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Biomedical subjects

H Kupferschmidt

Publications and source records attributed to H Kupferschmidt.

At least 19 recordsLinked to original sources
PubMed2003

[Acute drug poisoning].

The range of illicit substances of abuse is broad. Compounds of major importance are cannabinoids, opiates, cocaine, amphetamines, ecstasy, hallucinogens, phencyclidine, gammahydroxybutyrate, volatile nitrites, solvents, and nitrous oxide. The corresponding toxidromes vary considerably according to their mechanisms of action. Substances with a low general acute toxicity such as ecstasy may cause rare cases of severe or fatal complications. The therapy is rarely specific but symptomatic in most instances. Monitoring is important, and there is a need for a high index of suspicion for severe complications.

Cross-Cultural Comparison↗
PubMed2001

[Fatal brain edema after ingestion of ecstasy and benzylpiperazine].

HISTORY AND ADMISSION FINDINGS: A 23-year-old woman was hospitalized with headache, malaise and somnolence 11 hours after ingestion of A2 (benzylpiperazine), 7 hours after ingestion of ecstasy (MDMA), and large volume of fluids. On admission she had bradycardia (heart rate 48/min), hypertension (blood pressure 154/95 mm Hg), and reduced consciousness with diminished tendon reflexes and non-reacting pupils (Glasgow Coma Score 6). INVESTIGATIONS: Serum sodium was markedly decreased (115 mmol/l [normal 135-145]) with low plasma osmolality (246 mosm/kg [normal 280-300]). Other laboratory findings were within normal limits. TREATMENT AND COURSE: The patient had severe hypervolaemic hypotonic hyponatraemia. 40 minutes after admission she seized twice and was intubated. Brain CT scan showed massive cerebral oedema with beginning tonsillar herniation. Serum sodium concentration returned to normal within 38 hours, but the patient deteriorated neurologically with increasing tonsillar herniation detected in a second brain CT scan. The patient died 57 hours after admission. CONCLUSION: 13 cases of MDMA-associated severe hyponatraemia are reported. Intake of fluids after MDMA ingestion may lead to potentially fatal hypervolaemic hypotonic hyponatraemia with cerebral oedema. Symptoms appear about 8 hours (range 4-18) after MDMA ingestion. Even low doses of MDMA and fluids may lead to a serious outcome. The only risk factor is female gender. Measurement of serum sodium and brain CT scan is recommended in all patients with altered mental status after MDMA consumption.

Adult↗
PubMed2000

[Sudden coma in a 20-year-old man].

A 20-year-old male patient was brought to the emergency department by Emergency Medical Services after having been found unconscious. Upon arrival the patient was comatose with a GCS of 3, his vital signs were stable (with blood pressure 100/54 mmHg, heart rate 48 per minute, respiration rate 12 per minute and oxygen saturation 98% on room air). Both pupils were 3 mm, symmetric, and only minimally responsive. Approximately 2 hours after arrival the patient awoke and admitted having taken three ampoules of GHB (gamma hydroxybutyrate). GHB is a synthetic analog of gamma-amino butyric acid (GABA), a centrally inhibitory neurotransmitter. While GHB produces euphoria in low doses, small overdosing can result in severe poisoning with coma. The combination with other CNS depressants such as alcohol, opioids, and other narcotics is particularly dangerous. Physicians should be alerted to the clinical effects of GHB since abuse has become more widespread in Switzerland within the last months. In patients with unexplained coma the differential diagnosis of GHB-intoxication should be taken into consideration.

Adult↗
PubMed2000

Dose-dependent toxicity of diphenhydramine overdose.

