Recurrent mature cystic teratoma presenting as a perihepatic mass.
Explore the source record for details and available documents.
Abdominal Neoplasms↗
Biomedical subjects
S D Nelson
Publications and source records attributed to S D Nelson.
Large, deep, high-grade extremity sarcomas: treating tumors of the flexor fossae.
Limb salvage is now possible for the majority of patients with extremity sarcomas. Although overall prognosis is primarily based on tumor size and histologic grade, complete surgical excision and local control is essential for cure. There are, however, certain anatomic locations such as the flexor fossae in which a complete surgical margin is difficult to attain, and surgery without adjuvant therapy has a high local failure and amputation rate. We have found that preoperative adjuvant therapy consisting of chemotherapy and radiation followed by surgical excision with tumor-free margins has been successful in treating flexor fossa sarcomas with high limb salvage (96%), local control (89%) and overall survival rates (70%). These results are comparable to patients with similar large, high-grade extremity tumors in other compartmental locations.
Antineoplastic Combined Chemotherapy Protocols↗
The influence of specific and nonspecific potassium current blockade on the defibrillation energy requirement of biphasic shock.
UNLABELLED: Block of delayed rectifier potassium current (IK) is known to decrease defibrillation energy requirements (DERs). We tested the hypothesis that there would be no difference in DER reduction with a nonspecific IK (IKr + IKs) blocker, ambasilide, and a specific IKr blocker, dofetilide. METHODS: An anesthetized canine model (n = 30) of internal transvenous defibrillation with biphasic shocks was used. Ambasilide (n = 9; dose: 4.8 mg/kg, then 9.6 mg/kg/hour), dofetilide (n = 10; dose: 10 (micrograms/kg, then 3.6 (micrograms/kg/hour), or matched placebo (n = 11) were administered. DERs (J) were determined in triplicate using an increment-decrement protocol at baseline and during each treatment. ECG intervals were measured at baseline and during each treatment. ANOVA with post-hoc Bonferroni test was used for statistical analysis. RESULTS: Ambasilide resulted in a +23.5 +/- 4.06% prolongation of the QTc interval, while dofetilide resulted in a +20.5% +/- 3.76% prolongation of the QTc interval. Thus, the two drugs resulted in comparable prolongation of the QTc interval (P < 0.05 compared to placebo). Both drugs significantly reduced the DER (-17.7% +/- 5.33% reduction by ambasilide, and -21.9% +/- 5.21% reduction by dofetilide, P < 0.05 compared to placebo). There was no difference in the magnitude of DER reduction between the two treatments. CONCLUSIONS: Administration of equipotent doses (as indicated by QTc changes) of ambasilide or dofetilide had comparable effects on DERs. Selectivity of IK blockade has no significant effect on the magnitude of reduction in DERs.
Action Potentials↗
Improved clinical efficacy of external cardioversion by fluoroscopic electrode positioning and comparison to internal cardioversion in patients with atrial fibrillation.
BACKGROUND: Despite using different electrode positions, "conventional" external DC cardioversion in patients with atrial fibrillation is ineffective in 6%-50% of cases. An alternative when DC cardioversion is not successful is low energy internal cardioversion, which is performed at increased risk. We tested the hypothesis that optimization of electrode pad position under fluoroscopy to encompass as much atrial muscle as possible might improve the success rate of external cardioversion and thus minimize the need for internal cardioversion. METHODS: Fifteen (9 males, 6 females) patients (age: 54 +/- 15 years, weight: 124 +/- 35 kg) with chronic atrial fibrillation (> 8 weeks) who had undergone unsuccessful conventional external cardioversion entered the study. Repeat conventional external cardioversion with electrodes in standard (right anterior and left posterior) positions was followed by "optimized" external cardioversion by positioning electrodes under fluoroscopy (using metallic markers). In case of failure, internal cardioversion was performed. RESULTS: All 15 patients had undergone unsuccessful conventional external cardioversion with 360-J shocks. Eight patients (group A) reverted to sinus rhythm with one or two 360-J shocks using fluoroscopy-guided pad placement (53%). Six of the remaining 7 (86%) patients (group B) had successful internal cardioversion with biphasic shocks (12 +/- 3 J). The body weight and body mass index were statistically lower in group A vs group B (106 +/- 27 vs 145 +/- 33 kg, p = 0.03 and 35 +/- 8 vs 45 +/- 8 kg/m2, P = 0.48, respectively). There was no statistically significant in age, height, body surface area, duration of atrial fibrillation, amiodarone therapy, ejection fraction, or underlying heart disease. CONCLUSION: Unsuccessful external DC cardioversion, in some patients, is in part due to suboptimal conventional positioning of electrode pads that can be improved under fluoroscopic guidance by achieving the best possible vector encompassing the right and left atria. The optimized external cardioversion technique may minimize the need for internal cardioversion, which remains an effective approach when external cardioversion fails.
