissue (IBAT) were examined. For that purpose, adult Mill Hill hybrid hooded rats were receiving L-arginine, a substrate of NO synthases (NOSs), or N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOSs, as drinking liquids for 45 days. All experimental groups were divided into two sub-groups - acclimated to room temperature and cold. IBAT mitochondria were analyzed by transmission electron microscopy and stereology. L-Arginine treatment acted increasing the number of mitochondrial profiles per cell profile, as well as volume fraction of mitochondria per cell volume in animals maintained at room temperature. Cold-induced enhancement of number of mitochondrial profiles per cell profile was additionally increased in L-arginine-treated rats. Ultrastructural examinations of L-arginine-treated cold-acclimated animals clearly demonstrated thermogenically active mitochondria (larger size, lamellar, more numerous and well-ordered cristae in their profiles), which however were inactive in L-arginine-receiving animals kept at room temperature (small mitochondria, tubular cristae). By contrast, L-NAME treatment of rats acclimated to room temperature induced mitochondrial alterations characterized by irregular shape, short disorganized cristae and megamitochondria formation. These results showed that NO is a necessary factor for mitochondrial biogenesis and that it acts intensifying this process, but NO alone is not a sufficient stimulus for in vivo induction of mitochondriogenesis in brown adipocytes.

The role of nitric oxide in remodeling of capillary network in rat interscapular brown adipose tissue after long-term cold acclimation.

Cold exposure has been shown to increase blood flow in interscapular brown adipose tissue (IBAT). The aim of the present study was to evaluate the role of the L-arginine-nitric oxide (*NO) pathway on IBAT capillary network remodeling and its possible correlation with superoxide anion radical (O2(*-)). In the rats that received L-arginine (2.25%) or NG-nitro-L-arginine methyl ester (L-NAME, 0.01%) as a drinking liquid and maintained at room (22+/-1 degrees C) or low (4+/-1 degrees C) temperature for 45 days, IBAT capillaries were analyzed by stereology and observed by light and electron microscopy. Additionally, endothelial *NO synthase (eNOS) expression, nitrotyrosine immunoreactivity and both copper zinc superoxide dismutase (CuZnSOD) enzyme activity and immunohistochemical localization were examined. Stereological analyses of IBAT show that the capillary volume density, as well as capillary-to-brown adipocytes ratio, are increased in cold. L-arginine treatment increases, while L-NAME decreases both parameters, compared to respective controls. Those changes were accompanied by capillary dilatation observed by light and electron microscopy. The activity of CuZnSOD is lower in control cold-acclimated rats, as well as in both L-arginine-treated groups, when compared to control animals acclimated to room temperature. L-NAME treatment attenuates the effects both of cold and L-arginine on CuZnSOD and increases immunopositivity for CuZnSOD in room temperature-acclimated rats. Our results show that *NO induces remodeling of the IBAT capillary network by angiogenesis, and presumably that interaction with O2(*-) has a role in that modulation. The increased eNOS expression accompanied by an increased nitrotyrosine immunoreaction observed in both L-arginine-treated groups compared to corresponding controls strengthens this hypothesis.

Quantification of Helicobacter pylori resistance in functional and organic dyspepsia.

OBJECTIVE: To compare the efficacy of Helicobacter pylori eradication in patients with functional and organic dyspepsia. METHODS: The study included a cohort of 160 patients (115 with organic and 45 with functional dyspepsia) with dyspeptic symptoms and gastroscopically confirmed H. pylori infection. Triple therapy with omeprazole 20 mg, amoxicillin 1000 mg and metronidazole 400 mg (OAM) was administered twice a day for a week. Minimal inhibition concentration (MIC) was estimated on cultures from 41 patients with positive H. pylori for determination of antimicrobial sensitivity and primary resistance to amoxicillin and metronidazole. RESULTS: Endoscopic examination at least 6 weeks after therapy showed that 116 (72.5%) patients had H. pylori eradicated, whereas 44 (27.5%) were not. From the latter patients, 10 (23%) had functional dyspepsia and from 116 eradicated patients 35 (30%) had functional dyspepsia. Difference in efficacy of OAM therapy between patients with organic and functional dyspepsia was not significant (P > 0.5). Percentages of non-eradicated patients with organic and functional dyspepsia were 29.6 and 22.2%, respectively (ratio 1.3 : 1). MIC from 41 samples showed 18 (44%) in vitro resistant strains. There was no resistance to amoxicillin. CONCLUSIONS: There is no significant difference in H. pylori resistance to the same antibiotic between patients having functional or organic dyspepsia.