BACKGROUND: Diphenhydramine (DPHM) overdose is a frequent cause of acute poisoning. Although its clinical features are well known, information about the dose-dependent toxicity of DPHM is still scarce. The objective of this study was to investigate the dose-dependent toxicity of DPHM in patients with acute DPHM poisoning. METHODS: We have analyzed retrospectively all well-documented cases with DPHM monointoxications reported by physicians to the Swiss Toxicological Information Centre (STIC) between January 1984 and April 1996. In addition, a prospective study focusing on ingested DPHM doses and severity of symptoms was performed between May 1996 and December 1998. RESULTS: The retrospective and prospective studies included 232 and 50 patients with DPHM monointoxications, respectively. In both studies, mild symptoms (somnolence, anticholinergic signs, tachycardia, nausea/vomiting) occurred in 55-64%, moderate symptoms (isolated and spontaneously resolving agitation, confusion, hallucinations and ECG disturbances) in 22-27% and severe symptoms (delirium/psychosis, seizures, coma) in 14-18% of patients. Moderate symptoms occurred above ingested doses of 0.3 g DPHM. For severe symptoms the critical dose limit was 1.0 g DPHM. Although the frequency of delirium/psychosis remained constant or even decreased, coma and seizures were significantly (p<0.05) more frequent in the >1.5-g compared with the 1.0- to 1.5-g-dose group. CONCLUSIONS: These data demonstrate a clear dose-dependent acute toxicity of DPHM. They indicate that only patients with DPHM ingestions above 1.0 g are at risk for the development of severe symptoms and, therefore, should be hospitalized. Thus, the results contribute to the data basis required for a cost effective management of patients with DPHM overdose.

Adolescent↗
PubMed1997

[Bile duct cysts in adults].

INTRODUCTION: Bile duct cysts are rare, congenital dilations of the intrahepatic and/or extrahepatic biliary tract. Most of them present during childhood. The classical triad right upper quadrant pain, jaundice and abdominal mass is present only in a few instances. We report here the bile duct cysts which were diagnosed at our institution from 1989 to 1996. METHODS: 3245 consecutive endoscopic retrograde cholangiopancreatograms (ERCP) were evaluated retrospectively. Diagnosis was made when localized cystic dilations of the intrahepatic and/or extrahepatic biliary tract were present. Diffuse dilations of the intrahepatic and extrahepatic biliary tract were excluded. RESULTS: Bile duct cysts were found in 20 patients (17 females, 3 males) among 3245 ERCPs. Their mean age was 56 +/- 20 (median 64, range 10 to 83) years. The cyst types (according to the Alonso-Lej classification with the Todani modification) were type I in 11 (55%), type II, III and IV in two instances each (10%), and type V (or Caroli's disease) in 3 patients (15%). Leading symptoms were cholestasis in 14 patients, 10 of whom had abdominal pain, jaundice in 4 patients, and single cases of pancreatitis, cholangitis, and abdominal mass. In 2 patients the diagnosis was made incidentally. 10 patients had bile duct stones. We performed endoscopic sphincterotomy in 15 patients with concretions or persistent symptoms, 3 patients had cyst resection. One of these, with a type I cyst, already had a disseminated cholangiocarcinoma. 10 of 17 patients without cyst resection are currently symptom-free after complete removal of all gallstones. One male patient with cholecystolithiasis, who is not operable due to advanced liver disease, has recurrent cholangitis, 4 patients have died from causes unrelated to the bile duct cysts, and 2 patients are lost to follow up. CONCLUSION: Bile duct cysts in adults are rare. There is a preponderance in the female gender, and the most common type is the extrahepatic (choledochal) cyst. The leading symptoms are cholestasis and right upper quadrant pain. There is an increased risk of cholangiocarcinoma. In young patients the cysts should be entirely removed to prevent malignancy. Older persons are usually symptomless after complete removal of gallstones.

Adolescent↗
PubMed1997

[Follow-up and therapy of acute colchicine poisoning].

