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J A Vale

Publications and source records attributed to J A Vale.

At least 19 recordsLinked to original sources
PubMed2005

Changes in standard of candidates taking the MRCP(UK) Part 1 examination, 1985 to 2002: analysis of marker questions.

BACKGROUND: The maintenance of standards is a problem for postgraduate medical examinations, particularly if they use norm-referencing as the sole method of standard setting. In each of its diets, the MRCP(UK) Part 1 Examination includes a number of marker questions, which are unchanged from their use in a previous diet. This paper describes two complementary studies of marker questions for 52 diets of the MRCP(UK) Part 1 Examination over the years 1985 to 2001 to assess whether standards have changed. METHODS: Study 1, which used routinely collected information on the performance of 4405 marker items, used a statistical method to assess changes in performance across diets. Study 2 compared performances of individual candidates on 28 individual marker items that were shared by the 1996/2 and 2001/3 diets. RESULTS: Study 1 found evidence that candidate performance on the MRCP(UK) Part 1 Examination showed a gradual improvement over the period 1985 to 1997, which was followed by a sharp decline in performance until 2001. The 'dog-leg' in performance at 1997/3 was not an artefact of changed Examination Regulations, mix of UK and overseas candidates, or time from qualification until taking the Examination. Study 2 confirmed that performance in 2001/3 was significantly worse than in 1996/3, that the poorer performance was found in graduates of UK medical schools, and that candidates passing the Examination in 2001/3 performed less well than those passing in 1996/2. CONCLUSION: There has been a decline in the performance of graduates from UK medical schools taking the MRCP(UK) Part 1 examination. The reasons for this are not clear, but the finding has implications for medical education, and further studies are needed of performance in other postgraduate and undergraduate examinations. The use of norm-referencing as the sole method for setting the pass mark over this period meant that candidates passing the MRCP(UK) examination also had a lower standard. The MRCP(UK) Part 1 and Part 2 examinations now have their standard set by criterion-referencing.

Education, Medical, Graduate↗
PubMed2005

Position paper: Single-dose activated charcoal.

Single-dose activated charcoal therapy involves the oral administration or instillation by nasogastric tube of an aqueous preparation of activated charcoal after the ingestion of a poison. Volunteer studies demonstrate that the effectiveness of activated charcoal decreases with time. Data using at least 50 g of activated charcoal, showed a mean reduction in absorption of 47.3%, 40.07%, 16.5% and 21.13%, when activated charcoal was administered at 30 minutes, 60 minutes, 120 minutes and 180 minutes, respectively, after dosing. There are no satisfactorily designed clinical studies assessing benefit from single-dose activated charcoal to guide the use of this therapy. Single-dose activated charcoal should not be administered routinely in the management of poisoned patients. Based on volunteer studies, the administration of activated charcoal may be considered if a patient has ingested a potentially toxic amount of a poison (which is known to be adsorbed to charcoal) up to one hour previously. Although volunteer studies demonstrate that the reduction of drug absorption decreases to values of questionable clinical importance when charcoal is administered at times greater than one hour, the potential for benefit after one hour cannot be excluded. There is no evidence that the administration of activated charcoal improves clinical outcome. Unless a patient has an intact or protected airway, the administration of charcoal is contraindicated. A review of the literature since the preparation of the 1997 Single-dose Activated Charcoal Position Statement revealed no new evidence that would require a revision of the conclusions of the Statement.

Adsorption↗
PubMed2004

Biopsy of the red patch at cystoscopy: is it worthwhile?

OBJECTIVE: At cystoscopy red patches of urothelium are commonly seen within the bladder and frequently biopsied in order to exclude carcinoma in situ (CIS), which classically presents as a red, velvety patch. This appearance however is not specific and it is possible that many lesions are biopsied without significant benefit to the patient. The objective of this study was to determine whether routine biopsy of red patches seen in the bladder at cystoscopy is warranted. PATIENTS AND METHODS: 193 biopsies were taken from red patches seen at flexible and rigid cystoscopy during a 4-year period from December 1997 to January 2002 and examined by histopathology. Patients included in the study were those on cystoscopic follow-up for transitional cell carcinoma (TCC) of the bladder and those undergoing investigation for haematuria or lower urinary tract symptoms. RESULTS: In 193 (17.7% of total biopsies) red patch biopsies, malignancy was found in 23 (11.9%) and 18 of 23 (78.3%) were CIS. No malignancies were detected in red patches from patients under the age of 60 years. CONCLUSION: Red patch biopsy yields a positive finding of malignancy in 12% and was concluded to be a valuable exercise, particularly in those over the age of 60 years and on follow-up for TCC.

