Prävalenz der Hyperhomocysteinämie bei der Thrombangiitis obliterans: Spielt Homocystein pathogenetisch eine Rolle?

Stämmler, Frank; Diehm, Curt; Hsu, Emily; Stockinger, Klaus; Amendt, Klaus

doi:10.1055/s-2008-1043162

Cited by 28 publications

(15 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In our study, the plasma level of homocysteine was significantly higher in patients with Buerger’s disease as compared to atherosclerosis and healthy cases before treatment. (p < 0.001) The higher values of plasma homocysteine levels in Buerger’s disease patients and simultaneously the higher prevalence of tobacco usage in this group (90.9% of cases) and also higher plasma levels of homocysteine in smoker cases of 3 groups was compared to the initial measurement in all patients, suggests that tobacco could be the principle cause of hyperhomocysteinemia in such patients, which also has been revealed in other studies (4, 6, 12, 14). The effect of folic acid therapy on elevated homocysteine levels in some medical conditions has been evaluated in a variety of studies.…”

Section: Discussionsupporting

confidence: 77%

“…Buerger’s disease or Thromboangiitis obliterans (TAO) is a peripheral vascular disease with a questionable pathophysiology, natural course, and definitive treatment. Stammler (12) and Bergmark (13) have shown that the presence of high plasma levels of homocysteine in Buerger’s disease patients. So, hyperhomocysteinemia may play a meaningful role in the pathophysiology of Buerger’s disease.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of Folic Acid therapy on Homocysteine Level in patients with Atherosclerosis or Buerger’s Disease and in Healthy individuals: A clinical trial

et al. 2016

View full text Add to dashboard Cite

BackgroundHyperhomocysteinemia is considered a risk factor for atherosclerosis and some other vascular diseases such as Buerger’s disease.ObjectiveThe aim of this study was to measure the Homocysteine levels in 3 different groups of participants (Buerger’s disease, atherosclerosis patients, and healthy cases) and determine the therapeutic effect of folic acid therapy on homocysteine levels for these three groupsMethodsThis nonrandomized clinical trial study was conducted in the vascular and endovascular surgery research center of Mashhad University of Medical Sciences in Mashhad, Iran. This interventional study consisted of 44 participants of which 22 patients had Buerger’s disease and a control group of 22 healthy individuals, all of which were enrolled in this study. All of the study’s participants had their serum homocysteine levels measured both before and after 12 weeks of folic acid (5mg/day) therapy. The data analysis used fo data analysis was a Chi square and t-test or their non-parametrical equivalents for data analysis by means of Statistical Package for the Social Sciences (SPSS) version 16ResultsThe homocysteine levels were found to be significantly higher in patients with Buerger’s disease as compared to other groups before treatment with folic acid (Buerger = 21.8 ± 8.5 Mm/L, atherosclerosis = 17.3 ± 6.9, healthy = 13.8 ± 3.1; p < 0.001). After treatment with folic acid at 5 mg/daily for 12 weeks, the new plasma homocysteine levels did not show any significant difference (p = 0.38) between the Buerger’s disease group (14.6 ± 4.5 Mm/L) and atherosclerosis group (13.9 ± 4.7), but it was found to besignificantly higher in both groups when compared to the healthy group (10.7 ± 3.9, p<0.05). The plasma homocysteine level was reduced significantly when compared to its initial level in all 3 groups. The comparison of differences among three groups was found not to be significant (p=0.41)ConclusionsIt seems that supplementary therapy with folic acid at a dose of 5 mg daily may reduce the serum homocysteine levels significantly and may have a role in the development of vascular diseases such as Buerger’s disease. We suggest that folic acid should be considered as a routine agent in the Buerger’s disease therapeutic regimeClinical trial registrationThe trial was registered at the Thai Clinical Trials Registry (http://www.clinicaltrials.in.th) with the ID: TCTR20160601003.FundingThis study was not funded by any organization.

show abstract

Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Effect of Folic Acid therapy on Homocysteine Level in patients with Atherosclerosis or Buerger’s Disease and in Healthy individuals: A clinical trial

et al. 2016

View full text Add to dashboard Cite

show abstract

“…In the past years, several association between Buerger's disease and alteration of haemostasis have been suggested [5]. In these reports a role of hyperhomocysteinemia playing a pathogenetic role in Buerger's disease was ruled out, but univocal data are lacking since the majority of reports were based on single case observations or small populations [5,11,12]. On the other hand, reports on the role of MTHFR C677T gene variant, a cause of hyperhomocysteinemia, as a trigger factor of Buerger's disease did not confirm this association [13,14].…”

Section: Discussionmentioning

confidence: 99%

Buerger`s Disease and Hyperhomocysteinemia: Is there a Relationship?