Colchicine poisoning is a rare event. Its outcome is, compared to other drug intoxications, often serious or even fatal. Intaxications with colchicine may occur by ingestion of tablets as well as by consumption of meadow saffron leaves (Colchicum autumnale) that are often mistakenly collected instead of the leaves of ramson herb (Allium ursinum). Colchicine poisoning typically shows three phases: initially gastrointestinal symptoms predominate, in the second phase multiorgan failure may occur possibly leading to death. In case the patient survives, the third phase of recovery follows during which the patients often present with hair loss. The fatal dose of acute colchicine poisoning is estimated at about 0.9 mg/kg. Since hemodialysis and hemoperfusion are not effective measures because of the high volume of distribution, an aggressive primary decontamination with gastric lavage and activated charcoal is required as early as possible. A promising new aspect in the treatment of heavy colchicine overdose is the immunotherapy with colchicine-specific fab-fragments. At present this treatment is still in an experimental stage and has been applied so far to one patient with beneficial effects. Unfortunately colchicine-specific antibodies are not yet commercially available.

Adult↗
PubMed1996

[Pericarditis in chronic inflammatory bowel disease: underlying disease or side effects of therapy? Clinical problem solving].

Pericarditis and myocarditis are rare extraintestinal manifestations of chronic inflammatory bowel disease (ulcerative colitis and Crohn's disease). Pericarditis as a side effect induced by sulfasalazine or 5-aminosalicylic acid, drugs used in the therapy of these diseases, was first described only 7 years ago. In older case reports the relationship between the use of these drugs and pericarditis is unclear. We analyze the reported cases of 68 patients (38 men, 24 women) with ulcerative colitis (n = 45) or Crohn's disease (n = 15) who had one or more episodes of pericarditis or myopericarditis. Pericarditis was not associated with high activity of bowel disease in all cases. In most cases therapy with corticosteroids led to uneventful recovery. In drug induced pericarditis omission of the 5-ASA therapy was sufficient in a few cases. There was one fatal case (with myocarditis). The decision whether pericarditis is a symptom of the underlying disease or a side effect of the drug used for the treatment of the disease is not always easy. We present an analysis (clinical problem solving) of a pertinent observation in a patient with Crohn's disease and pericarditis, showing the dilemma of pericarditis in chronic inflammatory bowel disease and its therapy.

Adult↗
PubMed1996

[The absence of autoantibodies does not rule out autoimmune hepatitis].

UNLABELLED: The diagnosis of autoimmune hepatitis is mainly based on the finding of characteristic autoantibodies. Untreated patients have a poor prognosis because of rapid development of cirrhosis. Immunosuppressive treatment most often leads to remission. We report on 2 female patients aged 44 and 53 with autoimmune hepatitis. Initially no significant titers of autoantibodies against nuclear, cytosolic or microsomal components of the hepatocyte could be demonstrated. Seropositivity for autoantibodies was demonstrated 6 and 8 weeks later in the course. Immunosuppressive therapy with steroids resulted in rapid decrease of transaminases with persistent remission of autoimmune hepatitis. CONCLUSION: seropositivity for characteristic autoantibodies is not an absolute criterion for the diagnosis of autoimmune hepatitis. Patients with hepatitis of unknown origin should therefore be given a steroid treatment trial.

Adult↗
PubMed1996

[Clinico-pharmacological case (2). Bradycardia and ventricular tachycardia of the torsades de pointes type as a side effect of vasopressin: 3 case reports].

We present three patients with ornipressin-induced bradycardia, one of which developed also ventricular tachycardia of the torsade de pointes type. All three patients were treated with this vasopressin derivative because of bleeding esophageal varices due to portal hypertension in liver cirrhosis. Bradycardia ceased after discontinuing ornipressin therapy. One patient was treated successfully with atropine, one with isoprenalin and magnesium (he had to be defibrillated); the third patient recovered after cessation of ornipressin administration. Bradycardia is a known but rarely reported side effect of vasopressin and its derivatives. Animal studies suggest that this effect is due to its cardiodepressive action and also to a vagus-mediated reflex following vasopressin-induced increase in blood pressure. When injected directly into the ventricles of the brain, vesopressin leads to a decrease of the heart rate without affecting blood pressure; however, it remains unclear whether this mechanism is responsible for bradycardia after intravenous administration. Careful monitoring is essential during the treatment with vasopressin and its derivatives.

