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INTRODUCTION Accurate clinical diagnosis depends on the reliable recognition of signs and symptoms. This expertise comes from experience in seeing patients which has been traditionally gained over a long training period. Shortened specialist training (Modernising Medical Careers) has led to a greater reliance on structured teaching and skills transfer programmes. The accuracy of clinical diagnosis and the rate at which diagnostic skills improve during training is important for the assessment of trainees, and the delivery of care. PATIENTS AND METHODS This study assessed the accuracy of clinical diagnosis of skin lesions by two junior plastic surgery trainees. They were asked to diagnose 120 consecutive skin lesions seen in a pigmented skin lesion clinic in 2005, with the histological diagnosis being confirmed following subsequent excision. The process was repeated a year later in 2006 to enable the rate of correct diagnosis to be compared. RESULTS Initially, 53.3% of diagnoses were correct. A year later, this had risen to 65.0%. Twenty-two different skin pathologies were present in excised specimens, and skin cancers comprised 30%. The trainees demonstrated 93.8% sensitivity in their initial diagnosis of malignancy (95% CI, 79.2–99.2) and 97.4% a year later (95% CI, 86.5–99.9). However, specificity was 69.3% (95% CI, 58.6–78.7) in 2005 and 71.6% (95% CI, 60.5–71.4) in 2006. CONCLUSIONS Accuracy in the diagnosis of the wide range of skin conditions presenting to an out-patient clinic was shown to increase over a 1-year period. We feel that this improvement resulted from regular clinical exposure supported by a structured learning programme. The shortening of the specialist training period may affect the acquisition of diagnostic skills by trainees and impact on the confidence with which they commence consultant practice.

To the Editor: Stroke patients who are managed in an organized (stroke unit) setting are more likely to make a good recovery than those who receive conventional care in general wards, an effect that has been attributed to the coordinated rehabilitation input.1 However, recent descriptive information from 2 Norwegian trials2 3 now indicates that some of the benefits of stroke unit care may also be due to acute medical interventions. In particular, these units employed early mobilization and the routine use of intravenous saline, plus selective use of antipyretic and antibiotic medication, oxygen, and insulin.2 3 4 We therefore wished to test the hypothesis that stroke patients who manage to maintain key physiological variables (osmolarity, temperature, oxygen saturation, blood glucose) within a narrow physiological range are more likely to enjoy an early recovery and better functional outcome. We carried out a case-control study, recruiting consecutive individuals admitted to a large, urban teaching hospital with a clinical diagnosis of stroke in the previous 24 hours that was confirmed on CT scan. Patients were assessed on admission, day 3, and day 7 after stroke with the Scandinavian Stroke Scale, Barthel Index, and modified Rankin scale.5 Physiological variables were …

Seven female patients (mean age 86 years) with proven biochemical primary hypothyroidism were enrolled in a single-blind randomized crossover study, of standard daily versus twice-weekly thyroxine therapy, with each phase of one month's duration. The median daily dose of thyroxine was 100 μg (range 75 – 100 μg). Serum levels of thyroid hormones and thyrotrophin were very similar during twice-weekly thyroxine therapy to those during daily therapy and there were no statistically significant differences between trough and peak serum total triiodothyronine, free thyroxine, or thyrotrophin levels or systolic time intervals during twice-weekly thyroxine. Administration of thyroxine twice-weekly to elderly patients with primary hypothyroidism gives effective biochemical thyroid hormone replacement, with no evidence from the systolic time intervals of tissue thyrotoxicosis at expected peak thyroid hormone concentrations. Supervised twice-weekly thyroxine should be considered in patients with primary hypothyroidism who comply poorly with daily dosing.

OBJECTIVE: To compare the effects on renal function of captopril and enalapril in elderly patients with chronic heart failure. DESIGN: A multi-centre double-blind parallel-group comparison of the two angiotensin-converting enzyme (ACE) inhibitors, captopril (12.5 mg bid) and enalapril (2.5 mg bid). SUBJECTS: 80 elderly patients with chronic heart failure (41 in the captopril group, 39 in the enalapril group). MAIN OUTCOME MEASURES: The blood pressure and pulse rate response to the first dose of ACE inhibitor was assessed in all patients. Glomerular filtration rate (GFR) was measured radioisotopically by 99mTcDTPA or 51CrEDTA clearance after three and six months of each treatment. Subgroups were assessed for effective renal plasma flow (33 patients), exercise tolerance (25 patients) and by a symptom-oriented questionnaire (45 patients). RESULTS: No serious adverse effect on GFR was noticed. There was no significant difference between the two treatments in the mean baseline GFR or in changes from baseline at three and six months (captopril mean baseline GFR 49.6 ml min-1 1.76 m-2, enalapril 54.7 ml min-1 1.76 m-2; mean change (95% confidence interval) at three months captopril 12 ml min-1 (+3.0, +21.0), enalapril -2 ml min-1 (-13.0; +9.0); mean change at six months, captopril 3.7 ml min-1 (-6.7; +14.2), enalapril -6.0 ml min-1 (-21.0; +9.4). Significantly more patients given captopril had an improvement in GFR during the study period (26/31 compared with 20/31 enalapril-treated patients at three months, p = 0.0096, and 23/30 compared with 15/27 at six months, p = 0.021). There were no significant changes in effective renal plasma flow. Three patients treated with enalapril developed symptomatic hypotension within three days of starting treatment. Quality of life questionnaires revealed more gastrointestinal symptoms in the enalapril group (p = 0.039). CONCLUSIONS: Captopril seems marginally preferable to enalapril in the treatment of chronic heart failure in elderly patients.

