Complementary and alternative medicine provision in Europe--first results approaching reality in an unclear field of practices.

BACKGROUND: The demand for complementary and alternative medicine (CAM) treatment in the European Union (EU) has led to an increase in the various CAM interventions available to the public. Our aim was to describe the CAM services available from both registered medical practitioners and registered non-medical practitioners. METHODS: Our literature search comprised a PubMed search of any scientific publications, secondary references and so-called grey literature, a search of government websites and websites of CAM organisations to collect data in a systematic manner, and personal communications, e.g., via e-mail contact. Due to the different reliability of data sources, a classification was developed and implemented. This weighted database was condensed into tables and maps to display the provision of CAM disciplines by country, showing the distribution of CAM providers across countries. RESULTS: Approximately 305,000 registered CAM providers can be identified in the EU (~160,000 non-medical and ~145,000 medical practitioners). Acupuncture (n = 96,380) is the most available therapeutic method for both medical (80,000) and non-medical (16,380) practitioners, followed by homeopathy (45,000 medical and 5,800 non-medical practitioners). Herbal medicine (29,000 practitioners) and reflexology (24,600 practitioners) are mainly provided by non-medical practitioners. Naturopathy (22,300) is dominated by 15,000 (mostly German) doctors. Anthroposophic medicine (4,500) and neural therapy (1,500) are practised by doctors only. CONCLUSION: CAM provision in the EU is maintained by approximately 305,000 registered medical doctors and non-medical practitioners, with a huge variability in its national regulatory management, which makes any direct comparison across the EU almost impossible. Harmonisation of legal status, teaching and certification of expertise for therapists would be of enormous value and should be developed.

S1P modulator FTY720 limits matrix expansion in acute anti-thy1 mesangioproliferative glomerulonephritis.

FTY720 is a novel immune modulator whose primary action is blood lymphocyte depletion through interaction with sphingosine-1-phosphate (S1P) receptors. The present study analyzes the effect of FTY720 on both the early mesangial cell injury and the subsequent matrix expansion phase of experimental mesangioproliferative glomerulonephritis. Disease was induced by injection of OX-7 anti-thy1 antibody into male Wistar rats. In both protocols, FTY720 administration (0.3 mg/kg body wt) resulted in a selective and very marked reduction in blood lymphocyte count. In the injury experiment, the S1P receptor modulator was given starting 5 days before and continued until 1 day after antibody injection. FTY720 did not significantly affect the degree of anti-thy1-induced mesangial cell lysis and glomerular-inducible nitric oxide production. In the matrix expansion experiment, FTY720 treatment was started 1 day after antibody injection and continued until day 7. In this protocol, the S1P modulator reduced proteinuria, histological matrix expansion, and glomerular protein expression of TGF-beta(1), fibronectin, and PAI-1. Glomerular collagen III staining intensity was decreased. FTY720 reduced markedly glomerular lymphocyte number per cross section and to a lesser degree macrophage infiltration. In conclusion, FTY720 significantly limits TGF-beta(1) overexpression and matrix protein expression following induction of acute anti-thy glomerulonephritis, involving reductions in blood and glomerular lymphocyte numbers. The results suggest that lymphocytes actively contribute to matrix expansion in experimental mesangioproliferative glomerulonephritis. Our study expands on findings on FTY720's beneficial effects on tubulointerstitial and functional disease progression previously reported in anti-thy1-induced chronic glomerulosclerosis.

Platelet inhibition limits TGF-beta overexpression and matrix expansion after induction of anti-thy1 glomerulonephritis.

