Randomised clinical trial: yoga vs written self-care advice for ulcerative colitis.

BACKGROUND: Perceived stress seems to be a risk factor for exacerbation of ulcerative colitis. Yoga has been shown to reduce perceived stress. AIMS: To assess the efficacy and safety of yoga for improving quality of life in patients with ulcerative colitis. METHODS: A total of 77 patients (75% women; 45.5 ± 11.9 years) with ulcerative colitis in clinical remission but impaired quality of life were randomly assigned to yoga (12 supervised weekly sessions of 90 min; n = 39) or written self-care advice (n = 38). Primary outcome was disease-specific quality of life (Inflammatory Bowel Disease Questionnaire). Secondary outcomes included disease activity (Rachmilewitz clinical activity index) and safety. Outcomes were assessed at weeks 12 and 24 by blinded outcome assessors. RESULTS: The yoga group had significantly higher disease-specific quality of life compared to the self-care group after 12 weeks (Δ = 14.6; 95% confidence interval=2.6-26.7; P = 0.018) and after 24 weeks (Δ = 16.4; 95% confidence interval=2.5-30.3; P = 0.022). Twenty-one and 12 patients in the yoga group and in the self-care group, respectively, reached a clinical relevant increase in quality of life at week 12 (P = 0.048); and 27 and 17 patients at week 24 (P = 0.030). Disease activity was lower in the yoga group compared to the self-care group after 24 weeks (Δ = -1.2; 95% confidence interval=-0.1-[-2.3]; P = 0.029). Three and one patient in the yoga group and in the self-care group, respectively, experienced serious adverse events (P = 0.317); and seven and eight patients experienced nonserious adverse events (P = 0.731). CONCLUSIONS: Yoga can be considered as a safe and effective ancillary intervention for patients with ulcerative colitis and impaired quality of life. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT02043600.

Bioincompatibility--perspectives in 1993.

Bioincompatibility reactions related to the non-physiology of the procedure have plagued dialysis from its early days. Although the problem is certainly multifactorial, the present overview selectively focuses on some aspects of activation of late complement (C) components, the importance of which may have been underappreciated in the past. Dialysis patients are poised for intense C activation because of cumulation of the low molecular weight factor D, an intrinsically active serine esterase which is not inhibited by any known endogenous inhibitor and catalyzes an early step in the alternative pathway. C activation reflects the net balance between activation and inhibition, the latter particularly via factor H binding. Dialyzer membrane characteristics that are related to factor H binding and regulation of initial activation steps include not only membrane surface chemistry but also its microdomain structure. Kinetic studies of the generation of the terminal complement complex (TCC) suggest ongoing generation throughout the duration of a dialysis session (in contrast to the transient release of C-derived anaphylatoxins). Potential consequences of TCC generation include amplification of the non-C-dependent cell activation signals through L-fucose-dependent steps. Efforts to reduce TCC generation by membrane engineering, for example, end group derivatization and optimization of microdomain structure, open perspectives for the development of more biocompatible membranes.

Dystonie reactions and hallucinations: a rare adverse-effect?

Dystonie reactions and hallucinations: a rare adverse-effect? One of the intriguing side-effects of neuroleptics is the acute dystonie reaction like oculogyric crises. It is seldom mentioned that the dystonie reaction may be combined with hallucinations. This combination of acute dystonia with hallucinations may be explained by overstimulation of dopamine-receptors in the striatal neurons. Awareness of these hallucinations as a complication of neuroleptics is essential to prevent that neuroleptic dose will be increased; instead it must be lowered. Prevention of the dystonia is critical. These side effects may be suppressed with anti-parkinsonian drugs. Information to the patient in due time may prevent anxiety about the side effects.

Pharmacokinetics of verapamil in patients with renal failure.

The pharmacokinetics of verapamil was studied in patients with end-stage chronic renal failure and in normal subjects after i.v. injection of 3 mg and a single oral dose of 80 mg. Plasma levels of verapamil and its active metabolite norverapamil were measured by HPLC. After i.v. injection, the terminal phase half-life and total plasma clearance of verapamil in both groups were similar. Haemodialysis did not change the time course of plasma verapamil levels after i.v. administration. After a single oral dose, the plasma levels of verapamil and norverapamil in both groups of subjects were similar. Subsequently, normal volunteers and patients with renal failure were treated for 5 days with oral verapamil 80 mg t.d.s. There was no difference between the 2 groups of subjects in the trough and peak levels of verapamil or of norverapamil. Intravenous and oral administration of the calcium channel blocking agent had similar effects on blood pressure, heart rate and the PR-interval in the electrocardiogram in both groups. The study demonstrated that the disposition of verapamil was similar in normal subjects and in patients with renal failure.