Adolescent↗
Implantable defibrillators impedance measurement using pacing pulses versus shock delivery with intact and modified high voltage lead system.
At present the only method for measuring the high voltage system lead impedance in patients with an ICD is to deliver a low energy test shock. This is painful, requires sedation, and carries a risk of ventricular fibrillation induction. We sought to assess the shock lead and electrode function by calculating IMP using low voltage pacing pulses, and compared it to the measured impedance of a shock through the same lead. This was performed in both an intact and a modified lead system in order to mimic common clinical scenarios that alter lead system IMP (e.g., lead fracture). In an anesthesized canine model (n = 12) a standard (S) transvenous defibrillation lead (TDL), a modified (M) TDL (two-thirds of coil covered with heat-shrunk tubing), an active can (AC), and a M epicardial patch (EP) (two of four coils were disconnected) were used. Three configurations (C) were tested: C1:S/TDL-->AC, C2:M/TDL-->AC, and C3:M/TDL-->MEP. A measured IMP was obtained by an ICD using a 5-J shock as control. IMP was calculated using a 5-J shock, pacing pulses of 10-, 5-, 2-, and 1-V amplitude, as well as from a square wave drive train of low amplitude/high frequency signals (1 and 0.2 V, at 10 kHz) in all Cs. Ohm's law (V = IR) was utilized for measuring calculated IMP. As the surface area of the high voltage lead system decreased, the mean measured IMP (control) increased from C 1 to 3 (63 +/- 10, 95 +/- 4, and 127 +/- 20 omega, respectively). The correlation of calculated IMP from all Cs to measured impedance (control) remained high throughout the IMP range (range of correlation coefficient (r): 0.921-0.981). Calculated IMP using delivery of pacing pulses is highly correlated to IMP measured during shock delivery. This correlation remains high over a clinically significant range of high voltage lead system IMP changes. This study suggests that pacing pulses can be used to predict the IMP changes in the high voltage lead system which may occur clinically, reducing the need to deliver a shock for IMP measurement.
Animals↗
Primary musculoskeletal neoplasms: effectiveness of core-needle biopsy.
PURPOSE: To analyze the effectiveness of core-needle biopsy for evaluation of possible primary musculoskeletal neoplasms, which often are evaluated with open biopsy. MATERIALS AND METHODS: Core-needle biopsy was performed at a tertiary care institution in 141 patients suspected of having a mesenchymal neoplasm. In 85 patients, the lesion was in soft tissue; in 56 patients, the lesion was in bone. Eighty-nine patients had a malignant lesion, and 52 had a benign lesion. Twenty-eight patients had undergone previous surgery. RESULTS: In 105 (74%) patients, core-needle biopsy results were concordant with results from specimens subsequently obtained at surgery with respect to tumor histologic features and grade, or they provided sufficient diagnostic information to obviate surgery. In 36 (26%) patients, inaccurate core-needle biopsy results were obtained: In nine, results were imprecise about exact histologic features; in three, results were correct about histologic features but incorrect about tumor grade. In 25 (18%) patients, open biopsy was performed after core-needle biopsy. The accuracy and rate of performance of open biopsy for soft-tissue lesions were not significantly different from those for bone lesions. CONCLUSION: Percutaneous core-needle biopsy can be an effective alternative to open biopsy in the evaluation of possible mesenchymal neoplasms of either bone or soft tissue. Needle biopsy of such lesions, however, is best performed as part of a multidisciplinary team approach to tumor management.
Biopsy↗
Metabolism of (R)-(+)-pulegone and (R)-(+)-menthofuran by human liver cytochrome P-450s: evidence for formation of a furan epoxide.