Recent reports have suggested an association between terodiline hydrochloride and cardiac arrhythmias. We report 4 patients presenting over a six month period who developed polymorphic ventricular tachycardia (polymorphic VT) while receiving treatment with this agent. In each case there was prolongation of QT interval on electrocardiogram (ECG). Two patients had hypokalaemia associated with diuretic therapy. In the 3 cases in which follow-up ECG was available, QT interval returned to normal after discontinuation of terodiline. In order to define the effects of terodiline on corrected QT interval (QTc) and heart rate in the elderly, a prospective study was performed in 8 elderly in-patients treated with terodiline for urinary incontinence. After 7 days treatment with terodiline 12.5 mg twice daily, there was a significant increase in QT by a mean of 29 ms, QTc by 15 ms and a decrease in resting heart rate by a mean of 6.7 beats.min-1. Terodiline increases QTc and reduces resting heart rate in elderly patients. Both these effects may be associated with polymorphic VT, a potentially life threatening arrhythmia. This drug should be avoided in patients with other known risk factors for polymorphic VT, particularly hypokalaemia and cardiac disease.

EDITOR,—By applying American guidelines on neuroleptic use within nursing home facilities, Alice McGrath and Graham Jackson have deemed the prescription of these drugs for Glasgow nursing home residents to be potentially inappropriate in most cases.1 Their interpretation of the findings may be incorrect. No data are provided on the extent of behaviour problems among the patients studied. Previous research in similar settings suggests that a high prevalence of behaviour problems can be anticipated.2 3 Neuroleptic use may seem inappropriate in many cases because the …

We have given the selective 5 HT2 antagonist ritanserin in a dose of 10 mg twice daily for 4 weeks in a double-blind, randomized, placebo-controlled, parallel group study of 18 patients with untreated essential hypertension. The fall in single platelet count due to 5 HT-induced platelet aggregation was significantly reduced by ritanserin compared with placebo (p less than 0.05). There were no significant changes in supine or erect blood pressure or heart rate after ritanserin compared to placebo. Forearm blood flow, measured by mercury-in-strain gauge venous occlusion plethysmography, was not significantly altered by ritanserin. Ritanserin caused prolongation of the QTc interval by 41 (SEM 11) ms (p less than 0.05 compared to placebo) but had no detectable effect on QRS duration, features suggestive of Class III antiarrhythmic activity. These findings do not support an independent role of the 5 HT2 receptor in maintaining raised arterial pressure in essential hypertension.

We have studied eight adult atopic asthmatic patients in a randomized double-blind, placebo-controlled, cross-over trial in order to examine the effects of the 5 HT2 antagonist ketanserin on airways function (FEV1, FVC, V50(chi), and V25(pi]. Ketanserin did not significantly change resting bronchomotor tone. Treadmill exercise caused a similar maximal percentage fall in FEV1 after both drug [16.8 (3.7)%] and placebo [19.2 (4.2)%]; ketanserin did not significantly attenuate bronchoconstriction, measured over a 20-min period after exercise. These results suggest that 5 HT2 receptors do not play a major role in the control of resting bronchomotor tone or in exercise-induced bronchoconstriction in adult atopic asthmatic patients.

We have studied the acute effects of the serotonergic type-2 (5-HT2) antagonists ketanserin and ritanserin given as single oral doses to patients with essential hypertension. Ketanserin has alpha 1-antagonist properties, whereas ritanserin is largely devoid of alpha 1-receptor binding affinity. Ketanserin (40 mg orally) caused a significant reduction (p less than 0.03) of sitting mean arterial pressure over the 8-h period following drug administration by an average of 15.4 +/- 3.2 mm Hg (mean +/- SEM) as compared to a reduction of 8.5 +/- 2.2 following placebo. In contrast, ritanserin had no significant effect on blood pressure compared to placebo; sitting mean arterial pressure was reduced by 9.0 +/- 2.6 and 10.8 +/- 1.8 mm Hg after administration of 10 and 20 mg, respectively, of ritanserin. There were no significant differences in pulse rate among placebo, ketanserin, or ritanserin phases. Ritanserin caused a reduction in the hostility score (p less than 0.05) as measured by the Multiple Affect Adjective Check List; ketanserin had no significant effects. The highly selective 5-HT2 antagonist ritanserin, given in a dose which caused measurable alteration of psychological function tests, had no acute effects on blood pressure. The acute antihypertensive effects of ketanserin are not caused by 5-HT2 antagonism alone, but are likely to be dependent on its alpha 1-antagonistic properties.

Serotonin is a naturally occurring amine with vasoactive and platelet aggregating properties. It may be involved in the pathogenesis of hypertension. Almost all the serotonin circulating in blood is stored in platelets. Serotonin and other platelet contents are released from platelets during platelet aggregation, which occurs in a stepwise manner. Initially there is a reversible change in platelet shape from a disc to a spiny sphere, and then platelet clumping, and finally a release of platelet contents (Holm sen 1977). The contents of the dense granules, including serotonin, adenosine diphosphate, adenosine triphosphate, calcium and inorganic pyrophosphate, are released before the contents of the a granules, which include ~-thromboglobulin, platelet factor 4, acid hydro lases and fibrinogen (DeClerck 1986; Holmsen et al. 1977). Serotonin released during platelet aggregation could cause vasoconstriction, increased blood pressure and further platelet aggregation. The object of this study was to compare serotonin-induced and spontaneous platelet aggregation in whole blood, platelet serotonin content and plasma ~-thromboglobulin in patients with untreated essential hypertension and in a normotensive control group.