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The aim of the study was to evaluate the prevalence and character of non-steroid antiinflammatory drug (NSAID)-associated pathology in patients with rheumatic diseases (RD) in the Russian population. The study included questioning of 2537 RD patients (81% women and 19% men, mean age 55.8 +/- 14.2 years) who were taking NSAID, in 6 regions of Russia, between the October of 2003 and April of 2004. The results were analyzed using chi2 criterion, Fisher exact test, and Student t-criterion. 7.6% of the questioned and 14.7% of their relatives had ulcerous background [corrected] history (ulcers diagnosted prior to the beginning of treatment with NSAID). Most patients (70.1%) were taking non-selective NSAID (NSNSAID), chiefly diclophenac (50.9%). The most often used non-selective cyclooxygenasa-2 (COG-2) inhibitor was nimesulid, taken by 23.5% of the patients. 20.2% of patients were not aware of the influence of NSAID on the gastric and intestinal mucosa. 33.7% of the patients underwent esophagogastroduodenoscopy (EGDS) while taking NSAID. In 8.8% of the examined gastric or duodenal ulcers were found while they were taking NSAID; 1.5% of the examined developed gastro-duodenal hemorrhage or ulcer perforation. 53.1% of the questioned had gastroduodenal complaints; in most cases it was heartburn (37.3%), "heaviness" in the epigastral area (37.4%), and meteorism (37.4%). 51.3% of the patients associated gastroesopagial reflux and dyspepsia symptoms with intake of NSAID. 26.9% of the questioned associated stool disturbances and meteorism with NSAID intake. 32% of the patients took medications to eliminate gastrointestinal disorder symptoms. Patients taking selective COG-2 inhibitors had complaints less frequently than those who were taking NSNSAID (p = 0). Most frequently complaints were associated with intake of glucocorticoids (p = 0), low doses of aspirin (p = 0), smoking (p = 0), and elderly age (p = 0.007). Appearance of complaints was not associated with the dose of NSAID (diclophenac) (p = 0.257). 8.8% of the patients with ulcerous background were not aware of the effects of NSAID on the alimentory tract; 34.1% of the patients din not undergo EGDS withing the period of treatment with NSAID. Only 40.3% of patients were taking selective COG-2 inhibitors; 54.7% of patients were taking gastroprotective preparations. Alimentary tract pathology is a prevalent complication of therapy with NSAID in the Russian population. The most frequent gastrointestinal symptoms are subjective; they affect life quality substantially. Their risk factors are: elderly age, ulcer background, and glucocorticoid intake. Russian doctors do not take sufficient measures to prevent serious NSAID intake complications.

Asparate and alanine aminotransferase activity is approximately the same in different lobes of cerebral hemispheres of people with an uninjured central nervous system. The maximal activity of lactate, malate and succinate dehydrogenase is in the temporal lobes and thalami, the minimal one is in the corpus callosum. The activity of aminotransferases in the brain tumour lowers: in the dedifferentiated tumour the asparate aminotransferase shows a 23-24% decrease; in the case of the meningeal sarcoma it is 2.5 times as low: the activity of alaine aminogransferase is almost 10 times as low. The activity of malate dehydrogenase decreases in the neuroectodermal tumours and sharply (almost twice) in multiform glioblastoma. In the dedifferentiated meningiomas the activity of all the dehydrogenases is increased.

An acute intraperitoneal administration of ethanol (4-8 g/kg) produced a fall in the activity of malate-dehydrogenase (MDG), alanine- and aspartate-aminotransferase in homogenates and mitochondria of the cerebellum, large hemispheres and liver of the rats by 25 and 50 per cent, respectively. The activity of succinate-dehydrogenase (SDG) increased by 24 per cent in the large hemispheres and fell by 20 per cent in the liver and in the cerebellum homogenate. The activity of lactate-dehydrogenase (LDG) of the large hemispheres and liver mitochondria decreased by 30 per cent. A chronic (1 1/2-2 month long) ethanol intoxication produced a drop of the LDG and MDG in the mitochondria of the nerve structures and of aminotransferase in the liver. The SDG activity rose in the homogenate of the cerebellum, large hemispheres and of the liver by 80, 50 and 20 percent, respectively. The dehydrogenases and aminotransferases activity in the liver and nerve structures of rats in the state of abstinence was somewhat below the normal, but higher than in animals chronically consuming alcohol.

Chronically alcoholized intoxication (1.5--2 months) induces adaptation of cerebral neurones to changing equilibrium states of biochemical processes by altering the activity of enzymes of GABA metabolism, reduction of alanine and aspartate transaminase activity and increase of LDH and succinate dehydrogenase activity. In the cerebellum and cerebral hemispheres during alcohol abstinacy the activity of GABA-T, succinate dehydrogenase and aspartate transaminase was reduced while that of LDH and alanine transaminase was increased. The administration of fusarinic acid (100 mg/kg i. p.) to control animals induced a sharp increase of GAD activity in both structures of the brain. The stimulatory effects of fusarinic acid were not observed when it was administered to animals receiving alcohol chronically. Motor activity or rats was markedly reduced during chronical alcoholism and the first days of alcohol abstinacy (24--48 h), as well as following injection fusarinic acid and homopantothenic acid. The increase of locomotion and the vertical component of motor activity was observed only following one week or one month after alcohol abstinacy.