(R)-(+)-Pulegone, a monoterpene constituent of pennyroyal oil, is a hepatotoxin that has been used in folklore medicine as an abortifacient despite its potential lethal effects. Pulegone is metabolized by human liver cytochrome P-450s to menthofuran, a proximate hepatotoxic metabolite of pulegone. Expressed human liver cytochrome (CYP) P-450s (1A2, 2A6, 2C9, 2C19, 2D6, 2E1, and 3A4) were tested for their ability to catalyze the oxidations of pulegone and menthofuran. Expressed CYP2E1, CYP1A2, and CYP2C19 oxidized pulegone to menthofuran, with respective Km and Vmax values of 29 microM and 8.4 nmol/min/nmol P-450 for CYP2E1, 94 microM and 2.4 nmol/min/nmol P-450 for CYP1A2, and 31 microM and 1.5 nmol/min/nmol P-450 for CYP2C19. The human liver P-450s involved in the metabolism of menthofuran are the same as pulegone except for the addition of CYP2A6. These P-450s were found to oxidize menthofuran to a newly identified metabolite, 2-hydroxymenthofuran, which is an intermediate in the formation of the known metabolites mintlactone and isomintlactone. Based on studies with 18O2 and H218O, 2-hydroxymenthofuran arises predominantly from a dihydrodiol formed from a furan epoxide. CYP2E1, CYP1A2, and CYP2C19 oxidized menthofuran with respective Km and Vmax values of 33 microM and 0.43 nmol/min/nmol P-450 for CYP2E1, 57 microM and 0.29 nmol/min/nmol P-450 for CYP1A2, and 62 microM and 0.26 nmol/min/nmol P-450 for CYP2C19.
Animals↗
Diffuse bony metastasis from transitional cell carcinoma of urinary bladder: a case report and review of literature.
The incidence and mortality rate of bladder carcinoma remains high and is in fact increasing despite the application of new treatment strategies. Transitional cell carcinoma (TCC) is the most common carcinoma of the bladder (> 90% of cases). We report a case of a 60 year-old man with multiple bony metastases of TCC affecting the humerus, femur, spine, iliac wing, and ribs. The metastases were discovered within a year after first presentation of hematuria with a subsequent biopsy diagnosis of TCC of bladder, Grade 3 of 3 with no definite muscle invasion. Metastasis of TCC of bladder to bone is an uncommon occurrence when compared with breast and prostate carcinoma. This may be due to intrinsic properties of tumor cells and/or mechanisms of metastases. Recent studies confirm that bone is the preferred site of metastasis (35%) of TCC outside of the pelvis, with the spine being the most common site (40% of bony metastases). Histologic grading, emphasizing the presence of invasion, is generally accepted as being very important prognostically. The importance of diagnostic screening tests including urothelial biomarkers profile in reducing the mortality rate from first onset of hematuria is discussed such as tumor-associated antigen M344 and DD23.
Biopsy, Needle↗
Clinical characteristics of sudden death victims in heritable (chromosome 1p1-1q1) conduction and myocardial disease.
OBJECTIVES: The purpose of this study was to identify the clinical characteristics of family members at risk of sudden death. BACKGROUND: The significance of sudden death in heritable cardiac disorders with delayed expression is incompletely understood. Additional insights come from a four-decade experience of seven generations of a family of German origin with autosomal dominant (chromosome 1p1-1q1) cardiac conduction and myocardial disease. METHODS AND RESULTS: A total of 38 family members (20 males; 18 females) were identified with sudden death. Twenty-eight family members (mean age 48+/-8 years) from earlier generations had no pacemaker at the time of sudden death. In this group, 15 subjects were asymptomatic prior to sudden death. Ten family members with sudden death, from later generations, had chronically implanted pacemakers for high grade atrioventricular block. This group was older (mean age 57+/-2 years), with decreased functional status (New York Heart Association class II to IV), enlarged left atria, dilated left ventricles with reduced systolic function and documented ventricular fibrillation in three members. Twenty-eight family members with sudden death were descendants of sib lineages 2 or 6; 21 family members with sudden death were offspring of a parent who also suffered sudden death. CONCLUSION: Sudden death is an important late outcome in heritable (chromosome 1p1-1q1) cardiac conduction and myocardial disease. Pacemaker therapy is important for the treatment of symptomatic bradycardia, but it does not prevent sudden death. Family members who are beyond the third decade of life with reduced functional capacity, left ventricular dysfunction, pacemakers and who are the offspring of a parent with sudden death appear to be at greatest risk
Adult↗
Minimally invasive breast carcinoma staging using lymphatic mapping with radiolabeled dextran.