Doxorubicin toxicity to the skin: possibility of protection with antioxidants enriched yeast.

The possibility of skin protection against doxorubicin toxicity was examined after oral antioxidative pretreatment of the rats with yeast supplemented with selenium and vitamins E, C and A for 15 days. The activity and level of antioxidative defense components were monitored in the skin and blood 48 h after i.v. applied doxorubicin. In the blood, increased glutathione peroxidase activity in the erythrocytes, and amounts of vitamin E and glutathione in the plasma were found after the antioxidative treatment. It also led to an increase of the reductive capacity in the skin (increased thioredoxin reductase activity and reduced glutathione level). Doxorubicin alone, depleted reductive capacity, i.e. decreased the activity of thioredoxin reductase in the skin, as well as the content of reduced glutathione both in the skin and blood plasma. Depletion of reductive capacity represents one of the first harmful doxorubicin effects to the skin at the time when the changes of other antioxidative enzyme activities were not detectable. Reductive capacity in the skin of animals given antioxidative pretreatment was maintained elevated upon doxorubicin application in comparison with the corresponding control. Oral supplementation with antioxidants thus prevents toxic effects of doxorubicin in the skin and may contribute to the alleviation of its secondary cytotoxicity during the chemotherapy.

Seasonal changes in the antioxidative defense in ground squirrels (Citellus citellus): possible role of GSH-Px.

As seasonal hibernators, ground squirrels decrease their body temperature to 7 degrees C and hibernate during the winter. Maintenance at 30 degrees C prevents seasonal changes of body temperature and animals remain euthermic and active. We measured selenium (Se)-dependent glutathione peroxidase (GSH-Px), as well as the activity of other antioxidative components such as superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), and glutathione-S-transferase (GST) and the amount of low-molecular-weight antioxidants glutathione (GSH), ascorbic acid (AsA), and vitamin E (vit E) in spring, summer, and winter in ground squirrels continuously kept at a temperature of 30 degrees C. We examined liver and interscapular brown adipose tissue (IBAT) as thermogenic tissues, as well as the brain and the kidneys. During the winter, we found a decrease in enzymatic activity and an increase in the level of low molecular antioxidants in all tissues. Correlation analysis revealed a similarity in the composition of antioxidative defense (AD) among the tissues examined. The results obtained clearly demonstrated numerous correlative expressions of antioxidative components in this experimental model, especially of GSH-Px, suggesting the complexity of the system responsible for the maintenance of physiological homeostasis.

Seasonal changes in the activity of antioxidative defense in the kidneys of the euthermic ground squirrel (Citellus citellus).

The aim of this work was to determine the activity of the antioxidant enzymes: superoxide dismutase (EC 1.15.1.1; SOD), catalase (EC 1.11.1.6; CAT), glutathione peroxidase (EC 1.11.1.9; GSH-Px), glutathione-S-transferase (EC 2.5.1.18; GST), glutathione reductase (EC 1.6.4.2; GR) and the low molecular mass antioxidants: ascorbic acid (ASA) and vitamin E (vit E) in the kidney of ground squirrels during circannual changes. Keeping the ground squirrel at the temperature of thermic neutrality (30 degrees C) provides a stable euthermic state during the whole year and thus any change is due to the circannual rhythm. The highest specific activity of all examined antioxidative defense enzymes in the kidney was found in the spring, when ground squirrels are seasonally the most active. In the summer, lower specific activity of GSH-Px as well as of SOD and CAT were noted and, when expressed per g wet mass, only a decrease in GSH-Px activity was recorded. In the kidney of ground squirrels kept at 30 degrees C, the lowest specific activity of all examined enzymes was found during the winter and, when expressed per g wet mass, only the SOD activity was lower than in the spring and summer. Higher amounts of vitamins C and E were found in the ground squirrel kidneys in the summer. The results obtained in this work demonstrate that circannual regulation of metabolic activity, which is inherent to seasonal hibernators, is also expressed at the level of antioxidative defense in the kidneys.

