Tag 2 A40 / B21 Neuropathisches Schmerzsyndrom Diabetes

[Maxxel]

Ich hab auch D

[Unregistriert]

Der "Auslassversuch" ist meiner Meinung nach ein red herring(Da AEDs auch bei PNP angewendet werden) und spielt eigentlich in der Antiepileptischen Therapie ne Rolle, um zu schauen ob der Patient auch ohne AEDs anfallsfrei bleibt.
Allein der Grundsatz "ohne Konsequenz keine Diagnostik" würde auch eher E ausschließen.
Der Mehrwert aus der Untersuchung wäre: Ok, jetzt hat er wieder Schmerzen - Wie verwunderlich.
Zudem ist die PNP natürlich irreversibel, da hilft auch der neu eingestellte HbA1c nichts.

[drcox1]

Antwort E macht zwar irgendwie Sinn, aber wenn E richtig ist, wüsste ich nicht, warum C falsch sein soll. E besagt, man soll versuchen ohne Medi's auszukommen, aber wenn man Medis gibt, dann keine Monotherapie? Ich würde doch erst einmal mit einer Monotherapie anfangen dann. Jeder weiß doch, dass mehrere Medikamente Nebenwirkungen verstärken, die nimmt ja sicherlich noch andere Sachen.
Blöde Antwortkombination...

[Unregistriert]

Ja genau!nach 12 Jahren Diabetes sollen die PNP Symptome beim Auslassversuch besser werden!?!Hääää??

[CBehrendt1988]

http://www.ncbi.nlm.nih.gov/pubmed?term=22696371

"Abstract
BACKGROUND:
There are two types of diabetes. Type 1 diabetes affects younger people and needs treatment with insulin injections. Type 2 diabetes affects older people and can usually be treated by diet and oral drugs. Diabetic neuropathy affects 10% of patients with diabetes mellitus at diagnosis and 40% to 50% after 10 years. Enhanced glucose control is the best studied intervention for the prevention of this disabling condition but there have been no systematic reviews of the evidence.
OBJECTIVES:
To examine the evidence for enhanced glucose control in the prevention of distal symmetric polyneuropathy in people with type 1 and type 2 diabetes.
SEARCH METHODS:
We searched the Cochrane Neuromuscular Disease Group Specialized Register (30 January 2012), CENTRAL (2012, Issue 1), MEDLINE (1966 to January 2012) and EMBASE (1980 to January 2012) for randomized controlled trials of enhanced glucose control in diabetes mellitus.
SELECTION CRITERIA:
We included all randomized, controlled studies investigating enhanced glycemic control that reported neuropathy outcomes after at least one year of intervention. Our primary outcome measure was annual development of clinical neuropathy defined by a clinical scale. Secondary outcomes included motor nerve conduction velocity and quantitative vibration testing.
DATA COLLECTION AND ANALYSIS:
Two authors independently reviewed all titles and abstracts identified by the database searches for inclusion. Two authors abstracted data from all included studies with a standardized form. A third author mediated conflicts. We analyzed the presence of clinical neuropathy with annualized risk differences (RDs), and conduction velocity and quantitative velocity measurements with mean differences per year.
MAIN RESULTS:
This review identified 17 randomized studies that addressed whether enhanced glucose control prevents the development of neuropathy. Seven of these studies were conducted in people with type 1 diabetes, eight in type 2 diabetes, and two in both types. A meta-analysis of the two studies that reported the primary outcome (incidence of clinical neuropathy) with a total of 1228 participants with type 1 diabetes revealed a significantly reduced risk of developing clinical neuropathy in those with enhanced glucose control, an annualized RD of -1.84% (95% confidence interval (CI) -1.11 to -2.56). In a similar analysis of four studies that reported the primary outcome, involving 6669 participants with type 2 diabetes, the annualized RD of developing clinical neuropathy was -0.58% (95% CI 0.01 to -1.17). Most secondary outcomes were significantly in favor of intensive treatment in both populations. However, both types of diabetic participants also had a significant increase in severe adverse events including hypoglycemic events.
AUTHORS' CONCLUSIONS:
According to high-quality evidence, enhanced glucose control significantly prevents the development of clinical neuropathy and reduces nerve conduction and vibration threshold abnormalities in type 1 diabetes mellitus. In type 2 diabetes mellitus, enhanced glucose control reduces the incidence of clinical neuropathy, although this was not formally statistically significant (P = 0.06). However, enhanced glucose control does significantly reduce nerve conduction and vibration threshold abnormalities. Importantly, enhanced glucose control significantly increases the risk of severe hypoglycemic episodes, which needs to be taken into account when evaluating its risk/benefit ratio.