BACKGROUND: The sentinel lymph node is defined as the first lymph node to receive drainage from a primary tumor. Based on this concept, the authors set out to evaluate whether the status of the sentinel lymph node can accurately predict whether breast tumor cells have metastasized to the axillary lymphatic basin. METHODS: Radiolabeled dextran was injected into the site of the breast tumor. In the operating room, a portable gamma detector probe was used to identify the exact location of the sentinel lymph node(s). After identifying and excising the radioactive sentinel lymph node specimens, a routine axillary lymph node dissection was performed. All lymph nodes were then subjected to hematoxylin and eosin (H & E) staining, and the sentinel lymph nodes were subjected to additional cytokeratin immunohistochemistry. RESULTS: Of the 41 patients who participated in the study, 18 had tumor metastasis to their axillary lymph nodes. In all 18 of these cases, the sentinel lymph node(s) contained cancer detected by either H & E staining or cytokeratin immunohistochemistry. CONCLUSIONS: The status of the sentinel lymph node(s) appears to predict accurately whether breast tumor cells have metastasized to the axillary lymphatic basin. This new, minimally invasive technique for staging breast carcinoma should be further validated in a large, multi-institutional clinical trial.
Breast Neoplasms↗
Subnanomolar quantification of caffeine's in vitro metabolites by stable isotope dilution gas chromatography-mass spectrometry.
A method for the quantification of subnanomolar levels of in vitro metabolites of caffeine by an isotope dilution gas chromatographic-mass spectrometric (GC-MS) assay has been developed and applied. Trideuteromethylated analogs of each primary metabolite were synthesized and added after incubations of caffeine with human liver microsomes high in cytochrome P4501A2. HPLC separation of the metabolites prior to GC-MS quantification allowed the isolation of theobromine and paraxanthine which coeluted by GC and enabled quantification over a larger dynamic range. Quantitative analysis was performed on the n-propylated derivatives by selected-ion monitoring of either the M+. ions for the dimethylxanthines or [M-C3H6]+. ions for 1,3,7-trimethyluric acid. For the least abundant metabolite (1,3,7-trimethyluric acid), the detection level on column was 200 pg. Replicate analyses exhibited intra- and inter-day variability of 4.2 and 7.9%, respectively. This assay has been successfully used in the quantification of caffeine's primary metabolites in more than 180 incubations, at varying substrate concentrations and with multiple enzyme sources.
Caffeine↗
Oxidation of 1,3-butadiene to (R)- and (S)-butadiene monoxide by purified recombinant cytochrome P450 2E1 from rabbit, rat and human.
1,3-Butadiene (BD) is a gas used widely in the rubber and plastics industry as an intermediate in production processes and has been detected in automobile exhaust and cigarette smoke. BD requires metabolic activation to exert toxicity and has been shown to be carcinogenic in rodents. IARC has classified BD as a group 2A (probably carcinogenic to humans) carcinogen. The initial oxidation of BD to butadiene monoxide (BMO) occurs primarily via cytochrome P450 2E1 and two stereoisomers of BMO (R and S) can be formed. (R) and (S)-BMO are metabolized differently and demonstrate markedly different toxicities in isolated rat hepatocytes. This work examined the generation of (R) and (S)-BMO from BD by cytochrome P450 2E1 from rabbit, rat and human. BMO level was measured by GC-MS analysis and enantiomeric composition was determined by GC-FID. The greatest rate of formation of BMO from BD was obtained with rabbit cytochrome P4502E1 followed by human and then by rat. Enantiomeric distribution of R and S-BMO produced by the three species demonstrated no significant differences.
Animals↗
Role of CYP1A2 in the hepatotoxicity of acetaminophen: investigations using Cyp1a2 null mice.
