Am J Emerg Med 2001 Oct;19(6):527-8
Publication Types:
PMID: 11593481, UI: 21476793
Order this document
Am J Emerg Med 2001 Oct;19(6):525-6
PMID: 11593479, UI: 21476791
Am J Psychiatry 2001 Nov;158(11):1931-2
PMID: 11691710, UI: 21548755
Am J Psychiatry 2001 Nov;158(11):1827-34
Clinical Brain Disorders Branch, Intramural Research Program, NIMH, National Institutes of Health, Bethesda, MD, USA. eganm@intra.nimh.nih.gov
OBJECTIVE: First-degree relatives of patients with schizophrenia appear to have subtle neurological signs, suggesting that these measures could serve as intermediate phenotypes in genetic studies of schizophrenia. The strength of a possible genetic component is unknown, however, leaving it uncertain whether such traits could increase the power to find schizophrenia susceptibility loci. The authors' goal was to investigate the strength of this possible genetic component. METHOD: They estimated the relative risk of neurological impairments in a large group of siblings of patients with schizophrenia. Two standard neurological scales (the Neurological Evaluation Scale and the Woods Scale) were used to examine 115 patients, 185 of their siblings, and 88 normal comparison subjects. RESULTS: There were significant differences between the siblings of patients with schizophrenia and the normal comparison subjects only on the Woods Scale. Relative risk of neurological impairment was significantly increased in the sibling group, but the significance was weak to moderate. Neurological impairment was not redundant with several other intermediate phenotypic measures based on cognitive impairment. CONCLUSIONS: These data suggest that neurological signs cluster in patients with schizophrenia and their families and could possibly identify a unique component of genetic variance for risk of schizophrenia. However, the fairly low relative risk and the uncertain pathophysiology of such signs may limit their usefulness.
PMID: 11691688, UI: 21548733
Ann Emerg Med 2001 Nov;38(5):607-8
PMID: 11679882, UI: 21536138
Ann Emerg Med 2001 Nov;38(5):588-91
Maine Medical Center, Portland, ME, USA.
We present a case that illustrates the acute (<6 hours) metabolic and hemodynamic effects of the ingestion of a massive oral citric acid load. The principal findings included metabolic acidosis accompanied by an increase in the plasma anion gap that was not caused by L -lactic acidosis, hyperkalemia, and the abrupt onset of hypotension. A unique feature was a dramatic clinical improvement when ionized calcium was infused. The case illustrates the importance of considering the properties of the conjugate base (anion) of the added acid because, in this instance, the citrate anion had a unique and life-threatening consequence (lower ionized calcium level) that was rapidly reversible.
PMID: 11679874, UI: 21536130
Ann Emerg Med 2001 Nov;38(5):491-6
Department of Emergency Medicine and the Division of Biostatistics Indiana University School of Medicine, Indianapolis, IN, USA.
STUDY OBJECTIVE: We sought to compare the rate of akathisia after administration of intravenous prochlorperazine as a 2-minute bolus or 15-minute infusion. METHODS: We conducted a prospective, randomized, double-blind study in the emergency department of a central-city teaching hospital. Patients aged 18 years or older treated with prochlorperazine for headache, nausea, or vomiting were eligible for inclusion. Study participants were randomized to receive 10 mg of prochlorperazine administered intravenously by means of 2-minute push (bolus group) or 10 mg diluted in 50 mL of normal saline solution administered by means of intravenous infusion during a 15-minute period (infusion group). The main outcome was the number of study participants experiencing akathisia within 60 minutes of administration. Akathisia was defined as either a spontaneous report of restlessness or agitation or a change of 2 or more in the patient-reported akathisia rating scale and a change of at least 1 in the investigator-observed akathisia rating scale. The intensity of headache and nausea was measured with a 100-mm visual analog scale. RESULTS: One hundred patients were enrolled. One study participant was excluded after protocol violation. Seventy-three percent (73/99) of the study participants were treated for headache and 70% (70/99) for nausea. In the bolus group, 26.0% (13/50) had akathisia compared with 32.7% (16/49) in the infusion group (Delta=-6.7%; 95% confidence interval [CI] -24.6% to 11.2%). The difference between the bolus and infusion groups in the percentage of participants who saw a 50% reduction in their headache intensity within 30 minutes was 11.8% (95% CI -9.6% to 33.3%). The difference in the percentage of patients with a 50% reduction in their nausea was 12.6% (95% CI -4.6% to 29.8%). CONCLUSION: A 50% reduction in the incidence of akathisia when prochlorperazine was administered by means of 15-minute intravenous infusion versus a 2-minute intravenous push was not detected. The efficacy of prochlorperazine in the treatment of headache and nausea likewise did not appear to be affected by the rate of administration, although no formal statistical comparisons were made.
