Biomedical subjects
Publications and source records attributed to N J Warner.
The delusion that the usual passage of time has been changed and that time has been interfered with or is repeating itself is rare. Four patients with the delusion of warped time are presented and the significance of the symptom is discussed. The perception of the passage of time and its disorders is discussed.
Cognitive side-effects are commonly seen following electroconvulsive therapy which convey no therapeutic benefit but are troublesome to both patient and clinician. Various efforts have been made in the past to minimize these symptoms. Although modification of technical parameters related to ECT administration has led to some limited improvement in this regard, attention is now being increasingly focussed on pharmacological approaches. A number of agents have been explored in this context, however, as far as we are aware, the use of thiamine has not yet been investigated. We present three cases of elderly patients undergoing ECT for major depression in whom thiamine administration was associated with beneficial effects on post-ECT confusion. We review the evidence suggesting that thiamine deficiency may be implicated in the confusional state following ECT and recommend that consideration be given to its use in preventing and treating this problematic side-effect, especially in elderly patients.
We present three cases of travel-induced psychosis in an elderly population. The clinical presentations are described with a review of the literature.
The physical symptoms and side-effects reported by patients treated for early breast cancer with surgery (S), (breast conservation or mastectomy), radiotherapy (R) and chemotherapy (C) are reported. As part of a large quality-of-life study, eligible patients were invited to complete a questionnaire at three and 12 months after treatment for early breast cancer. Symptoms 2 weeks after surgery were retrospectively collected at the 3-month questionnaire. Comparing the commonly used different therapy combinations (S, S+R, S+C and S+R+C) we found the only loco-regional symptom to show a significant difference between these groups was chest tightness (P<0.001). Both anxiety about attending for and discomfort during C were significantly higher than during R (P<0.00005 and 0.00001 respectively). We found that the addition of R and, or, C to S resulted in surprisingly little variation in physical side-effects.
This article presents a five-point framework to help health-care providers understand and manage important psychosocial issues related to Langerhans cell histiocytosis (LCH). It entails frank and open discussions with patients and their families of how the disease can affect them individually and collectively. Each point is explained and then applied to two different cases. The framework is applicable to all chronic pediatric diseases, but is particularly relevant for rare conditions with unknown etiologies such as LCH.
We present five case reports of elderly ladies with delusions of pregnancy. This symptom is discussed with reference to the cases and a review of the literature.
This report reviews the tolerability profile of enalapril, an angiotensin-converting enzyme (ACE) inhibitor, in the treatment of patients with congestive heart failure. Data have been collected from 546 patients treated with enalapril for up to 9 months in clinical trials other than the Cooperative North Scandinavian Enalapril Survival Study. Results in patients treated with enalapril (n = 193) or placebo (n = 195) in double-blind, controlled clinical trials show that the incidences of death, serious adverse experiences, and adverse experiences requiring discontinuation of double-blind therapy, as well as the overall incidence of such experiences, were similar in the 2 groups. However, certain adverse experiences that are related to the mechanism of action of ACE inhibitors were seen more often after enalapril than after placebo treatment. Dizziness and hypotension were the most frequent adverse experiences reported in patients with heart failure treated with enalapril. The most frequent laboratory adverse experiences were increases in blood urea nitrogen and serum creatinine levels. hyperkalemia was also seen in patients receiving enalapril. It is possible to identify patients at risk of these experiences before initiating treatment with enalapril and to take certain measures (such as withholding or reducing the dose of diuretic drugs and discontinuing potassium supplements or potassium-sparing diuretic drugs) to reduce the likelihood that hypotension, increases in blood urea nitrogen and serum creatinine levels, or hyperkalemia will occur. Angioedema, a recognized adverse effect of ACE inhibitors, was not seen in the clinical trials reviewed here. Cough , another recognized adverse effect of these agents, was seen infrequently and rarely resulted in the discontinuation of enalapril.(ABSTRACT TRUNCATED AT 250 WORDS)
This review will discuss the safety profiles of the angiotensin-converting enzyme (ACE) inhibitors captopril, enalapril and lisinopril in patients with hypertension. In general, the safety profiles of ACE inhibitors compare favourably with those of other agents used for the treatment of hypertension. Adverse effects are not common when ACE inhibitors are used at the currently recommended doses. The adverse experiences that do occur with ACE inhibitors can be divided into 3 categories. Hypotension, hyperkalaemia and renal impairment are related directly to the blockade of the angiotensin-converting enzyme. Attention to the clinical condition, including concomitant therapy, reduces the risk of these adverse effects of ACE inhibition. Other adverse effects such as cough and angioedema also occur with all ACE inhibitors. The mechanisms are poorly understood, making it difficult to predict in which patients they will occur. Adverse effects such as rash, dysgeusia, neutropenia and proteinuria, which were reported relatively frequently in the early experience with captopril, are reported less frequently with lower doses of captopril and do not appear to be a problem with other ACE inhibitors such as enalapril and lisinopril.