Acetaminophen (APAP) is known to cause centrilobular hepatic necrosis under overdose conditions. This is thought to be mediated via the P450-generated reactive intermediate N-acetyl-p-benzoquinone imine (NAPQI). Initially, NAPQI is detoxified by conjugation with glutathione (GSH), but once GSH is depleted, NAPQI reacts more extensively with hepatic proteins leading to hepatocellular damage. The P450 isoforms thought to be responsible for APAP hepatotoxicity in humans are CYP2E1, CYP1A2, and CYP3A4, and thus, we have investigated the effect of murine Cyp1a2 on APAP hepatotoxicity using Cyp1a2 knockout mice (Liang et al., Proc. Natl. Acad. Sci. USA 93, 1671-1676, 1996). Doses of 250 mg/kg were markedly hepatotoxic in these mice, and surprisingly, deaths only occurred in the knock-out and heterozygote mice over a 24-h period after dosing. Furthermore, there were no significant differences among survivors of any genotype in serum ALT concentrations, a well correlated indicator of APAP hepatotoxicity in mice. Finally, no differences were observed in the urinary metabolites excreted ove the 24-h period, including those derived from GSH conjugation of the major reactive metabolite NAPQI. Consistent with the effects on hepatotoxicity and metabolism, 2 h after hepatotoxic doses (500 mg/kg, i.p.) of APAP no significant differences were observed in total whole liver homogenate nonprotein thiol concentrations among the three genotypes even though hepatic thiols were decreased compared to control animals (> 90%). In addition, when the liver cytosol and microsome samples were examined by immunoblotting for the presence of APAP-protein adducts using a specific antiserum, there were no observable differences in either the intensity of staining or in the spectrum of adducts formed between APAP-dosed mice of any genotype. The cumulative data suggest that Cyp1a2 doses not play a significant role in APAP hepatotoxicity in these mice.
Acetaminophen↗
Oxidation of acetaminophen to its toxic quinone imine and nontoxic catechol metabolites by baculovirus-expressed and purified human cytochromes P450 2E1 and 2A6.
Acetaminophen (APAP), a widely used analgesic and antipyretic agent, is bioactivated by cytochromes P450 to cause severe hepatotoxicity. APAP is oxidized by two pathways to form a toxic intermediate, N-acetyl-p-benzoquinone imine (NAPQI), and a nontoxic catechol metabolite, 3-hydroxy-APAP (3-OH-APAP). We investigated the role of P450 2E1 and 2A6 in APAP oxidation by using baculovirus-expressed and highly purified forms of human P450 2E1 and 2A6. An electrochemical HPLC assay was developed to quantify both oxidative metabolites simultaneously. For the first time, it was demonstrated that human P450 2E1 selectively oxidized APAP to NAPQI (assayed as its glutathione conjugate, GS-APAP), whereas human P450 2A6 selectively oxidized APAP to 3-OH-APAP. At 1 mM APAP, the relative ratio for the formation of GS-APAP vs 3-OH-APAP with human P450 2E1 was approximately 6:1, whereas the ratio with human P450 2A6 was 1:3. Apparent Km and Vmax values for the formation of GS-APAP by human P450 2E1 were 1.3 mM and 6.9 nmol/min/nmol of P450, respectively, whereas they were 4.6 mM and 7.9 nmol/min/nmol of P450 for P450 2A6. Apparent Km and Vmax values for the formation of 3-OH-APAP by human P450 2E1 were 4.0 mM and 2.5 nmol/min/nmol of P450, respectively, whereas they were 2.2 mM and 14.2 nmol/min/nmol of P450, respectively, for P450 2A6. Thus, although at toxic doses of APAP P450 2E1 is the more efficient catalyst for the formation of the toxic metabolite NAPQI, P450 2A6 also can contribute significantly to NAPQI production.
Acetaminophen↗
QRS duration widening: reduced synchronization of endocardial activation or transseptal conduction time?
Antegrade activation of the His-Purkinje system (HPS) results in synchronized activation of the right ventricular (RV) and left ventricular (LV) endocardia forming normal, narrow QRS duration (QRSD). An alteration in septal activation and transseptal conduction time have been reported to be the causes for QRSD widening seen with bundle branch block. However, reduced synchronization of activation of RV and LV endocardia as another potential mechanism for QRSD widening has not been systematically studied. Fifteen consecutive patients underwent radiofrequency ablation (RFA) for treatment of supraventricular tachycardia. After RFA, mean QRSD in normal sinus rhythm was 86 +/- 8 ms with mean HV interval of 40 +/- 5 ms. Right atrial (RA), coronary sinus (CS), simultaneous (S) RA-CS, RV apex (RVA), LV apex (LVA), and SRVA-LVA pacing were performed. Mean QRSD with RA, CS, SRA-CS pacing was similar to normal sinus rhythm (87 +/- 7, 87 +/- 8 and 88 +/- 8 ms respectively). Mean QRSD was significantly longer with SRVA-LVA and either RVA or LVA pacing alone compared to normal sinus rhythm (106 +/- 8, 146 +/- 12 and 157 +/- 13 ms, respectively). However, QRSD was significantly shorter with SRVA-LVA pacing compared to either RVA or LVA pacing alone (P < 0.0001). We conclude that shorter QRSD with SRVA-LVA pacing compared to either RVA or LVA pacing alone is due to elimination of transseptal conduction delay; longer QRSD with SRVA-LVA pacing compared to sinus or atrial paced rhythm is due to reduced synchronization of endocardial activation secondary to ectopic entry of impulses into the HPS network and inability to take advantage of the branching structure of the HPS. Therefore, in addition to transseptal conduction delay, reduced synchronization of endocardial activation is another potential mechanism for QRSD widening.