BACKGROUND: Although a role of platelets is well established in atherosclerosis, only little is known about their contribution to pathologic renal matrix expansion. The present study analyzes the effect of the platelet inhibitor clopidogrel on the early injury and subsequent repair phase of experimental anti-thy1 glomerulonephritis. METHODS: In male Sprague-Dawley rats, acute anti-thy1 glomerulonephritis was induced by intravenous injection of OX-7 antibody. In protocol 1 (injury), clopidogrel was given starting 5 days before antibody injection. One day after disease induction, parameters of mesangial cell injury (glomerular cell number, inducible NO synthesis, and macrophage infiltration) were analyzed. In protocol 2 (repair), clopidogrel treatment was started one day after antibody injection. On day 6, parameters of glomerular repair [glomerular matrix score, expression of transforming growth factor (TGF)-beta 1, fibronectin, and plasminogen activator inhibitor (PAI)-1] and thrombosis (aneurysm formation and fibrinogen deposition) were determined. In both protocols, an additional group of rats was treated with the angiotensin-converting enzyme (ACE) inhibitor enalapril. RESULTS: In the injury protocol, platelet inhibition did not affect mesangial cell lysis, glomerular NO production, and macrophage infiltration, while ACE inhibition was protective. In the repair protocol, clopidogrel significantly limited aneurysm formation and fibrinogen deposition, as well as glomerular matrix expansion, TGF-beta 1, fibronectin, and PAI-1 expression. In comparison, enalapril was less effective in preventing glomerular thrombosis, but was significantly superior to clopidogrel in limiting matrix protein expression and accumulation. CONCLUSION: The present study shows that platelets play a significant role in the sequence from mesangial cell injury to renal matrix expansion in anti-thy1 glomerulonephritis. The results, directly comparing renin-angiotensin-system and platelet inhibition, suggest that platelets contribute less than angiotensin II to TGF-beta overexpression and matrix accumulation in this model of acute glomerular wound repair.

NO mediates antifibrotic actions of L-arginine supplementation following induction of anti-thy1 glomerulonephritis.

UNLABELLED: NO mediates antifibrotic actions of L-arginine supplementation following induction of anti-thy1 glomerulonephritis. BACKGROUND: L-Arginine plays a complex role in renal matrix expansion, involving endogenous metabolism into nitric oxide (NO), polyamines, L-proline and agmatine. Supplementing dietary L-arginine intake has been shown to limit transforming growth factor (TGF)-beta 1 overproduction and matrix accumulation in rats with induced anti-thy1 glomerulonephritis (GN). The present study tests the hypothesis that this beneficial effect on in vivo TGF-beta overexpression is mediated via the generation of NO. METHODS: One day after induction of anti-thy1 GN, male Wistar rats fed a normal protein diet were assigned to the following groups: (1) normal controls; (2) GN; (3) GN-Arg (plus 500 mg L-arginine/day); (4) GN-Arg-NAME [plus 500 mg L-arginine/day and 75 mg/L of the NO synthase inhibitor nitro-L-arginine-methyl ester (L-NAME) in the drinking water]; and (5) GN-Molsi (10 mg/day of the NO donor molsidomine). In protocol 1, treatment lasted until day 7, and in protocol 2, until day 12 after disease induction, respectively. Analysis included systolic blood pressure, a glomerular histologic matrix score, and the glomerular mRNA and protein expression of the key fibrogen TGF-beta1, the matrix protein fibronectin, and the protease inhibitor plasminogen activator inhibitor type 1 (PAI-1). RESULTS: Blood pressure was normal in untreated anti-thy1 animals and not significantly affected by any of the treatments. Compared to untreated nephritic rats, administration of both L-arginine and molsidomine reduced glomerular TGF-beta 1 overexpression significantly and to a similar degree in both protocols, while the beneficial effect of L-arginine was abolished by concomitant NO synthesis inhibition. Glomerular matrix accumulation, fibronectin and PAI-1 mRNA and protein expression closely followed the expression of TGF-beta 1. CONCLUSION: The present study shows that L-arginine's antifibrotic action in normotensive anti-thy1 GN is mainly mediated by endogenous production of NO. The data suggest that NO limits in vivo TGF-beta overexpression in a pressure-independent manner and that NO donors may be of benefit in the treatment of human fibrotic renal disease.