Adult↗
PubMed2004

Position Paper on urine alkalinization.

This Position Paper was prepared using the methodology agreed by the American Academy of Clinical Toxicology (AACT) and the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT). All relevant scientific literature was identified and reviewed critically by acknowledged experts using set criteria. Well-conducted clinical and experimental studies were given precedence over anecdotal case reports and abstracts were not considered. A draft Position Paper was then produced and presented at the North American Congress of Clinical Toxicology in October 2001 and at the EAPCCT Congress in May 2002 to allow participants to comment on the draft after which a revised draft was produced. The Position Paper was subjected to detailed peer review by an international group of clinical toxicologists chosen by the AACT and the EAPCCT, and a final draft was approved by the boards of the two societies. The Position Paper includes a summary statement (Position Statement) for ease of use, which will also be published separately, as well as the detailed scientific evidence on which the conclusions of the Position Paper are based. Urine alkalinization is a treatment regimen that increases poison elimination by the administration of intravenous sodium bicarbonate to produce urine with a pH > or = 7.5. The term urine alkalinization emphasizes that urine pH manipulation rather than a diuresis is the prime objective of treatment; the terms forced alkaline diuresis and alkaline diuresis should therefore be discontinued. Urine alkalinization increases the urine elimination of chlorpropamide, 2,4-dichlorophenoxyacetic acid, diflunisal, fluoride, mecoprop, methotrexate, phenobarbital, and salicylate. Based on volunteer and clinical studies, urine alkalinization should be considered as first line treatment for patients with moderately severe salicylate poisoning who do not meet the criteria for hemodialysis. Urine alkalinization cannot be recommended as first line treatment in cases of phenobarbital poisoning as multiple-dose activated charcoal is superior. Supportive care, including the infusion of dextrose, is invariably adequate in chlorpropamide poisoning. A substantial diuresis is required in addition to urine alkalinization in the chlorophenoxy herbicides, 2,4-dichlorophenoxyacetic acid, and mecoprop, if clinically important herbicide elimination is to be achieved. Volunteer studies strongly suggest that urine alkalinization increases fluoride elimination, but this is yet to be confirmed in clinical studies. Although urine alkalinization is employed clinically in methotrexate toxicity, currently there is only one study that supports its use. Urine alkalinization enhances diflunisal excretion, but this technique is unlikely to be of value in diflunisal poisoning. In conclusion, urine alkalinization should be considered first line treatment in patients with moderately severe salicylate poisoning who do not meet the criteria for hemodialysis. Urine alkalinization and high urine flow (approximately 600 mL/h) should also be considered in patients with severe 2,4-dichlorophenoxyacetic acid and mecoprop poisoning. Administration of bicarbonate to alkalinize the urine results in alkalemia (an increase in blood pH or reduction in its hydrogen ion concentration); pH values approaching 7.70 have been recorded. Hypokalemia is the most common complication but can be corrected by giving potassium supplements. Alkalotic tetany occurs occasionally, but hypocalcemia is rare. There is no evidence to suggest that relatively short-duration alkalemia (more than a few hours) poses a risk to life in normal individuals or in those with coronary and cerebral arterial disease.

Alkalies↗
PubMed2004

Position paper: gastric lavage.

Gastric lavage should not be employed routinely, if ever, in the management of poisoned patients. In experimental studies, the amount of marker removed by gastric lavage was highly variable and diminished with time. The results of clinical outcome studies in overdose patients are weighed heavily on the side of showing a lack of beneficial effect. Serious risks of the procedure include hypoxia, dysrhythmias, laryngospasm, perforation of the GI tract or pharynx, fluid and electrolyte abnormalities, and aspiration pneumonitis. Contraindications include loss of protective airway reflexes (unless the patient is first intubated tracheally), ingestion of a strong acid or alkali, ingestion of a hydrocarbon with a high aspiration potential, or risk of GI hemorrhage due to an underlying medical or surgical condition. A review of the 1997 Gastric Lavage Position Statement revealed no new evidence that would require a revision of the conclusions of the Statement.

