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DOI: 10.1055/s-2007-973603
© Georg Thieme Verlag KG Stuttgart · New York
Neuentstehung eines Diabetes mellitus unter antihypertensiver Therapie
New-onset diabetes mellitus during antihypertensive treatmentPublikationsverlauf
eingereicht: 18.01.2007
akzeptiert: 8.2.2007
Publikationsdatum:
21. März 2007 (online)

Zusammenfassung
Eine arterielle Hypertonie ist häufig mit einer Insulinresistenz vergesellschaftet und prädispositioniert zur Entwicklung eines Diabetes mellitus. Faktoren für die häufige Ko-Morbidität von Hypertonie und Diabetes umfassen die hohe Rate an Übergewicht und Adipositas bei Patienten mit Hypertonie, Hypertonie-assoziierte Veränderungen der Mikrozirkulation (Remodeling und Rarefikation), gesteigerte Aktivität des sympathischen Nervensystems bei Hypertonie und eine Reihe möglicher zellulärer Funktionsänderungen. Eine medikamentöse Hypertoniebehandlung kann die Inzidenz eines neu diagnostizierten Diabetes erhöhen (Diuretika und ß-Rezeptorenblocker), reduzieren (ACE-Hemmer und AT1-Antagonisten) oder intermediäre Effekte auslösen (Kalziumantagonisten). Die unterschiedlichen Effekte der verschiedenen Antihypertensiva auf den Kohlenhydratstoffwechsel hypertensiver Patienten lassen sich weitgehend mit der unterschiedlichen Beeinflussung der Hypertonie-assoziierten Veränderungen der Mikrozirkulation und der Sympathikusaktivität erklären. Die verschiedenen Raten an neu diagnostiziertem Diabetes mellitus bei der Therapie mit „alten” vs. „neuen” Antihypertensiva gehen über die Behandlungszeit kontinuierlich auseinander, so dass sich für die bei Hypertonie meist notwendige Langzeittherapie niedrige „numbers needed to treat” (NNT) berechnen lassen. Ein neu aufgetretener Diabetes mellitus ist in Interventionsstudien mit einer Beobachtung bis etwa 5 Jahre nicht mit einer gesteigerten Rate kardiovaskulärer Ereignisse assoziiert. Langzeitdaten zeigen jedoch überwiegend, dass ein unter Hypertoniebehandlung entstandener Diabetes prognostisch ungünstig ist. Differenzialtherapeutisch sprechen diese Befunde gegen Diuretika und b-Rezeptorenblocker und für eine Bevorzugung von ACE-Hemmstoffen und AT1-Antagonisten bei der Hypertoniebehandlung, insbesondere bei Patienten mit gesteigertem Diabetesrisiko.
Summary
Arterial hypertension is frequently associated with insulin resistance and type 2 diabetes mellitus. Factors in this close association include the high rate of overweight and obesity in hypertensive patients, hypertension-associated changes within the microvasculature (arteriolar remodelling and capillary rarefaction), increased activity of the sympathetic nervous system and a number of possible molecular and cellular changes. Drug treatment of hypertension can further increase (diuretics, beta-blockers) or decrease (ACE inhibitors, angiotensin II receptor antagonists) the rate of new-onset diabetes or may have intermediate effects (calcium-channel blockers). The differing effects of the various antihypertensive drugs on the incidence of new-onset diabetes can largely be explained by their differential effects on hypertension-associated alterations within the microvasculature and on the activity of the sympathetic nervous system. In long-term studies, the difference between "new" and "old" antihypertensive drugs in their effect on the rate of new-onset diabetes continues to grow so that small "numbers needed to treat" (NNT) can be calculated. In interventional studies lasting up to five years, new-onset diabetes is not associated with excess cardiovascular events or mortality. However, preliminary data from long-term observations predominantly suggest that new-onset diabetes during antihypertensive therapy has an unfavorable prognosis. These findings argue against diuretics and b-blockers and for suggest that ACE inhibitors and angiotensin II receptor blockers in the treatment of hypertension, especially in those patients with an increased metabolic risk.
Schlüsselwörter
antihypertensive Therapie - Diabetes - unerwünschte Nebenwirkungen
Key words
antihypertensive treatment - diabetes - side effects
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Prof. Dr. med. Rainer Düsing
Universitätsklinikum Bonn, Medizinische Poliklinik
Wilhelmstraße 35-37
53111 Bonn
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