Effect of selenium-enriched yeast pretreatment on the antioxidative defense in the skin of rats exposed to heat shock.

Skin protection against heat shock and the specificity in the organization of antioxidative defenses were examined in rats given oral antioxidative pretreatment with selenium (Se)-enriched yeast and vitamins E, C, and A for 15 days and then exposed to hyperthermia. The activity of antioxidative enzymes in the skin and the liver was monitored 1 hour and 3 hours after heat shock. Glutathione peroxidase (GSH-Px) activity was increased in the skin after heat shock in the groups supplemented with antioxidants, but not in the controls. In contrast, the activity of liver GSH-Px was increased only in the controls receiving antioxidants. Heat shock led to a decrease in liver superoxide dismutase (SOD) activity at 1 hour in the antioxidant-supplemented group, but this was unchanged in the liver of all other groups and in the skin. The activity of thioredoxin reductase (TR) in the skin was increased in the antioxidant supplemented group 1 hour after heat shock, whereas the hepatic thioredoxin reductase activity was decreased. The activities of catalase (CAT), glutathione reductase (GR), and glutathione-S-transferase (GST) were unaffected by either treatment. These results suggest that supplementation with antioxidants protects the skin against heat shock, especially with respect to the GSH-Px and TR activity. The different response of the skin in comparison with the liver probably reflects differences in organization and regulation of antioxidative defenses.

Glutathione-dependent antioxidant enzyme activities and glutathione content in the rat brain at different stages of oestrous cycle.

Enzymatic activities of glutathione peroxidase, glutathione-S-transferase, glutathione reductase and catalase, as well as the glutathione content were measured in the brain tissue of regularly cycling rats at dioestrus, proestrus and estrus. The activity of glutathione peroxidase was found to be suppressed at proestrus, whereas that of catalase was increased at dioestrus. Glutathione transferase and glutathione reductase activities, as well as the glutathione content appeared to be stable during the oestrous cycle. These results suggest that, in the female rat, glutathione peroxidase and catalase activities in the brain tissue are influenced by the ovarian hormone status.

Seasonal variation in the antioxidant defense system of the brain of the ground squirrel (Citellus citellus) and response to low temperature compared with rat.

Seasonal variation in the activity of antioxidant enzymes (superoxide dismutase (EC 1.15.1.1.; SOD), catalase (EC 1.11.1.6; CAT), glutathione peroxidase (EC 1.11.1.9; GSH-Px), glutathione reductase (EC 1.6.4.2; GR), glutathione-S-transferase (EC 2.5.1.18; GST) and low-molecular-weight antioxidants: ascorbic acid (AsA), vitamin E (VIT E) and glutathione (CSH+GSSG) were examined in the brain of the ground squirrels (Citellus citellus) maintained at 30 degrees C during the whole year. The highest activity (per mg protein) of antioxidant defense (AD) enzymes was found in the spring and was much lower in the summer. A further decrease in activity of CAT, GSH-Px and GST was observed in the winter. The highest levels of AsA and glutathione were recorded in winter in comparison with spring and summer. AD system in the brain of the ground squirrel and rates (maintained at thermoneutrality) exposed to low temperature (4 degrees C) for 3, 6 or 24 hr during the summer was studied as well. Summer was chosen as a period of stable euthermia for ground squirrels and in thermoregulation similar to rats. Consumption of free fatty acid and glucose during the acute exposure to low temperature was found to be species specific. In the ground squirrel, an increase in the specific activities of SOD, after 3, 6 and 24 hr, CAT after 3 and 6 hr and GR after 6 hr of exposure to low temperature was detected. When activities were expressed in U/g wet mass, an increase of SOD after 3, 6 and 24 hr (P < 0.02, P < 0.02, P < 0.005) and CAT and GSH-Px 3 hr (P < 0.01) upon exposure to low temperature was observed. In the rats, no changes in the specific activities of these enzymes after exposure to low temperature were recorded and only an increase in GST activity (U/g wet mass) after 6 hr exposure was registered. Low-molecular-weight AD components in both animal species were unchanged upon short-term exposure to low temperature. The species-specific differences in brain AD between the rats and the ground squirrels after short exposure to low temperature may be ascribed to seasonal changes of the brain activity in the latter.