Animals↗
PubMed2003

Reliability of the MRCP(UK) Part I Examination, 1984-2001.

OBJECTIVES: To assess the reliability of the MRCP(UK) Part I Examination over the period 1984-2001, and to assess how the reliability is related to the difficulty of the examination (mean mark) and to the spread of the candidates' marks (standard deviation). METHODS: Retrospective analysis of the reliability (KR20) of the MRCP(UK) examination recorded in examination records for the 54 diets between 1984 and 2001. RESULTS: The reliability of the examination showed a mean value of 0.865 (SD 0.018, range 0.83-0.89). There were fluctuations in the reliability over time, and multiple regression showed that reliability was higher when the mean mark was relatively high, and when the standard deviation of the marks was high. CONCLUSIONS: The reliability of the MRCP(UK) Examination was maintained over the period 1984-2001. As theory predicted, the reliability was related to the average mark and to the spread of marks.

Clinical Competence↗
PubMed2002

Magnetic resonance imaging-guided laser thermal ablation of renal tumours.

OBJECTIVE: To test the hypothesis that magnetic resonance imaging (MRI)-guided laser thermal ablation (LTA) of inoperable renal tumours is a safe, tolerable and potentially effective treatment. PATIENTS AND METHODS: Nine patients (aged 56-81 years) with malignant renal tumours underwent percutaneous LTA under MRI guidance in a 0.5 T open magnet. Real-time colour thermal mapping was used to monitor tumour ablation, and the follow-up was with gadolinium-enhanced MRI at 6 weeks and (where appropriate) 3-4 months after the procedure. Tumour volume and percentage tumour enhancement before and after ablation were compared. The percentage of tumour ablated on real-time T1-weighted thermal maps was compared with that on gadolinium-enhanced follow-up MRI. RESULTS: The mean (range) follow-up was 16.9 (3-32) months after the first ablation. The mean tumour size did not change significantly, but the mean percentage of viable tumour decreased significantly from 73.7% before to 29.5% after ablation (P = 0.012, Wilcoxon signed-ranks test). Thermal maps correlated moderately well with follow-up MRI in predicting the extent of tumour ablation (Pearson correlation coefficient 0.55). There were two minor and one major complication. CONCLUSION: In this pilot study of patients unsuitable for surgery, MRI-guided LTA of renal tumours was safe, feasible (being well tolerated by the patient) and significantly reduced enhancing tumour volume by a mean of 45%.

Aged↗
PubMed2001

Bone loss associated with the use of LHRH agonists in prostate cancer.

Hypogonadism is a recognised cause of osteoporosis in men. When patients with advanced prostate cancer are treated with luteinising hormone releasing hormone (LHRH) agonist analogues their circulating testosterone levels decline and these patients may develop fractures.We have undertaken a cross-sectional study on a cohort of patients treated with goserelin (n=41) and compared their bone density and bone turnover with patients with prostate cancer not on goserelin and elderly patients living in the community.There was no difference in bone density between the patients on treatment and those living in the community and there was a similar incidence of osteoporosis (50 and 42%, respectively). The bone marker measurements were higher in the treated patients: urine N-telopeptide (NTX) 80.1 (9) (mean (s.e.)) BCE/mmol, compared to 30.1 (2.9), P<0.001 in elderly patients; and bone alkaline phosphatase 41.9 (6.1) u/l in treated patients and 20.7 (1.5) in untreated prostate cancer patients, P<0.002. Patients on treatment with radionuclide scan evidence of metastases did not have higher bone marker values than those with negative scans.As increased bone turnover and low bone density are associated with enhanced risk of osteoporotic fractures, we suggest that patients on LHRH agonist analogues should receive advice and possibly anti-bone resorptive treatment with bisphosphonates to prevent further bone loss and fractures.Prostate Cancer and Prostatic Diseases (2001) 4, 161-166.

Journal Article↗
PubMed2000

Mechanisms of toxicity, clinical features, and management of acute chlorophenoxy herbicide poisoning: a review.

