[Silibinin and its hepatoprotective action from the perspective of a toxicologist]. / Sylibinina i jej dzialanie hepatoprotekcyjne z punktu widzenia toksykologa.

Silibinin is the most active component of a complex of flavonoids -silymarin contained in fruit milk thistle (Sylibum marianum). Its mechanism of action is complex and highly beneficial in protecting hepatocytes. On the one hand this compound blocks the penetration of various toxins (for example amanitin) into the hepatocytes not allowing in this way for the cell death and on the other hand, it prevents apoptosis through intracellular. It protects the liver from oxidative intracellular free radicals by increasing the activity of enzyme superoxide dismutase and peroxidase, as well as by increasing the concentration of glutathione and the activity of the peroxidase. Silibinin strengthens and stabilizes the cell membranes, inhibits the synthesis of prostaglandins associated with the lipid peroxidation and promotes regeneration of liver through the stimulation of protein synthesis and effect on the production of new hepatocytes. A particularly interesting topic from the perspective of a toxicologist is the application of silibinin in Amanita phalloides poisoning. Clinical trials conducted in this respect are very encouraging. The other beneficial application of silibinin is in therapy of the alcoholic liver cirrhosis. The evidence shows that the use of silymarin leads to a significant reduction in liver-related mortality and even reduction in the number of patients with encephalopathy in the course of the disease. Application of silibinin goes beyond liver disease and expands in the direction of cancer and even diabetes. What is interesting is the fact, that the substance of herbal origin occurring in the environment is so strong, favorable, beneficial and multidirectional. Science has contributed to improving the bioavailability of silibinin thus making it more effective.

[The harmfulness of drugs and slimming substances--a toxicologist's point of view]. / Szkodliwosc leków i srodków wspomagajacych odchudzanie--punkt widzenia toksykologa.

Obesity in rapidly developing countries has recently become an epidemic. That is why the need to fight against this chronic disease is becoming more and more apparent. In order to lose weight it is necessary to achieve negative energy balance either by increasing physical activity or using a low calorie diet. When these methods are ineffective, pharmacotherapy is used. The criterion for the application of medical treatment is a BMI above 30 kg/m2 or above 27 along with the presence of other risk factors. Drugs for weight loss fall into three groups: appetite inhibitors, those increasing energy expenditure by enhancing thermogenesis and those inhibiting the absorption of food in the intestines. This paper presents an overview of these classes of drugs and dietary supplements with an emphasis on their adverse effects and the possibility of poisoning. Despite the fact that in Poland only one drug - orlistat has been registered for the treatment of obesity, the availability of other products is unlimited due to the Internet. This fact, and the tendency of patients to treat obesity by themselves using pharmacological substances, poses a major threat and a challenge to the toxicologist.

[Severe tricyclic antidepressants poisoning--a case study]. / Ciezkie zatrucie trójcyklicznymi antydepresantami--opis przypadku.

Long QT syndrome is a disease characterized by periodic or constant prolongation of QT interval and attacks of ventricular polymorphic tachycardia known as torsade de pointes. It may appear as a result of various medicines application, both anti-arrhythmic and non-cardiovascular. Currently, a list of medicines which may cause proarrhythmic action in consequence of QT prolongation is long and constantly updated. It contains tricyclic antidepressants, which are the most toxic antidepressants currently used and are often the cause of poisoning and hospitalization on toxicology wards. The paper presents the case of a 20-year-old man, treated in the clinical toxicology ward, after severe poisoning with tricyclic antidepressants. The patient, treated many times in our toxicology centre, had very high concentration of tricyclic antidepressants in the serum (2768 ng/ml). The concentration above 1000 ng/ml indicates serious life-threatening poisoning. Very severe symptoms of cardiotoxicity were observed: in ECG - wide QRS (160 ms) with heart rate 120-150 per minute, ventricular tachycardia, periodically polymorphic, prolongation of QT interval, hypotonia (80/60 mm Hg) and also recurrent attacks of seizures. Also metabolic/respiratory acidosis was stated (pH - 7.089; pCO2 - 56.9 mm Hg, HCO3 - 16.8 mmol/l). Gastric lavage, activated charcoal were administered, symptomatic and supportive treatment according to the intensive therapy rule was applied, including sodium bicarbonate, magnesium sulfate and vasopressors intravenous infusion. High concentration of the drug, unknown after ingestion and significantly developed symptoms of cardiotoxicity caused, that the treatment was ineffective. The case described shows that treatment of severe poisoning with tricyclic antidepressants and induced acquired long QT syndrome is still a challenge.

