Use of nasal mupirocin for eradicating meticillin-resistant Staphylococcus aureus: a dilemma?
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Biomedical subjects
Publications and source records attributed to F L Wu.
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BACKGROUND: The carcinogenic effect of betelnut chewing leading to oral cancer is well known. Betelnut chewing may also affect the autonomic nervous system. In this report, we present another potential hazard of betelnuts, milk-alkali syndrome. CASE REPORT: Two patients who had chewed a large quantity of betelnuts developed hypercalcemia, metabolic alkalosis, and renal insufficiency. They ingested a large amount of calcium carbonate from a local special paste used for betelnut preparation, the main ingredient of which is ground oyster shell. The symptoms and metabolic abnormalities disappeared promptly after abstinence from betelnut chewing and administration of saline solution. Improvement of renal function was observed in both patients. Analysis of the calcium content of the paste suggested that the patients might have ingested 9 g and 6 g of calcium carbonate per day, respectively. CONCLUSION: This is the first report of milk-alkali syndrome not caused iatrogenically, but by recreational usage of oyster shell preparations of betelnuts.
The preliminary results of an interdisciplinary active surveillance adverse drug reaction (ADR) reporting program conducted from April 1992 to December 1993 in the family medicine ward of National Taiwan University Hospital are presented. During this period, every admitted patient was screened for any possible drug-related problems; suspected ADRs were evaluated and documented. The USA Food and Drug Administration's definition of ADR was used, and Naranjo's scale was used to estimate the probability of drug-induced events. A total of 41 ADRs were identified in 38 patients. Among these 41 cases, 18 ADRs occurred during hospitalization, and 23 were the reason for hospitalization. The incidence of ADRs rated as probable or highly probable during hospital stay was 2.0%, or 2.7% if possible reactions were included (based upon 666 hospital admissions to the unit during the study period). The occurrence of admissions due to ADRs rated as highly probable or probable was 2.7%, or 3.5% if possible reactions were included. Twenty-one ADRs (51.2%) were type A reactions and 20 (48.8%) were type B. Thirty-three ADRs (80.5%) were classified as serious or moderate. There was no mortality. Further studies are warranted to determine the incidence of ADRs in different patient populations in Taiwan.
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Dog model of acute pancreatitis, induced by intrapancreatoductal injection of fresh trypsin-bile mixture, was used to investigate the effects of naloxone on hemodynamic changes in acute pancreatitis. In the control group, acute pancreatitis was induced and characterized hemodynamically by the decrease in maximum positive and negative dP/dt (+/- dP/dtmax), cardiac output (CO) and cardiac index (CI), and increase in pulmonary vascular resistance (PVR) and systemic vascular resistance (SVP), as well as early reduction of pancreatic blood flow (PBF). In the naloxone treated group, naloxone was given intravenously 10 minutes after the induction of acute pancreatitis (80 micrograms/kg as a bolus + 80 micrograms/kg/h for 3 hours). It was found that naloxone significantly increased PBF and the +/- dP/dtmax effectively prevented the significant decrease in CO, CI and increase in PVR, SVR observed in untreated acute pancreatitis; and significantly reduced the severity of pancreatitis, as assessed by both histological staging and mortality rate. These results suggest that naloxone appears to limit the progression from edematous to hemorrhagic pancreatitis through preserving PBF and improving systemic hemodynamics at the early phase of acute pancreatitis; hence the hypothesis that endogenous opioid peptides may play a role in the pathophysiology of acute pancreatitis.
A dog model was used to measure the hemodynamic changes in acute pancreatitis (AP) caused by intraductal injection of fresh trypsin-bile mixture and to investigate the efficacy of dopamine in the treatment of AP. Dopamine was administered intravenously for 3 hours at a dose of 0.6 mg/kg/hour starting 10 min after the induction of AP. Hemorrhagic pancreatitis was characterized by a fall in cardiac output (CO), systemic arterial pressure (SAP), an increase in pulmonary vascular resistance (PVR), systemic vascular resistance (SVR) and the development of early reduction of pancreatic blood flow (PBF). Administration of dopamine produced a significant increase in PBF and leads to a normalization in CO, SAP, PVR and SVR. In addition, dopamine significantly reduced the severity of the AP, as assessed by histological staging and mortality rate. These results suggest that dopamine can limit the progression from edematous to hemorrhagic pancreatitis and prevent irreversible pancreatic damage through preserving PBF at the early phase of AP.
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Endogenous opioid peptides may play a role in the genesis of pancreatic damage in acute pancreatitis. The effects of naloxone on the haemodynamic changes in acute pancreatitis were investigated by inducing it in dogs with pancreatic ductal injection of fresh trypsin-bile mixture. In the control group (n = 8), acute pancreatitis was characterized haemodynamically by falls in the maximum positive and negative dP/dt (+/- dP/dt), cardiac output (CO) and cardiac index (CI), and increases in the pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR) as well as an early reduction of pancreatic blood flow (PBF). In another set of eight dogs (naloxone group), naloxone was given intravenously 10 min after the induction of acute pancreatitis (80 micrograms/kg as a bolus + 80 micrograms/kg/h for 3 h). Compared with untreated dogs, naloxone significantly increased PBF and the +/- dP/dtmax; prevented the significant decreases in CO and CI and increases in PVR and SVR, and reduced significantly the severity of pancreatitis, as assessed by both the histological staging and the mortality rate. These results suggest that naloxone limits the progression of acute pancreatitis from oedematous to haemorrhagic form. It is proposed that endogenous opioid peptides may play a role in the pathophysiology of acute pancreatitis.
Lidocaine-induced seizures have been reported after topical administration. A 30-year-old, 48-kg women with acquired immunodeficiency syndrome, chronic end-stage renal failure, anemia, congestive heart failure (CHF), cardiomyopathy, and increased liver function tests was admitted to the hospital with fever, chills, and dry cough. Bronchoscopy was performed to rule out Pneumocystis carinii pneumonitis; the patient experienced seizure activity after administration of a total dose of topical lidocaine 300 mg. Plasma drug concentration measured shortly after seizure, and at 4 and 22 hours after seizure were 12.0, 7.6, and 1.4 mg/L, respectively. A direct correlation exists between clinical symptoms and blood level of lidocaine; as the level increases to 8-12 mg/L the probability of seizure increases. The extent of absorption and bioavailability after airway administration depends on tissue vascularity, sites and techniques of application, patient's disease state, and, most important, the dose/unit body weight. The lidocaine dose should be titrated slowly and patients monitored for altered mental status. The dose often has to be decreased empirically in patients with liver disease or CHF. Efforts should be made to deliver minimum amounts of the drug to the lower respiratory tract, since its pharmacokinetics at that site are similar to those with intravenous administration.