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Biomedical subjects

K Hruby

Publications and source records attributed to K Hruby.

At least 37 records · Page 2Linked to original sources
PubMed1983

[Pharmacotherapy of Amanita phalloides poisoning using silybin].

A total of 18 cases of Amanita phalloides poisoning was treated by combined chemotherapy during 1980 and 1981. After attempted primary elimination of the toxin all patients received silybin as basic therapy mainly by infusion and, in two instances, silymarin orally. In order to investigate the effect of silybin therapy a retrospective study of the followed-up case records was made. The cases were arbitrarily classified into three groups of severity (light, medium and severe) according to clinical and laboratory findings. A close relationship was found between the severity of the intoxication and the time elapsed before commencement of silybin therapy. The time interval between mushroom intake and the commencement of the silybin administration averaged 71.5 hours in the "severe" group compared with 46 and 33.8 hours, respectively, in the "medium" and "light" groups. The mean silybin dosage was 33 mg/kg body weight/day; the mean duration of silybin therapy was 81.6 hours. With the exception of one fatality in a particularly high dosage suicidal intoxication, all patients survived. Administration of silybin within about 48 hours after mushroom intake seems to be an effective measure to prevent severe liver damage in Amanita phalloides poisoning.

Adult↗
PubMed1983

[Poisoning with clonidin hydrochloride in children and adults].

In this study clinical findings are presented of 31 patients with clonidinee intoxication and the therapeutic measures taken in these cases are discussed. In toddlers poisoning is seen after ingestion of a single tablet of 150 micrograms clonidine, whilst in adults poisoning may occur already at a dosage just exceeding the therapeutic limit, which is subject to wide individual variation (1 to 3 tablets). Primary elimination procedures must be instituted at these dosages, but, because of the rapid absorption of clonidine, gastric lavage and induced emesis provide no benefit to patients with complete symptomatology or those who took the overdose several hours before. Chlorpromazine-like effects, hypotension and bradycardia proved to be the outstanding features. Respiratory depression, disturbances of myocardial conduction or hypertension were less frequent. Symptoms lasted for a mean of 15.5 +/- 8.6 hours, with a range of 4 to 36 hours. Fluid therapy and, as necessary, dopamine for hypotension, phentolamine for hypertension and atropine for bradycardia caused prompt improvement in addition to essential measures such as meticulous control of respiratory function, body temperature and of ECG changes. There was no need to implement the central clonidine antagonist, tolazoline in any of these cases.

Adolescent↗
PubMed1983

[Accidental fatal formaldehyde poisoning].

A previously healthy man accidentally swallowed 20 to 50 ml of Formalin (25%). Relevant clinical findings after the accident were: severe metabolic acidosis, severe disseminated intravascular coagulation and renal failure. He died 7 hours after formaldehyde ingestion-presumably from toxic pulmonary oedema. Relevant post-mortem findings were: massive pulmonary damage (toxic oedema), leather-like thickening of the gastric wall and multiple subendocardial haemorrhages. The treatment of formaldehyde poisoning is briefly discussed.

Acidosis↗
PubMed1983

[Dry senile maculopathy: prevention and treatment in risky cases].

In 33 cases of advanced unilateral dry senile maculopathy in which the fellow eye showed initial affection but still had a visual acuity of 6/12, the visual acuity of the better eye was preserved in 27 cases for an average of 4 years and 2 months by sustained intramuscular injections of retinal phosphatides (Etaretin). Four cases did not respond to the therapy and 2 patients may be considered borderline cases. If one eye approaches a terminal stage, sustained phosphatide treatment should be instituted as soon as initial retinal lesions appear in the fellow eye. The incorporation of radioactively labelled phospholipids in the retina following subcutaneous applications has been demonstrated in animal experiments. The quantity of the incorporated phospholipids may be considered sufficient for a therapeutic effect. A further thorough clinical investigation would be desirable.

Female↗
PubMed1983

Chemotherapy of Amanita phalloides poisoning with intravenous silibinin.

1 A total of 18 cases of Amanita phalloides intoxication was treated by combined chemotherapy during 1980 and 1981. After attempted primary elimination of the toxin all patients received silibinin as basic therapy mainly by infusion and in two instances orally. 2 In order to evaluate the effect of silibinin therapy a retrospective study of the followed-up case records was made. The cases were arbitrarily classified into three groups according to the severity of liver damage (light, medium and severe). 3 There was found a close relationship between the severity of liver injury and the delay between mushroom ingestion and the onset of silibinin therapy. With the exception of one fatality in a particularly high dosage suicidal intoxication, all patients survived. 4 Administration of silibrinin even up to 48 h after mushroom ingestion appears to be an effective measure to prevent severe liver damage in Amanita phalloides poisoning. Contrarily, the onset of general supportive treatment together with penicillin therapy which was throughout several hours before silibinin administration did not correlate with the severity of liver damage.

Adult↗
PubMed1982

[New aspects of chlorprothixen-poisoning (author's transl)].

