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001-es BibID:BIBFORM023401
Első szerző:Fülesdi Béla (aneszteziológus)
Cím:Cerebrovascular reactivity and reserve capacity in type II diabetes mellitus / Fülesdi B., Limburg M., Bereczki D., Káplár M., Molnár C., Kappelmayer J., Neuwirth G., Csiba L.
Dátum:1999
ISSN:1056-8727
Megjegyzések:The aim of the study was to test the hypothesis that cerebrovascular reserve capacity and cerebrovascular reactivity are impaired in patients suffering from non insulin-dependent diabetes mellitus. We also intended to investigate factors which may influence resting cerebral blood flow velocity and cerebrovascular reserve capacity. A total of 28 patients suffering from type II diabetes mellitus and 20 healthy control subjects were studied. Based on diabetes duration patients were divided into two groups: subjects with > 10 years and those with < or = 10 years disease duration. Middle cerebral artery mean blood flow velocities were measured at rest and after intravenous administration of 1g acetazolamide. Cerebrovascular reactivity and reserve capacity were calculated. Blood glucose, insulin, glycosylated hemoglobin, hemostatic factors (fibrinogen, alpha-2 macroglobulin and von Willebrand factor antigen) were determined. Cerebrovascular reactivity and reserve capacity values were compared between the two diabetic subgroups and controls. Correlations between laboratory parameters and cerebrovascular reserve were investigated by linear regression analysis. Resting cerebral blood flow velocity was similar in controls and in the two diabetic subgroups. Cerebrovascular reactivity was elevated for a shorter time in patients with > 10 years disease duration than in controls and short-term diabetic patients. Cerebrovascular reserve capacity was lower in the long-term diabetes group (means +/- SD: 39.6 +/- 20.7%) than in patients with < or = 10 years disease duration (63.3 +/- 17.4%, p < 0.02 after Bonferroni correction). Cerebrovascular reserve capacity was inversely related to the duration of the disease (R = 0.53, p < 0.003). None of the determined laboratory factors had any relation with resting cerebral blood flow and cerebrovascular reserve capacity. The vasodilatory ability of cerebral arterioles is diminished in long-standing type II diabetes mellitus.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal Of Diabetes And Its Complications. - 13 : 4 (1999), p. 191-199. -
További szerzők:Limburg, Martien Bereczki Dániel (1960-) (neurológus) Káplár Miklós (1965-) (belgyógyász, diabetológus) Molnár Csilla (1962-) (aneszteziológus) Kappelmayer János (1960-) (laboratóriumi szakorvos) Neuwirth Gyula Csiba László (1952-) (neurológus, pszichiáter)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:BIBFORM023404
Első szerző:Hidasi Eszter (neurológus)
Cím:No correlation between impairment of cerebrovascular reserve capacity and electrophysiologically assessed severity of neuropathy in noninsulin-dependent diabetes mellitus / Hidasi E., Káplár M., Diószeghy P., Bereczki D., Csiba L., Limburg M., Fülesdi B.
Dátum:2002
Megjegyzések:Microvascular abnormalities have an important role in the most frequent neurological complications of diabetes mellitus: neuropathy and cerebrovascular disorders. Severity of neuropathy as well as of cerebral microvascular damage can be quantitatively evaluated by instrumental methods like nerve conduction studies and transcranial Doppler. In the present study, we investigated whether a correlation exists between the severity of peripheral neuropathy and the impairment of cerebrovascular reserve capacity (CRC) in 20 patients with Type 2 diabetes mellitus. METHODS: CRC was measured by transcranial Doppler and defined as the maximal percentage increase in blood flow velocity in the middle cerebral artery within 20 min after an intravenous dose of 1000 mg of acetazolamide. Nerve conduction studies of the median, ulnar, peroneal, and sural nerves were performed. Severity of neuropathy was scored based on conduction velocities, amplitudes, and distal latencies. RESULTS: There was no correlation between the neuropathic score and CRC (R= .003, P= .99). Neither CRC nor the neuropathic score correlated significantly with age, duration of diabetes, and serum values of HbA(1c), glucose, insulin, von Willebrand factor, and alpha(2) - macroglobulin. Severity of neuropathy but not CRC correlated with microalbuminuria (R= .47, P= .038 and R= .14, P= .54). Improper treatment reflected by HbA(1c) >10% was associated with significantly more severe albuminuria, higher actual blood glucose level, higher von Willebrand factor activity, and marginally higher neuropathic score (21 vs. 13, P=.096), but was not associated with CRC (44% vs. 42%, P= .81). When duration of diabetes was dichotomized to 15 years and less or over 15 years, CRC was significantly smaller (35% vs. 50%, P= .036) and neuropathy was more severe in the subgroup with longer diabetes duration (19 vs. 11.5 points, P= .07). CONCLUSIONS: Although both CRC and peripheral nerve function are affected more severely in patients with long-lasting Type 2 diabetes mellitus, damage in the cerebrovascular system and in the long peripheral nerves occur independently. As in diabetes mellitus pathological changes in autonomic and large peripheral nerves develop simultaneously, decreased CRC in diabetic patients might be predominantly due to structural changes of resistance arteries or to metabolic than to neurogenic factors.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Diabetes and its Complications. - 16 : 3 (2002), p. 228-234. -
További szerzők:Káplár Miklós (1965-) (belgyógyász, diabetológus) Diószeghy Péter (1948-) (ideg- és elmeszakorvos) Bereczki Dániel (1960-) (neurológus) Csiba László (1952-) (neurológus, pszichiáter) Limburg, Martien Fülesdi Béla (1961-) (aneszteziológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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