[Sodium azide poisoning--a rare reason of hospitalization in toxicological units--case report]. / Zatrucie azydkiem sodu--rzadka przyczyna hospitalizacji w osrodkach toksykologicznych--opis przypadku.

Sodium azide poisonings are a rare reason for hospitalization in toxicological units. They are observed as rarely as once within a number of years per hospital. Consequently, an algorithm for the optimum procedure of treating such intoxications does not exist and, as a result, there is a need to describe every single clinical case. A female, aged 55, was directed to the toxicological unit from a county hospital after swallowing four tablets of sodium azide, 150 mg each, in the form of preservative for fresh milk samples. Two hours after the incident a gastric lavage was performed and the tableting blend was retrieved. In the clinical examination higher concentration of lactic acid, ALAT and TSH were observed. In the ECG record unspecific aberrations in the ST segment were noticed. Due to the patient's general good condition and the fact that the tableting blend had been retrieved from the gastric rinse, further use of the antidote indicated in the therapy of cyanide intoxications was abandoned. Symptomatic treatment was used along with the patient's eight-day observation. In the described case the early decontamination prevented the development of acute poisoning.

[Myocardial infarction in the course of ethylene glycol poisoning--a case report]. / Zawal serca w przebiegu zatrucia glikolem etylenowym--opis przypadku.

The following paper describes the case of the 59-year-old patient moved from Clinical Cardiology to the Centre of Clinical Toxicology because of severe ethylene glycol poisoning, which occurred in the course of myocardial infarction of inferior wall. Ethylene glycol concentration was 85 mg/dl, the blood pH - 6.9, troponin >50 ng/ml, CK-MB 297.1 U/L. ECG current of injury was found at the bottom of the wall cuts reflective reductions in section ST in leads I, aVL and the precordial leads. In the coronarography was RCA occlusion, OM critical stenosis and suspected mouth of LAD stenosis. RCA urgent angioplasty was performed with implantation of bare metal stents 5. In addition, toxicological treatment consisted of mechanical ventilation, hemodialysis, ethanol, and intensive medical care. On 19 day of hospitalization the patient in good general condition was discharged home.

[Noncardiogenic pulmonary edema in the course of poisoning with clozapine, ketoprofen and thiethylperazine]. / Niekardiogenny obrzek pluc w przebiegu zatrucia klozapina, ketoprofenem i tietylperazyna.

Pulmonary edema is a severe, potentially fatal clinical condition. It happens, when interstitial fluid is accumulating in the alveoli, impeding proper gas exchange. Typically we distinguish cardiogenic and noncardiogenic pulmonary edema. The article describes the case of severe pulmonary edema, which occurred in a young woman, free of cardiac diseases, about 30 hours after a suicidal drug poisoning (clozapine, ketoprofen, thiethylperazine). Both clozapine and ketoprofen intoxication, may be severe. Complications in these poisonings affect not only the central nervous system, but also the circulatory or respiratory system and may even occur several hours after the overdose of these drugs. The study considered the causes and possible mechanisms of pulmonary edema in poisoning with these drugs.

[Extremely severe metabolic acidosis and multi-organ complications in ethylene glycol intoxication: a case study]. / Skrajnie ciezka kwasica metaboliczna i powiklania wielonarzadowe w przebiegu zatrucia glikolem etylenowym--opis przypadku.

The paper presents the case of a female, 36, hospitalised in the Lublin Regional Center of Clinical Toxicology, diagnosed with heavy ethylene glycol intoxication. The patient suffered from metabolic acidosis with pH at 6.6, bases shortage - 35,5 mmol/l, renal failure, acute respiratory failure, symptoms of CNS damage such as prolonged coma, followed by dysphasia and the lower limbs paresis persisting for a few weeks. During the treatment, ethanol was used as a competitive inhibitor of alcoholic dehydrogenase along with hemodialyses, intensive symptomatic treatment, care and rehabilitation. In spite of the severe course of the intoxication, the procedures employed with the patient resulted turned out to be effective, with total renal failure regression, lower limb paresis regression, speech function regain and regular motor apparatus function regain and the regaining of speech and regular motor apparatus functions. The case description proves that intensive therapy might lead to recovery even in cases of extreme metabolic acidosis.