Micco¹,

Fiore²,

Micco³

et al. 2009

TOATHERTJ

View full text Add to dashboard Cite

Thromboangiitis obliterans, also known as Buerger's disease, is a cause of juvenile lower limb ischaemia. Buerger's disease is idiopathic and one of diagnostic criteria is the absence of atherosclerotic risk factors other than smoking. A possible involvement of thrombophilia has been investigated and the role of hyperhomocysteinemia is still matter of discussion. We describe 9 patients with Buerger's disease followed-up for the past 3 years. We found a significant increase in circulating homocysteine levels (mean: 31.6 in patients vs 8.2 μmol/L in control subjects). We also analyzed the C677T mutation of MTHFR; 5/9 Buerger's patients were heterozygotes and 4/9 homozygotes for the mutation as compared with 3 heterozygotes in the control group. Our data, although preliminary, suggest a possible role of homocysteine in the pathogenesis of Buerger's disease as one of the causes of endothelial dysfunction. The role of MTHFR C677T variant must be further evaluated in larger trials involving patients with Buerger's disease.

show abstract

“…Studies have shown a possible relationship between TAO and hypercoagulable states, although the details of such relation are still unknown. There are cases associated with deficiencies in protein S and protein C [7], antiphospholipid antibodies [8] and hyperhomocysteinemia [9]. A study has demonstrated that high concentrations of anticardiolipin antibodies are correlated with an earlier and more severe form of the condition, including higher amputation rates [10].…”

Section: Introductionmentioning

confidence: 99%

Determination of Kininogens Levels and Kallikrein/Kininase II Activities in Patients with Thromboangiitis Obliterans

Dellalibera-Joviliano

Joviliano

Évora

2010

Scand J Immunol

View full text Add to dashboard Cite

Some components of the kinin system such as plasma kallikrein levels, the activities of tissue kallikrein (including saliva) and kininase II and the concentrations of kininogen fractions (low‐molecular weight/LKg and high‐molecular weight/HKg) were evaluated in the plasma of patients with thromboangiitis obliterans (TAO) presenting clinical symptoms of the condition. Twenty TAO were diagnosed by means of the traditional Shionoya and Olin criteria and later classified into non‐smokers (n = 11) and active smokers (n = 9). Fifty‐three normal, non‐smoking/smoking individuals (control) were also studied. Kininogen levels were determined by ELISA; the activities of kallikreins and kininase II were determined using selective substrates. The levels of enzymes (kallikreins and kininase II) and protein (kininogens) were significantly higher in patients with TAO who were active smokers compared to the control groups (no matter whether control individuals were active smokers or non‐smokers, P < 0.001 for all comparisons). Interestingly, regardless of the time of disease onset, a significant increase in the levels of these components of the kinin system was also observed in patients when TAO active smokers were compared with TAO ex‐smokers (P < 0.01 for all analysed parameters). Activation of the kinin system in patients with TAO may indicate the involvement of vasodilatation in an attempt to control vascular changes, thereby favouring the deposition of immune complexes at the vascular level because of nicotine stimulation. Moreover, our results corroborate the idea that TAO can be an autoimmune disorder with specific mechanisms.

show abstract

Prävalenz der Hyperhomocysteinämie bei der Thrombangiitis obliterans: Spielt Homocystein pathogenetisch eine Rolle?

Abstract: Hyperhomocysteinaemia occurs frequently in patients with TAO. It may play an important and nicotine-independent role in its pathogenesis.

Cited by 28 publications

References 0 publications

Effect of Folic Acid therapy on Homocysteine Level in patients with Atherosclerosis or Buerger’s Disease and in Healthy individuals: A clinical trial

Effect of Folic Acid therapy on Homocysteine Level in patients with Atherosclerosis or Buerger’s Disease and in Healthy individuals: A clinical trial

Buerger`s Disease and Hyperhomocysteinemia: Is there a Relationship?

Determination of Kininogens Levels and Kallikrein/Kininase II Activities in Patients with Thromboangiitis Obliterans

Contact Info

Product

Resources

About