The effect of a synthetic analogue of atrial natriuretic peptide (Ileu-ANP) on haemodynamic, hormonal, and electrolyte excretion indices was studied in 7 patients with chronic congestive heart failure. Patients received in random order placebo or Ileu-ANP infusions (5 micrograms/min) for 4 h on 2 separate occasions, at least 1 week apart. Compared with placebo, Ileu-ANP caused significant reductions in mean systemic arterial pressure, mean pulmonary artery pressure, pulmonary diastolic pressure, and right atrial pressure. These changes were sustained for at least 2 h after infusion. Cardiac output increased from 6.2 to 7.4 l/min at 60 min, then returned to pre-infusion levels. Despite considerable falls in systemic pressure there was no significant increase in heart rate or plasma noradrenaline. With Ileu-ANP infusion, plasma renin activity, angiotensin, arginine vasopressin, aldosterone, and cortisol values were not significantly different from placebo values. Plasma cortisol and aldosterone increased after stopping Ileu-ANP. Neither urine volume nor sodium excretion rate was significantly increased by Ileu-ANP.
Quinidine elevates serum digoxin concentration in part by reducing the volume of distribution of digoxin, which implies that quinidine displaces digoxin from tissues. The purposes of this study were to: 1) measure the effect of quinidine on tissue digoxin concentrations, and 2) determine if quinidine alters the relation between myocardial digoxin concentration and digoxin effect on myocardial monovalent cation transport. Eighteen dogs were treated with tritiated digoxin until the steady-state serum digoxin concentration was between 1.0 and 1.5 ng/ml. All dogs continued receiving the same dose of digoxin while nine dogs were given quinidine as well. Quinidine was continued until the serum digoxin concentration had increased by at least 25%. At the end of treatment, the serum digoxin concentration in dogs treated with digoxin was 1.2 +/- 0.1 ng/ml compared with 2.1 +/- 0.5 ng/ml in dogs treated with digoxin and quinidine in combination (p less than 0.001). Digoxin concentration in myocardium, skeletal muscle, liver, kidney, stellate ganglion, vagus nerve, femoral nerve, brain and brainstem medulla was higher in dogs treated with a combination of digoxin and quinidine than in dogs treated with digoxin alone, but remained proportional to the serum digoxin concentration in all tissues except the brainstem medulla. Myocardial monovalent cation transport was measured using rubidium-86. The effect of digoxin on myocardial monovalent cation transport did not increase as the serum and myocardial digoxin concentrations increased after quinidine administration.
The pharmacokinetics of sulindac have been studied after a single 200 mg oral dose in six normal subjects and five patients with surgical ileostomies. The plasma concentration-time curves for sulindac were similar in both groups up to 12 hours after dosing, indicating similar absorption of the drug. Higher plasma concentrations of sulindac were found in normal subjects after 12 hours, but this late phase accounted for only 12% of the total AUC in the subjects. The sulfone metabolite showed a similar pattern, with no statistically significant difference in the total AUC, but in patients with ileostomy there was a halving of the AUC after 12 hours. Plasma concentrations of the active sulfide metabolite were similar in both groups up to 12 hours, but negligible concentrations were detected in the plasma of patients with ileostomy after 12 hours. Thus the AUC after 12 hours, which represented 55% of the total AUC in normal subjects, was reduced to only 7% in patients with ileostomy. The rate of reduction of sulindac in vitro by ileostomy effluent was only one hundredth that by normal feces. Our results suggest that the gut microflora are an important site of reduction of sulindac in man. Comparison of AUC values suggests that about half the total sulfide is formed by the gut bacteria, probably from sulindac excreted in the bile.
To study the relationship of the serum digoxin concentration to the digoxin effect on monovalent cation transport during the quinidine-digoxin interaction, we used radiolabeled rubidium to measure monovalent cation active transport in myocardial biopsy samples from dogs. In a preliminary study, we showed that quinidine did not affect rubidium uptake by myocardial samples from intact dogs. Then, we studied four groups, each consisting of 13 dogs, which received either saline, low dose digoxin, high dose digoxin, or low dose digoxin plus quinidine treatment. In these groups of dogs, the following steady state serum digoxin concentrations were achieved: saline-treated, 0 ng/ml; low dose digoxin, 1.2 +/- 0.2 ng/ml (mean +/- SD); high dose digoxin, 2.4 +/- 0.4 ng/ml; and low-dose digoxin plus quinidine treated, 2.3 +/- 1.1 ng/ml. Compared to control values, rubidium uptake was decreased by 17% in dogs treated with low dose digoxin (P less than 0.05) and by 38% in dogs treated with high dose digoxin (P less than 0.01 vs. saline-treated, P less than 0.01 vs. low dose digoxin). Although low dose digoxin plus quinidine-treated dogs had the same mean serum digoxin concentration as the high dose digoxin-treated dogs, rubidium uptake in low dose digoxin plus quinidine-treated dogs was decreased by only 17% compared to control (P less than 0.05 vs. saline-treated, (P less than 0.01 vs. high dose digoxin). During the quinidine-digoxin interaction in the intact dog, the reduction in myocardial rubidium uptake is less than expected from the increase in serum digoxin concentration.
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