Aged↗
PubMed1996

[Virus titre and histological inflammation activity in chronic hepatitis C].

We determine the correlation between viremia in serum specimens, transaminase activity (ALT and AST) and histological grading in 37 patients with chronic hepatitis C. In addition we compared two PCR methods for hepatitis C virus (HCV)-RNA in serum specimens. For the histological grading we used a modified Knodell score. For detection and quantification we measured the viremia (HCV-RNA titer) with a standardized "nested primer" PCR (end-point dilution method) and the commercially available Amplicor HCV Monitor. The mean HCV-RNA and AST level was significantly higher in patients with a histologically active inflammation. In the individual patient we could not conclude from the titer of HCV-RNA on the histologic grading because of the wide range of the results. We did not find a significant difference in ALT in patients having varying histological gradings. HCV-RNA titer and transaminases (ALT and AST) did not correlate significantly. The HCV-RNA titer was significantly marked in older patients (above 40 years) and patients having sporadic hepatitis than in younger patients and patients with chronic hepatitis after drug abuse. The "nested primer" PCR (end-point dilution method) was more sensitive for detection of HCV-RNA in serum specimens than Amplicor HCV Monitor. The lack of HCV-RNA with Amplicor HCV Monitor in 12 of 37 patients (32%) did not rule out viremia. We conclude that in patients with a chronic hepatitis C marked viremia points to a histologically active inflammation. In the individual patient we could not conclude from the titer of HCV-RNA on the histological grading. Because of the lower sensitivity of Amplicor HCV Monitor it is necessary to confirm negative results with a "nested primer" PCR.

Adult↗
PubMed1996

[Endoscopic therapy of bile leakage following laparoscopic cholecystectomy].

Biliary leakages are more frequent in laparoscopic than in open cholecystectomy. The aim of our study was to evaluate the diagnostic and therapeutic value of endoscopic retrograde cholangiography (ERC) in the management of bile leakages after laparoscopic cholecystectomy. The primary management was endoscopic sphincterotomy and extraction of remaining gallstones in the common bile duct to provide a decrease of biliary pressure, allowing closure of the fistulas. We report on 20 patients with bile leakage at ERCP, presenting between January 1991 and October 1995 with persistent bile discharge out of drainages, increasing fluid collections subhepatic (termed bilomas) or in the free peritoneal cavity (cholascos), abdominal pain, fever, cholestasis, intraoperatively diagnosed choledocholithiasis, and subhepatic abscess in one case. In 19 cases, after fluoroscopic visualization of the biliary tree and the leak, endoscopic sphincterotomy was performed. The biliary leaks were located at the cystic duct remnant (n = 12), at the gallbladder fossa (n = 5), or at lesions at the hepatic or common bile duct (n = 2). In 7 patients residual common bile duct stones were endoscopically removed. Most patients had localized small subhepatic fluid collections (n = 13) and the others had cholascos (n = 6). The leaks closed with endoscopic sphincterotomy alone in 11 patients, 4 patients had endoscopic sphincterotomy plus percutaneous or laparoscopic drainage of the bile collections, and 4 patients underwent laparotomy. All 6 cases with cholascos but only 2 of the 13 patients with localized collections underwent a second therapeutic procedure (drainage, laparotomy). Five of these procedures were performed within 7 days of ERCP, in most cases due to persistent bile leak. We conclude that biliary leakages after laparoscopic cholecystectomy require laparotomy only exceptionally. Endoscopic sphincterotomy, combined with percutaneous drainage in the case of large collections, represents a safe and successful strategy ensuring closure of the leaks in most cases.

Aged↗
PubMed1995

Case report: reversible QT prolongation with torsades de pointes in a patient with pimozide intoxication.