PMID: 11679859, UI: 21536115
Ann Pharmacother 2001 Jul-Aug;35(7-8):870-3
Psychiatry Department, Eastern Virginia Medical School, Norfolk 23507, USA. mcdaniww@mccoy.evms.edu
OBJECTIVE: To report a psychiatric patient who developed serotonin syndrome after a medication overdose and whose marked mydriasis was quickly reversed by administration of cyproheptadine. This phenomenon was confirmed when other cases of serotonin syndrome were studied. METHOD: In the index patient as well as in three subsequent cases of serotonin syndrome, pupil diameter, muscle tone, mental status, and vital signs were monitored before and after a test dose of cyproheptadine as medications were discontinued and antiserotonergic therapy begun. RESULTS: In each patient, cyproheptadine produced rapid reversal of mydriasis within one hour of the initial dose. Other signs of serotonin syndrome remitted more slowly. As the signs and symptoms of serotonin syndrome remitted and pupils returned to normal size and reactiveness, cyproheptadine therapy seemed to produce mydriasis after each dose. Cessation of therapy after this point did not result in recurrence of symptoms. One patient developed serotonin syndrome twice. Two patients developed serotonin syndrome during treatment with medications that are partial serotonin antagonists (mirtazapine and nefazodone). CONCLUSIONS: Rapid reversal of mydriasis in serotonin syndrome by cyproheptadine may serve as a specific suppressive test for the condition, and possibly may add to our understanding of the syndrome. Treatment with cyproheptadine is not thought to abbreviate the illness, but provides symptomatic relief while symptoms persist.
PMID: 11485136, UI: 21377364
Forensic Sci Int 2001 Oct 15;122(1):75-8
Glasgow Dental Hospital and School, 378 Sauchiehall Street, G2 3JZ, Scotland, Glasgow, UK.
The occurrence of distortion in human bite marks is well recognised. A forensic classification of distortion is suggested which is based upon the causative factors and their inter-relationships. The terms primary distortion and secondary distortion are introduced and described. The objective of this classification is to emphasise the need for a scientific approach to the recognition and interpretation of the types of distortion found in human bite marks. The relationships between distortion, distinctive features and superimposition techniques in bite mark analysis are discussed.
PMID: 11587871, UI: 21472249
Gastroenterol Clin Biol 2001 Jun-Jul;25(6-7):716-7
PMID: 11673741, UI: 21526975
Hum Exp Toxicol 2001 Apr;20(4):185-8
Department of Environmental Medicine, University of Rochester Medical Center, New York 14642, USA.
Utilizing information obtained from the X-ray fluorescence linear scanning along a single strand of hair in a recent fatal exposure to dimethylmercury, it was possible to determine the circumstances leading to the fatal result. When the Dartmouth chemistry professor displayed symptoms of mercury toxicity, samples of her urine and blood were found to have considerable amounts of mercury by a commercial laboratory. The Dartmouth medical people immediately started treatment with a chelator on January 29, 1997 to remove the mercury, and sent the first samples of blood, urine and hair taken on January 31, 1997 to our laboratory. Our X-ray fluorescence analysis of a single strand of hair shown in Figure 1 shows a single large peak of intake of mercury confirming the information revealed by examination of her laboratory notebook that she had spilled some dimethylmercury about 5 months previous to the date the hair sample was taken. Figure 2 shows two peaks, the peak closest to the scalp end of the hair shows the effect of the large amount of mercury released by the chelator, part of which appeared in the blood. Utilizing the start of the first increase in the blood level as August 14, 1996, and the second as caused by the chelator on January 29, 1997, a count of the number of 2-mm points measured between the two dates gives an accurate growth of the hair during that time. A close examination of Figure 1 indicates that it required five points, each of 2 mm, along the hair to reach the maximum. This indicates a time period of 10 mm of growth equal to 23 days during which a large concentration of methylmercury was entering the blood as evidenced by the hair concentration. The professor died on June 11, 1997.