INTRODUCTION: Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation, and disruption of acetylcoenzyme A metabolism. Between January 1962 and January 1999, 66 cases of chlorophenoxy herbicide poisoning following ingestion were reported in the literature. FEATURES FOLLOWING INGESTION: Adjuvants in the formulations may have contributed to some of the features observed. Vomiting, abdominal pain, diarrhea, and, occasionally, gastrointestinal hemorrhage were early effects. When present, hypotension was predominantly due to intravascular volume loss, although vasodilation and direct myocardial toxicity may have contributed in some cases. Neurotoxic features included coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation, and paralysis. Hypoventilation occurred not infrequently, usually in association with central nervous system depression, but respiratory muscle weakness was a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, and myotonia were observed and increased creatine kinase activity was noted in some cases. Other clinical features reported included metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia, and hyperventilation. Twenty-two of 66 patients died. FEATURES FOLLOWING DERMAL AND INHALATIONAL EXPOSURE: Substantial dermal or inhalational 2,4-dichlorophenoxyacetic acid exposure has occasionally led to systemic features but no such reports have been published in the last 20 years and no fatalities have been reported at any time. Substantial dermal exposure has been reported to cause mild gastrointestinal irritation after a latent period followed by progressive mixed sensory-motor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have also occurred after occupational inhalation exposure, with or without dermal exposure. MANAGEMENT: In addition to supportive care, alkaline diuresis to enhance herbicide elimination should be considered in all seriously poisoned patients. Limited clinical data suggest that hemodialysis produces similar herbicide clearance to alkaline diuresis without the need for urine pH manipulation and the administration of substantial amounts of intravenous fluid in an already compromised patient. CONCLUSIONS: While chlorophenoxy herbicide poisoning is uncommon, ingestion of a chlorophenoxy herbicide can result in serious and sometimes fatal sequelae. In severe cases of poisoning, alkaline diuresis or hemodialysis to increase herbicide elimination should be considered.

2,4-Dichlorophenoxyacetic Acid↗
PubMed2000

Mechanisms of toxicity, clinical features, and management of diquat poisoning: a review.

USES: Diquat (1,1'-ethylene-2,2'-bipyridilium) is a nonselective bipyridyl herbicide, related structurally to paraquat, which is used both as a contact herbicide and a preharvest desiccant. In comparison to paraquat, diquat is used much less widely in agriculture. MECHANISMS OF TOXICITY: Diquat is a potent redox cycler and is readily converted to a free radical which, in reaction with molecular oxygen, generates superoxide anions and subsequently other redox products. These products can induce lipid peroxidation in cell membranes, and potentially cause cell death. FEATURES: Over the period 1968-1999, only 30 cases of diquat poisoning were reported in detail in the literature, of which 13 (43%) were fatal. Local and systemic effects have been reported following diquat exposure, with systemic features being invariably associated with ingestion. In severe and usually fatal cases, gastrointestinal mucosal ulceration, paralytic ileus, hypovolemic shock, acute renal failure, and coma have been reported. MANAGEMENT: After rapid confirmation of the diagnosis using a qualitative urine test, gut decontamination may be considered in patients who present within 1 hour of a life-threatening ingestion (>6 g). Supportive measures including fluid and electrolyte replacement should then be employed. Although hemofiltration and hemodialysis are of proven value if renal failure supervenes, there is no clinical evidence that hemodialysis or hemoperfusion removes toxicologically significant amounts of diquat, thereby reducing the risk of organ failure and preventing a fatal outcome in severe cases.

Animals↗
PubMed2000

Chemical contamination of private drinking water supplies in the West Midlands, United Kingdom.

INTRODUCTION: In the United Kingdom, private drinking water supplies are subject to much less stringent sampling and testing regimes than are public supplies. Information regarding the quality of private drinking water supplies is disparate and poorly defined. The aim of this study was to collate the data for chemical contamination of private drinking water supplies in the West Midlands, a region of Central England with a population of 5.3 million. METHODS: The most recent year's data on the number of private supplies, the number of supplies sampled, and the number and type of failures for chemical parameters were obtained from District and Local Authorities in the West Midlands Region. RESULTS: Data covered 12-month periods during 1995-1996. Of the 6013 private supplies identified, samples from 1297 had been tested for chemical parameters during the period of the study. A total of 420 individual failures for chemical parameters were reported in 386 water supplies. The majority of breaches of United Kingdom and European Union standards were due to increased concentrations of nitrates (270), magnesium (21), manganese (17), and iron (15). Increased turbidity was present in 27 cases. Only 6 samples breached the standard for lead and 6 for pesticides. CONCLUSIONS: Over a quarter of the supplies tested during the period of the study were in breach of United Kingdom and European Union legislation. Of the reported failures, the high concentrations of nitrate and nitrite, lead, copper, and sulfate are of concern to health and remedial action is warranted. Regular sampling of private drinking water supplies remains necessary to prevent risk to health from a wide variety of toxic contaminants.