Activity of antioxidant defense enzymes and glutathione content in some tissues of the Belgrade (b/b) laboratory rat.

The activity of antioxidant defense (AD) enzymes--superoxide dismutase (SOD, EC 1.15.1.1.), catalase (CAT, EC 1.11.1.6.), glutathione peroxidase (GSH-Px, EC 1.11.1.9.), glutathione-S-transferase (GST, EC 2.5.1.18), glutathione reductase (GR, EC 1.6.4.2) and glutathione (GSH) content of the anemic Belgrade (b/b) laboratory rats--were measured and analyzed in liver, spleen, lung, heart, brain and testes in comparison with nonanemic controls. The activities of hepatic Mn SOD, CAT, GSH-Px and GST (P < 0.02, P < 0.01 and P < 0.005) were decreased in anemic, comparing with nonanemic animals, whereas the spleen CuZn SOD, Mn SOD, CAT and GSH-Px (P < 0.005, P < 0.02, P < 0.005 and P < 0.01) activities were increased. In the lung of anemic rats, Mn SOD, GSH-Px and GR (P < 0.005, P < 0.01, P < 0.05) activities were higher, whereas GST (P < 0.01) activity was lower in relation to nonanemic ones. In anemic rats, heart Mn SOD (P < 0.05) activity was increased, brain GSH-Px (P < 0.005) activity was lower, whereas GR (P < 0.02) activity was higher compared with nonanemic controls. CuZn SOD (P < 0.05) activity in the testes was elevated and GSH-Px (P < 0.05) reduced in anemic animals. GSH content was decreased in the liver (P < 0.01), lung and brain (P < 0.005) and increased in the spleen (P < 0.02) of anemic rats in relation to the controls. Our data suggest phenotype specific differences in the AD system of the Belgrade (b/b) rat tissues in comparison with nonanemic controls.

Effect of long-term exposure to cold on the antioxidant defense system in the rat.

Catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), and glutathione-S-transferase (GST) activities as well as glutathione (GSH), ascorbic acid (AsA), and vitamin E concentrations were analyzed in the blood, liver, brain, interscapular brown adipose tissue (IBAT), and small intestine of rats exposed to low environmental temperature (4 degrees C; 35, 75, and 105 d of exposure) and in controls of the same age exposed to an environmental temperature of 22 +/- 2 degrees C. Prolonged cold exposure resulted in an increase in GSH-Px in IBAT and in small intestine after 35, 75, and 105 d of exposure. Catalase activity in cold-exposed animals was higher in IBAT after 75 and 105 d of cold exposure. Glutathione reductase activity was greater in brain after 35 d, in liver after 75 d, and in IBAT after 105 d of exposure to low temperatures as compared to the controls. In contrast, GST activity was lower in liver and IBAT after 35 and 75 d of cold exposure. AsA and GSH (determined only 105 d after cold exposure) were markedly higher in IBAT, whereas plasma GSH was lower and plasma AsA was higher in cold-exposed animals. The observed changes in analysed components of the antioxidant defense system under conditions of prolonged exposure to low temperature suggest that a reorganization the activity of this system at the molecular level occurred. Although other studies indicate that a 21-d cold exposure is sufficient for adaptation of thermogenesis, the present study shows that in general, longer periods are required for the registration of the changes in the antioxidant defense system.

[The effect of atmospheric conditions on the occurrence of peptic ulcer hemorrhage]. / Utjecaj atmosferskih uvjeta na ucestalost krvarenja iz peptickog ulkusa.