PMID: 11393270, UI: 21284456
Int J Dermatol 2001 Jul;40(7):458-61
Department of Dermatology, Soroka University Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
PMID: 11679003, UI: 21536863
Int J Dermatol 2001 Jul;40(7):427-30
Department of Internal Medicine, Lakeside Hospital, Metairie, Louisiana 70001, USA. MHoldi1540@compuserve.com
PMID: 11678994, UI: 21536854
J Emerg Med 2001 Oct;21(3):285-7
PMID: 11604287, UI: 21490376
J Hepatol 2001 May;34(5):783-5
PMID: 11434632, UI: 21327491
J Indian Med Assoc 2001 Jun;99(6):311, 314-5, 318-20
Department of Medicine and Gastroenterology, Institute of Postgraduate Medical Education and Research, Calcutta.
The hepatotoxic action of arsenic, when used as a therapeutic agent, has long been recognised. Data on liver involvement following chronic exposure to arsenic-contaminated water are scanty. The nature and degree of liver involvement are reported on the basis of hospital based studies in patients who consumed arsenic contaminated drinking water for one to 15 years. Two hundred forty-eight patients with evidence of chronic arsenic toxicity underwent clinical and laboratory examination including liver function tests and hepatitis B surface antigen (HBsAg) status. Liver biopsy was done in 69 cases; in 29 patients, liver arsenic content was estimated by neutron activation analysis. Hepatomegaly was present in 190 of 248 patients (76.6%). Non-cirrhotic portal fibrosis was the predominant lesion (91.3%) in liver histology. The maximum arsenic content in liver was 6 mg/kg (mean 1.46 [0.42], control value 0.16 [0.04]; p <0.001); it was undetected in 6 of 29 samples studied. The largest number of patients with liver disease due to chronic arsenicosis from drinking arsenic contaminated water are reported. Non-cirrhotic portal fibrosis is the predominant lesion in this population. Hepatic fibrosis has also been demonstrated due to long term arsenic toxicity in an animal model. Initial biochemical evidence of hepatic membrane damage, probably due to reduction of glutathione and antioxidant enzymes, may be seen by 6 months. Continued arsenic feeding resulted in fatty liver with serum aminotransferases elevated at 12 months and hepatic fibrosis at 15 months.
PMID: 11678619, UI: 21533580
MMWR Morb Mortal Wkly Rep 2001 Oct 19;50(41):893-7
On September 11, 2001, following the terrorist incidents in New York City and Washington, D.C., CDC recommended heightened surveillance for any unusual disease occurrence or increased numbers of illnesses that might be associated with the terrorist attacks. Subsequently, cases of anthrax in Florida and New York City have demonstrated the risks associated with intentional release of biologic agents. This report provides guidance for health-care providers and public health personnel about recognizing illnesses or patterns of illnessthat might be associated with intentional release of biologic agents.
PMID: 11686473, UI: 21542674
Pediatr Emerg Care 2001 Aug;17(4):313-4
PMID: 11493841, UI: 21385763
Toxicol Pathol 2001 Mar-Apr;29(2):242-9
Department of Molecular Medicine Genetics Institute/Wyeth Research, Andovter, Massachusetts 01810, USA.
Acetaminophen intoxication results in hepatotoxicity associated with increased serum concentrations of hepatocellular leakage enzymes such as aspartate aminotransferase, lactate dehydrogenase, and alanine aminotransferase, centrilobular degeneration and necrosis, and activation of Kupffer cells. Recombinant human Interleukin-11 (rhIL-11) downregulates the production of proinflammatory mediators from activated macrophages and has direct effects on hepatocyte gene expression. Based on these biological activities of rhIL-11, the effect of pretreatment with rhIL-11 in a murine model of acetaminophen-induced hepatotoxicity was examined. Administration of 500 microg/kg acetaminophen to B6C3F1 mice resulted in progressive hepatotoxicity as demonstrated by elevated serum concentrations of hepatocellular leakage enzymes and TNFalpha and histopathology. Pretreatment with 250 or 500 microg/kg of subcutaneously administered rhIL-11 2 hours before acetaminophen administration reduced serum concentrations of hepatocellular leakage enzymes and TNFalpha by 40-50%. This was associated with a statistically significant decrease in mean severity score for centrilobular hemorrhage and necrosis from grade 3 to grade 2 for rhIL-11-treated animals compared to vehicle. These results indicate that treatment with rhIL-11 has a protective effect in a model of acetaminophen-induced liver damage.
PMID: 11421492, UI: 21314323
the above reports in Macintosh PC UNIX Text HTML format documents on this page through Loansome Doc