Studies of salivary flow in borderline hypertension: effects of drugs acting on structures innervated by the autonomic nervous system.

Salivary flow and the influence of drugs on this were studied in subjects with borderline hypertension and in normotensive subjects. Saliva production at rest was lower in borderline hypertensive subjects than in normotensive subjects. Plasma catecholamine levels were similar in both groups of subjects studied. Intravenous injections of propranolol and phentolamine did not enhance saliva secretion in the borderline hypertensive group, whereas atropine caused the secretion to decrease in both groups. Intravenous infusions of neostigmine led to a dose-dependent increase of salivary flow. The dose-response curve for the stimulating effect of neostigmine on saliva production was shifted to the right in borderline hypertensive as compared with normotensive subjects. The results of the study support the assumption that in subjects with borderline hypertension parasympathetic influence on the salivary glands is reduced.

Studies on salivary flow in borderline hypertension.

Salivary flow and the influence of drugs on this variable were studied in subjects with borderline hypertension and in normotensive control subjects. Saliva production under resting conditions was 0.85 +/- 0.08 g/min in normotensive subjects and 0.51 +/- 0.04 g/min in borderline hypertensive subjects. In both groups of subjects studied, salivary secretion was decreased by atropine but propranolol and phentolamine had no effect. The stimulating effect of neostigmine on saliva production was more pronounced in normotensive than in borderline hypertensive subjects. Thus, in order to increase salivary flow by 1 g/min 28 +/- 0.9 micrograms/min neostigmine had to be infused intravenously in normotensives compared with 41 +/- 3.8 micrograms/min in borderline hypertensives. The results of the study suggest that subjects with borderline hypertension have a reduced parasympathetic drive to the salivary glands.

Studies on the autonomic nervous system in borderline hypertension.

Parameters of the autonomic nervous system were studied in normotensive subjects (NT; standing blood pressure (BP) less than or equal to 125/85 mmHg) and in subjects with borderline hypertension (BHT; 140/90 less than or equal to standing BP less than 160/100 mmHg). No differences in plasma noradrenaline and adrenaline levels were found between NT and BHT subjects, neither at rest nor during exercise at 75% of maximum work capacity. The dose of noradrenaline required to increase systolic BP by 10 mmHg was significantly higher in NT than in BHT subjects (5.13 +/- 0.42 vs 3.50 +/- 0.57 microgram . min -1). No difference between NT and BHT subjects was found in the dose of isoprenaline required to increase heart rate by 20 beats . min -1 (1.21 +/- 0.12 vs 1.09 +/- 0.11 microgram . min -1), suggesting decreased parasympathetic activity in the former group. The enhanced pressor effect of noradrenaline, together with the decreased parasympathetic activity, could explain the elevated blood pressure and heart rate in subjects with borderline hypertension.

The sympathetic nervous system and the renin-angiotensin system in borderline hypertension.

1. Plasma catecholamine levels as well as plasma renin activity and plasma renin concentration were compared in normotensive volunteers and in subjects with borderline hypertension. All subjects were studied at rest and during bicycle ergometry. 2. The two groups of volunteer subjects did not differ in the plasma concentrations of noradrenaline and adrenaline, both at rest and during physical activity. The same was true for plasma renin activity and plasma renin concentration. Furthermore, urinary excretion of noradrenaline, adrenaline and 4-hydroxy-3-methoxymandelic acid was similar in both groups. 3. The results do not support the assumption that there is increased sympathetic activity in subjects with borderline hypertension.

Studies on the effects of propanolol on plasma catecholamine levels in patients with essential hypertension.

The influence of the beta receptor blocking agent propranolol on plasma catecholamine concentrations was studied in eight patients with essential hypertension. The study was of single blind crossover design. Propranolol given in oral doses ranging from 60 to 240 mg daily for a period of 3 weeks decreased blood pressure and heart rate. The beta-adrenergic blocking agent caused plasma catecholamine levels to increase both at rest and during bicycle exercise. Chromatographical analysis showed that concentrations of noradrenaline as well as of adrenaline rose during treatment with propranolol. However, dopamine-beta-hydroxylase activity in plasma was not altered. Furthermore, the urinary excretion of noradrenaline, adrenaline and 4-hydroxy-3-methoxy mandelic acid did not change during beta receptor blockade. The results are compatible with the assumption that antihypertensive doses of propranolol by decreasing cardiac output cause an activation of the sympatho-adrenal system.