Environmental Monitoring↗
PubMed1999

MR-guided laser thermoablation of inoperable renal tumors in an open-configuration interventional MR scanner: preliminary clinical experience in three cases.

A minimally invasive technique for performing magnetic resonance (MR)-guided laser interstitial thermoablation (LITT) for inoperable renal tumors is described. Three patients were treated using a percutaneous technique with real-time MR guidance in an open access interventional MR scanner. Laser therapy was delivered using a neodymium-YAG source via a water-cooled applicator system. Thermal lesions were monitored in real time using a color thermometry sequence. All patients were discharged the following day with no complications. Follow-up with gadolinium-enhanced MRI in a conventional high-field system confirmed necrosis in targeted tissue, and further treatment is planned for one patient. We concluded that LITT can be useful in treating inoperable renal malignancy and merits further evaluation. J. Magn. Reson. Imaging 1999;10:545-549.

Aged↗
PubMed1999

Therapeutic review: is ascorbic acid of value in chromium poisoning and chromium dermatitis?

INTRODUCTION: Repeated topical exposure to chromium(VI) may cause an allergic contact dermatitis or the formation of chrome ulcers. Systemic toxicity may occur following the ingestion of a chromium(VI) salt, from chromium(VI)-induced skin burns, or from inhalation of chromium(VI) occurring occupationally. Soluble chromium(VI) salts are usually absorbed more easily and cross cell membranes more readily than trivalent chromium salts, and, therefore chromium(VI) is more toxic than chromium(III). In experimental studies, endogenous ascorbic acid in rat lung, liver, and kidney and human plasma, effectively reduces chromium(VI) to chromium(III). The administration of exogenous ascorbic acid has been advocated therefore in the treatment of systemic chromium poisoning and chromium dermatitis to enhance the extracellular reduction of chromium(VI) to the less bioavailable chromium(III). REVIEW: In vitro experiments confirm that the addition of ascorbic acid to plasma containing chromium(VI) leads to a dose-dependent reduction of chromium(VI) to chromium(III). In animal studies, parenteral ascorbic acid 0.5-5 g/kg significantly reduced chromium-induced nephrotoxicity when administered 30 minutes before parenteral sodium dichromate and up to 1 hour after parenteral sodium chromate dosing. Parenteral ascorbic acid 0.5-5 g/kg also reduced mortality when given orally up to 2 hours after oral potassium dichromate dosing. However, the administration of parenteral ascorbic acid more than 2 hours after parenteral chromate in these experimental studies did not protect against renal damage, and parenteral ascorbic acid given 3 hours postparenteral chromate increased toxicity. In addition, there is no confirmed clinical evidence that the administration of ascorbic acid lessens morbidity or mortality in systemic chromium poisoning. A possible reason for the lack of benefit of ascorbic acid when administration is delayed, is that chromium(VI) cellular uptake has occurred prior to ascorbic acid administration. Topical 10% ascorbic acid has been claimed to reduce significantly the healing time of experimentally induced chrome ulcers in guinea pigs. The proposed mechanism is reduction on the skin surface of chromium(VI) to chromium(III). Several case reports suggest that topical ascorbic acid is effective in the management of chromium dermatitis but this has not been confirmed in controlled clinical trials and, moreover, the practical difficulties of frequent application are likely to limit its usefulness. DISCUSSION: Based on experimental studies, substantial amounts of ascorbic acid would need to be administered, preferably parenterally, soon after exposure to prevent systemic toxicity from chromium(VI) in humans. However, as ascorbic acid is a metabolic precursor of oxalate, the administration of ascorbic acid in high dose could lead to acute oxalate nephropathy, particularly in the presence of renal failure. While smaller doses of ascorbic acid (e.g., 10 g intravenously) are not toxic, such doses probably will not reduce the mortality from systemic chromium poisoning. CONCLUSION: There is currently insufficient evidence to advocate the use of ascorbic acid in the management of systemic chromium toxicity. Topical ascorbic acid may reduce dermal hexavalent chromium exposure, but this observation must be confirmed in controlled studies.

Animals↗