Antiphospholipid antibody syndrome and vasoocclusive diseases

Doko, S; Katsumura, T; Fujiwara, Takashi; Ishiguro, Hiroshi; Hara, Masaki

doi:10.1055/s-0031-1275949

Cited by 1 publication

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“…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

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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.

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