Pimozide is a diphenylpiperidine neuroleptic with well characterized cardiovascular side effects including QT prolongation. So far, life-threatening cardiac arrhythmias, in particular torsades de pointes, have not been described in patients treated with pimozide. The authors describe a patient in whom torsades de pointes developed after the ingestion of 800 mg pimozide as a suicide attempt. After intravenous treatment with lidocaine and magnesium, the patient recovered completely and the QT interval had normalized 5 days after the intoxication. Potential mechanisms leading to torsades de pointes in patients treated with pimozide are discussed.

Electrocardiography↗
PubMed1995

Plasma and hepatic carnitine and coenzyme A pools in a patient with fatal, valproate induced hepatotoxicity.

Reduced hepatic mitochondrial beta-oxidation and changes in the plasma carnitine pool are important biochemical findings in valproate induced liver toxicity. The carnitine pools in plasma and liver and the liver coenzyme A (CoA) pool in a patient with fatal, valproate induced hepatotoxicity were measured. In plasma and liver the free and total carnitine contents were decreased, whereas the ratios short chain acylcarnitine/total acid soluble carnitine were increased. The long chain acylcarnitine content was unchanged in plasma, and increased in liver. The total CoA content in liver was decreased by 84%. This was due to reduced concentrations of CoASH, acetyl-CoA, and long chain acyl-CoA whereas the concentrations of succinyl-CoA and propionyl-CoA were both increased. The good agreement between the plasma and liver carnitine pools reflects the close relation between these two pools. The observed decrease in the hepatic CoASH and total CoA content has so far not been reported in humans with valproate induced hepatotoxicity and may be functionally significant.

Adult↗
PubMed1993

[Epidemiology of the plague. Changes in the concept in research of infection chains since the discovery of the plague pathogen in 1894].

Three major plague epidemics have been recorded worldwide up to this day: the Justinian plague in the 6th century, the Black Death in the 14th century and the recent 20th century pandemic. The latter occurred at a time of advanced microbiological knowledge which permitted the etiology and the modes of transmission and spread of this bacterial infectious disease to be clarified. The present thesis is an attempt to describe the changes in plague research that occurred during that period of time. While the German, Austrian, British, Russian and Egyptian plague Commissions studying the Indian plague outbreak after 1896 contributed only little to the fundamental epidemiological knowledge on plague, several individual researchers succeeded in discovering some of the key facts in the etiology and transmission of the disease. Alexandre Yersin discovered the pathogenic agent of plague (Hongkong 1894), E.H. Hankin, P.L. Simond (Bombay 1898) and J.A. Thompson (Sydney 1900) recognized the role of rat plague, M. Ogata (Formosa 1897) and P.L. Simond (Bombay 1898) observed the transmission of the disease by fleas, and A.W. Bacot and C.J. Martin (1914) described the specific mechanism of transmission of plague. Accordingly, fleas transmit plague from rat to man, the efficiency of the flea as a vector depending on a blocking phenomenon specific of each flea species. The Indian rat flea (Xenopsylla cheopis) has been recognized the most efficient vector. Although the involvement of wild rodents was already known shortly after the turn of this century, the concept of sylvatic plague (the plague of wild rodents) as opposed to murine plague (the plague of commensal rodents) only emerged between 1920 and 1950. It led to taking stock of all hosts and vectors of the disease and thereby defining the natural foci of plague. According to this concept plague is primarily a disease of wild rodents which have been carrying it together with their fleas since ever. As man and urban rats only become infected occasionally, they do not constitute chronic foci. The occurrence of persistent foci rather depends on the interaction of resistant and sensitive wild rodents (burrowing animals) as was discovered by French researchers in the Middle East as late as the 1950s and 1960s. The concept of rodent-dependent transmission was somewhat attenuated by the discovery of direct interhuman transmission by French researchers between 1930 and 1965.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