Adolescent↗
(R)-(+)-Menthofuran is a potent, mechanism-based inactivator of human liver cytochrome P450 2A6.
(R)-(+)-Menthofuran is a potent, mechanism-based inactivator of human liver cytochrome P450 (CYP or P450) 2A6. Menthofuran caused a time- and concentration-dependent loss of CYP2A6 activity. The inactivation of CYP2A6 was characterized by a Ki of 2.5 microM and a kinact of 0.22 min-1 for human liver microsomes and a Ki of 0.84 microM and a kinact of 0.25 min-1 for purified expressed CYP2A6. Addition of various nucleophiles, a chelator of iron, or scavengers of reactive oxygen species or extensive dialysis failed to protect CYP2A6 from inactivation. An antibody to metallothionein conjugates of a suspected reactive metabolite of menthofuran was used to detect reactive menthofuran metabolite adducts with CYP2A6. These adducts were formed only in the presence of NADPH-P450 reductase and NADPH. Glutathione, methoxylamine, and semicarbazide did not prevent adduction of reactive menthofuran metabolites to CYP2A6, however. The menthofuran metabolite formation/CYP2A6 inactivation partition ratio was determined to be 3.5 +/- 0.6 nmol/nmol of P450. Menthofuran was unable to inactivate CYP1A2, CYP2D6, CYP2E1, or CYP3A4 in a time- and concentration-dependent manner.
Animals↗
Epidemic of liver disease caused by hydrochlorofluorocarbons used as ozone-sparing substitutes of chlorofluorocarbons.
BACKGROUND: Hydrochlorofluorocarbons (HCFCs) are used increasingly in industry as substitutes for ozone-depleting chlorofluorocarbons (CFCs). Limited studies in animals indicate potential hepatotoxicity of some of these compounds. We investigated an epidemic of liver disease in nine industrial workers who had had repeated accidental exposure to a mixture of 1,1-dichloro-2,2,2-trifluoroethane (HCFC 123) and 1-chloro-1,2,2,2-tetrafluoroethane (HCFC 124). All nine exposed workers were affected to various degrees. Both compounds are metabolised in the same way as 1-bromo-1-chloro-2,2,2-trifluoroethane (halothane) to form reactive trifluoroacetyl halide intermediates, which have been implicated in the hepatotoxicity of halothane. We aimed to test whether HCFCs 123 and 124 can result in serious liver disease. METHODS: For one severely affected worker liver biopsy and immunohistochemical stainings for the presence of trifluoroacetyl protein adducts were done. The serum of six affected workers and five controls was tested for autoantibodies that react with human liver cytochrome-P450 2E1 (P450 2E1) and P58 protein disulphide isomerase isoform (P58). FINDINGS: The liver biopsy sample showed hepatocellular necrosis which was prominent in perivenular zone three and extended focally from portal tracts to portal tracts and centrilobular areas (bridging necrosis). Trifluoroacetyl-adducted proteins were detected in surviving hepatocytes. Autoantibodies against P450 2E1 or P58, previously associated with halothane hepatitis, were detected in the serum of five affected workers. INTERPRETATION: Repeated exposure of human beings to HCFCs 123 and 124 can result in serious liver injury in a large proportion of the exposed population. Although the exact mechanism of hepatotoxicity of these agents is not known, the results suggest that trifluoroacetyl-altered liver proteins are involved. In view of the potentially widespread use of these compounds, there is an urgent need to develop safer alternatives.
Biomarkers↗
Clinical significance of an equivocal signal-averaged electrocardiogram.
Patients with an equivocal signal averaged electrocardiogram (SAECG) had less heart disease and better prognosis than patients with overtly abnormal SAECGs. An equivocal SAECG should not prompt further invasive diagnostic testing for ventricular tachycardia unless other clinical risk factors are present.
Aged↗