Polyhexamethyleneguanidine hydrochloride (PHMG) is an antimicrobial biocide of the guanidine family. In the period from August 2006 to May 2007, more than 12500 patients were admitted to hospital with a history of drinking illegal cheap "vodka" in 44 different regions in Russia, of whom 9.4% died. In reality, the "vodka" was an antiseptic liquid composed of ethanol (˜93%), diethyl phthalate, and 0.1-0.14% PHMG (brand name "Extrasept-1").
We performed an analysis of the clinical features and outcome in four poisoning treatment centers in the cities of Perm, Ekaterinburg, Irkutsk, and Khabarovsk. A total of 579 patients (215 females and 364 males) with similar symptoms were included.
The main symptoms on admission included jaundice (99.7%), skin itch (78.4%), weakness (96%), anorexia (65.8%), dizziness (65.3%), nausea (54.8%), vomiting (22.6%), stomach ache (52.7%), diarrhea (32%), and fever (50%). Mild symptoms were found in 2.5% of cases, moderate in 63%, and severe in 34.5%. Laboratory results were (mean ± SD): total bilirubin 249 ± 158 µmol/L, direct bilirubin 166 ± 97 µmol/L, cholesterol 14 ± 8 mmol/L, alanine aminotransferase 207 ± 174 IU/L, aspartate aminotransferase 174 ± 230 IU/L, alkaline phosphatase 742 ± 751 IU/L, and gamma-glutamyltranspeptidase 1199 ± 1095 IU/L. Patients generally recovered over a period of 1-5 months, although high levels of alkaline phosphatase and gamma-glutamyltranspeptidase were still found in all patients examined after 6 months. Sixty-one patients (10.5%) died between 23 and 150 days after poisoning. Local cholestasis, inflammatory infiltration, and fibrosis developing into cirrhosis were found by liver biopsy.
Acute liver injury caused by PHMG-hydrochloride or PHMG in combination with either ethanol or diethyl phthalate can be characterized as cholestatic hepatitis with a severe inflammatory component causing high mortality.
INTRODUCTION: Poisoning is a common cause of emergency visits and hospital admission in Western countries. The purpose of this study was to assess the incidence and type of toxic exposures presenting to emergency medical facilities in Iceland. MATERIALS AND METHODS: The study was prospective and included all patients with confirmed or suspected poisoning presenting to hospitals and rural medical centers providing emergency services in Iceland during the twelve-month period from April 2001 until March 2002. RESULTS: A total of 1,121 toxic exposures were documented representing an incidence of 3.91 cases per 1,000 inhabitants per year. The female to male ratio was 1.23. The majority of exposures (56.7%) occurred in the patient's home, 60% were deliberate, 72% had drugs and/or alcohol as their main cause, and 11% involved illicit drugs. Exposures to chemicals other than drugs were usually unintentional. CONCLUSION: Toxic exposures requiring emergency medical care are common in Iceland. Self-poisonings by ingestion of prescription drugs and/or alcohol accounted for the majority of cases.
The indices of mortality due to intoxication by alcohol and its surrogates in a region studied during the 90-ies essentially differ depending on an information source. An analysis of the alcoholic situation in the region and en elaboration of preventive measures cannot be limited to data on the consumption of alcohol (provided by the State Statistics Committee) showing only the volume of statistically registered sales of alcoholic beverages through the trade network. If this factor is ignored, erroneous conclusions can be made on both the volumes of average-per-capita consumption of alcohol and on the reasons of changes in people's health indices.
Medical cards of 1,116 inpatient victims of surrogate alcohol poisoning and 242 cases of its fatal outcome associated with jaundice were available for analysis form Irkutsk Region and other regions of the Russian Federation in the second half of 2006 and early 2007. The study revealed differences in hepatic lesions depending on the chemical nature of toxicants. Mixtures containing guanidine derivatives caused highly specific irreversible disturbance of bile transport in hepatocytes and biliary capillaries in the absence of cholestasis at the level of biliary ducts. Changes in hepatocytes of different type and genesis appear to be due to other toxic components and may be of use for the establishment of causal relation between hepatic lesions and concrete toxic mixtures.