Over the past 8 years the Poison Information Centre of Vienna was confronted 24 times with acute chlorproxithene (CPTX) poisoning. In adults doses of 2 g and more caused severe intoxication, but serious toxic manifestations were observed already at low dosage in children (after the ingestion of less than 5 mg/kg body weight). In one case unexpected death due to cardiac failure occurred as long as 49 hours after CPTX intake. The favorable outcome in one patient treated with gut, as well as gastric lavage indicates that this therapeutic strategy may be of value in the management of CPTX intoxication.

Chlorprothixene↗
PubMed1982

The effect of histamine2 and muscarine receptor antagonists on plasma levels of parathyroid hormone and calcitonin.

Long-term administration of cimetidine, a histamine2 receptor antagonist, has been reported to normalize elevated parathyroid hormone (PTH) concentrations in patients with secondary [1] and primary hyperparathyroidism [2] and even to improve the clinical symptoms. We have compared the effect of cimetidine and pirenzepine on PTH and calcitonin (CT) plasma levels in a short-term trial on patients with secondary hyperparathyroidism. After cimetidine a significant effect on PTH was seen within 30 min lasting 30 min and after pirenzepine, within 60 min and lasting 60 min. The effect on CT was only significant after cimetidine.

Adult↗
PubMed1982

[The intoxication with cyclizin in infancy and adult age (Experiences of a contamination-information-central office) (author's transl)].

Epidemiological, clinical and therapeutic aspects obtained from 38 cases of intoxication with the antiemetic drug "cyclizine" in children and adults are discussed. The relative frequency of accidentally or purposely performed overdosage shows a decreasing tendency. The introduction of regulations after the prescription of cyclizine compounds, leaving a limited dose available without prescription and the introduction of a safety package to prohibit misuse by children are reported in their relationship with the epidemiologic data. A toxic dose of 5 mg/kg body weight, a minimal lethal dose (MLD) of about 80 mg/kg are evaluated and compared with previous published data. Differences of age in the development of the clinical picture of the cyclizine-intoxication with a disposition for the evolvement of convulsions in children compared to the total lack of convulsions in adults have to be pointed out. The management of overdoses follows general principles of treatment like gastric lavage, supporting care and includes the specific treatment with the antidote "physostigmin-salicylate", which causes a shortening of the time of recovery.

Adolescent↗
PubMed1982

Accidental ingestion of NaF tablets by children--report of a poison control center and one case.

Accidental ingestion by children of NaF tablets for caries prophylaxis is a frequent event. However, our own experience from the Poison Information Centre in Vienna and reports from other centers show that these accidents usually do not present a serious risk. The mechanism of fluoride toxicity and symptoms of poisoning are briefly reviewed. The case of a boy who died after ingesting 16 mg fluoride/kg, but whose cause of death is not certain beyond doubt, is discussed.

Child, Preschool↗
PubMed1982

[Pharmacotherapy in severe liver failure].

In severe liver failure pharmacokinetics and pharmacodynamics of different drugs are changed as compared to normals. The disturbances observed may be due to hepatic or extrahepatic mechanism, which allows a rough classification of the different drugs. The hepatic clearance of a drug is dependent upon blood perfusion of the liver (flow limited elimination) or upon the metabolic capacity of the liver (capacity limited elimination). Extrahepatic factors are protein binding and changes of the distribution volumes. Adjustment of the initial and chronic doses of any drug should depend primarily upon the pharmacokinetic profile of the drug and secondarily upon the clinical effects. Repeated measurements of drug levels can only be done in special hospitals and in patients severely in danger. Classification of drugs into groups with high, medium or low therapeutic risk may help, when a treatment plan is drawn up and may economize control of the patient.

Biotransformation↗
PubMed1981

[Pharmacokinetics of beta-methyldigoxin and beta-acetyldigoxin in patients with cirrhosis of the liver (author's transl)].

In this prospective randomised study 12 patients suffering from cirrhosis of the liver (stable phase) and 12 healthy male volunteers were treated with either 0.3 mg beta-methyldigoxin (Lanitop) or 0.4 mg beta-acetyldigoxin (Novodigal) daily, orally. Every day the total serum digoxin concentrations of the patients and volunteers were measured by radioimmunoassay. Both digoxin and beta-methyldigoxin are measured by this method. In subjects receiving beta-methyldigoxin therapy the ratio of beta-methyldigoxin to digoxin in the serum was determined by liquid chromatography. The digoxin levels in patients with cirrhosis treated with beta-methyldigoxin were statistically significantly higher than in healthy volunteers. In patients with cirrhosis the proportion of serum beta-methyldigoxin averaged 77.7% of the total digoxin concentration, whereas the proportion was only 37.5% in healthy volunteers. With beta-acetyldigoxin there was no statistically significant difference between patients with cirrhosis and healthy volunteers. Alterations in pharmacokinetics may cause the higher total serum digoxin concentrations in cirrhotic patients. The following factors seem to be important: longer elimination half life, changes in distribution volume and reduced renal clearance. There is greater danger of digitalis toxicity in patients with cirrhosis of the liver on standard dosage of beta-methyldigoxin than on standard dosage of beta-acetyldigoxin.

Acetyldigoxins↗