[Serotonin syndrome in the course of drug-poisoning--case presentation]. / Zespól serotoninergiczny w przebiegu zatrucia lekami--opis przypadku.

UNLABELLED: Serotonin syndrome is caused by excess serotonin in the central nervous system. It usually occurs as adverse drug-therapy (neuroleptic agents, monoamine oxidase inhibitors, serotonin reuptake inhibitors and others). CASE PRESENTATION: a 50-year-old woman with a history of depression, was admitted to our hospital, due to suicidal drug poisoning (moclobemide- 4500 mg, venlafaxine 1050 mg, mianserin 300 mg and cytisine 30mg). She was also drunk. The patient was unconscious and sweaty, on the ECG tachycardia (120/min) was observed. In addition, several hours after admission, the patient developed acute respiratory failure, we observed myoclonus, lockjaw, body temperature increased to 37.3 degrees Celsius, and blood pressure was 170/80 mmHg. During the neurological examination there was a tendency to bilaterall Babinski sign and the nystagmus was present. The patient was intubated, and we started an intravenous infusion of Relanium. In laboratory studies: ethanol: 2.52 g/l, tests for benzodiazepines and tricyclic antidepressants were negative, WBC 13.1 tys/microl, CPK was elevated to 372 U/L, other parameters (electrolytes, transaminases, serum total protein, glucose, CRP, creatinine) were normal. The patient required intensive care and treatment during the next two days. The diagnosis of serotonin syndrome was based on the Hunter's criteria, which are more sensitive and more specific than Sternbach's criteria. The patient was discharged from hospital in good condition.

[Is it possible to survive metabolic acidosis with pH measure below 6.8? A study of two cases of inedible alcohol intoxication]. / Czy mozliwe jest przezycie kwasicy metabolicznej o wartosci pH ponizej 6,8? Opis 2 przypadków klinicznych zatrucia alkoholami niespozywczymi.

26 of serious inedible alcohol (ethylene glycol and methanol) intoxications have been observed in Lublin Regional Center of Clinical Toxicology during 2010/2011 (18 mounths). As a result of such intoxications, metabolic acidosis and acute renal failure and other organs injury develop. The writings inform that it is possible to survive a pH spectrum between 6.8 and 7.8, whereas beyond these values protein denaturation and death proceed. The paper presents two cases of intoxication with ethylene glycol and ethylene glycol, methanol together where the lowest pH values in capillary blood were recorded below 6.8. The first case is of a male, 45, who was diagnosed glycol concentration at 283.3 mg/dl, with the lowest pH value obtained in the gasometric examination of capillary blood at 6.712. The other case is of another male, 54, who had probably drunk condenser liquid. Ethylene glycol and methanol's concentration were 535 mg/dl and 37.5 mg/dl correspondingly, whereas the lowest capillary blood pH value was recorded at 6.745. Both men had been addicted to alcohol for many years. The treatment demanded multiple hemodialyses, respiratory therapy, catecholamine intravenous injections as well as intensive pharmacological treatment resulting from multi-organ complications. The intoxication in either case was non-lethal.

[Myocardial infarction secondary to carbon monoxide poisoning--a study of two cases]. / Zawal serca w przebiegu zatrucia tlenkiem wegla--opis dwóch przypadków klinicznych.

The carbon monoxide poisoning still remains a main cause of fatal poisoning. The carbon monoxide poisoning occurs after inhalation of carbon monoxide. Carbon monoxide binds strongly to molecules, such as cytochrome oxidase, myoglobin, hemoglobin, causing hypoxia of tissues and organs. Carbon monoxide converts hemoglobin to carboxyhemoglobin and makes transport of oxygen through the body impossible and causes severe hypoxia. The only treatment is administering 100% oxygen or providing hyperbaric oxygen therapy. The central nervous system and heart are the most sensitive to hypoxia. We present the cases of two young people with no history of chronic diseases (a 24-year-old man and a 39-year-old woman) who were diagnosed NSTEMI in the course of severe carbon monoxide poisoning. Both poisoning cases were severe, both patients were unconscious when they were admitted to our hospital. We observed elevation of serum troponin level and changes in ECG (e.g. atrial fibrillation) significant for myocardial infarction.