The influence of atmospheric factors on the frequency of bleeding from the peptic ulcer was studied within the period from April 1, 1984, to March 31, 1989, consequently through 1826 days. The average daily atmospheric pressure, the average daily temperature and the relative humidity have been examined. There were 1102 cases of bleeding peptic ulcer, 537 bleeding gastric ulcers and 565 bleeding duodenal ulcers. During the study period there were 454 days with bleeding form ventricular ulcer and 465 days with bleeding from duodenal ulcer. There was 793 days with bleeding form either lesion. The discriminatory analysis demonstrated that the atmospheric pressure is the variable that discriminates the days with bleeding and the days prior to bleeding from the days without bleeding. The relative humidity occurs as the relevant discriminatory variable in the days prior to bleeding for the duodenal ulcer group and for the entire group. The centroids of the discriminatory function demonstrate that the days with ulcer bleeding are characterized by the fall of atmospheric pressure. The factor analysis of meterological variables clearly shows the correlation of the atmospheric pressure and the bleeding regardless to the localisation of bleeding ulcer, where the greatest number of bleedings is correlated with lower atmospheric pressure. We conclude that the incidence of bleeding form the peptic ulcer of the stomach and duodenum correlates in great measure with low atmospheric pressure in the days prior to bleeding and in the days of bleeding, as well as with fall of atmospheric pressure in the days of bleeding with respect to previous day.(ABSTRACT TRUNCATED AT 250 WORDS)

Ulcerative colitis in Zagreb, Yugoslavia: incidence and prevalence 1980-1989.

We present a ten-year incidence of ulcerative colitis in Zagreb, Yugoslavia. The study included both outpatients and inpatients regardless of the extent and severity of the disease. The mean annual incidence rate was 1.5 per 100,000 inhabitants for the period of 1 January 1980 through 31 December 1989. There was no increase in the incidence of ulcerative colitis during the study period. A prevalence rate estimate of 21.4 per 100,000 inhabitants was based on July 1985 official estimated population. The results confirm the low frequency of ulcerative colitis in central Europe.

Prophylactic administration of ranitidine after sclerotherapy of esophageal varices.

The present trial was carried out to determine the usefulness of H2-receptor antagonist drug therapy for the prevention of esophageal bleeding and esophageal varices in patients who underwent sclerotherapy. According to randomization, out of the 58 patients, 28 received, along with the usual standard therapy, ranitidine and 30 received placebo. Ranitidine, 50 mg, was administered intravenously over a period of 3 days every 8 hours, and then 150 mg of ranitidine was given per os in the evening for one month. For improvement of hemostasis and during the elective sclerotherapies, 1% polidocanol was used as the sclerosant. During each puncture, 2 ml was injected. Injections were paravasal and intravasal. After sclerotherapy, endoscopic examinations were carried out on the third day and one month later. Necrosis was noted in 42% of the patients and esophageal mucosal inflammation in 26%. Esophageal ulcers did not occur. There was no statistically significant difference between the two groups in terms of age, sex ratio, cause of liver cirrhosis, and the Child's classification. The size of the esophageal varices had no effect on the development of esophageal mucosal changes in correlation with the quantity of sclerosant. The comparison of the two groups of patients, sclerosed for hemorrhage and sclerosed electively, showed no statistically significant difference regarding esophageal mucosal changes. No differences between the ranitidine and placebo groups of patients were observed in this indication. It can be concluded that esophageal mucosal changes probably arise as a consequence of the sclerosant, its concentration, quantity and mode of application.(ABSTRACT TRUNCATED AT 250 WORDS)

Epidemiology of Crohn's disease in Zagreb, Yugoslavia: a ten-year prospective study.

A ten-year prospective study of Crohn's disease was carried out in Zagreb, Yugoslavia. It included both inpatients and outpatients regardless of the extent and severity of the disease. The mean annual incidence rate was 0.7 per 100,000 between 1 January 1980 and 31 December 1989. There was no increase in the incidence of Crohn's disease during the study period. The prevalence of Crohn's disease was 8.3 per 100,000 on 31 December 1989. The results confirm the low frequency of Crohn's disease in central and southern Europe.