جستجوی مقالات مرتبط با کلیدواژه "thromboangiitis obliterans" در نشریات گروه "پزشکی"

Buerger’s disease, also known as Thromboangiitis Obliterans (TAO), is a progressive, inflammatory vascular disease with unknown etiology. To address the degree of T cell immunosenescence in this inflammatory disease, the frequency of senescent T cells expressing CD57 and/or CD153 (CD30L) in patients with TAO. In this study, nine male cigarette smoker patients with TAO, nine male healthy cigarette smokers, and nine male healthy non-smoker blood donors were enrolled. PBMCs were extracted from the blood of all participants and stored in liquid nitrogen before use. The percentages of senescent T cells were detected by flow cytometry. The results were analyzed using non-parametric statistical tests. The frequencies of senescent CD3+CD4+CD57+CD153+ and CD3+CD4+CD57-CD153+ T cells significantly increased in patients compared with the non-smoker controls (p=0.01 and p=0.04, respectively). The frequency of senescent CD3+CD4-CD57-CD153+ T cells was higher in patients compared with the smoker controls (p=0.02). In patients with TAO, CD57+CD153- cells were more frequent in CD3hiCD4- and CD3hiCD4+ T cells compared with the CD3loCD4- and CD3loCD4+ T cells (p=0.008 and p=0.0002, respectively). Conversely, the frequency of CD57-CD153+ T cells was significantly higher in CD3loCD4- T cells compared with the CD3hiCD4- T cells (p=0.004). The percentage of CD3+CD4+CD57+CD153- T cells correlated negatively with smoking level in smoker controls (p=0.02, Spearman r=-0.80). Elevated frequencies of senescent CD4+CD57+CD153+ and CD4+CD57-CD153+ T cells in patients compared with non-smoker and smoker controls suggest the contribution of immunosenescence in TAO.

During the gathering of demographic data for the biobank on Buerger’s Disease (BD), we found that, after the clinical manifestation of BD, the patients usually became infertile, and the age of their last child was compatible with the time of disease diagnosis. The aim of this study was to evaluate the underlying cause of secondary infertility in BD patients.

Anti-sperm antibodies (ASA), testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) in the sera of 39 male BD patients were measured and compared with 39 age-matched Caucasian male controls.

Six patients declared that they suffered from impotency. The ASA level was positive in 25.6% of the patients and 2.4% of the controls (p= 0.003, CC= 6.96). The mean levels of testosterone in the patients and controls were 393.12±32.9 ng/dl and 354.37±30.9 ng/dl, respectively. The mean levels of LH in the patients and controls were 0.88±0.12 mIU/r and 0.85±0.1 mIU/r, respectively. The mean levels of FSH in the patients and controls were 4.1± 0.35 mIU/r and 3.56±0.33 mIU/r, respectively. No significant difference in the serum levels of testosterone, LH, or FSH was found between the patients and controls (p> 0.05). The spermograms of three ASA-negative patients demonstrated impaired sperm motility. 

Anti-sperm antibodies, disturbed genital circulation, autonomic dysfunction and sperm motility may be responsible for secondary infertility in Buerger’s Disease.

Buerger's disease (thromboangiitis obliterans) may be a rare peripheral vascular disease that sometimes affects young male smokers. This study presents surgical treatment options for 315 Buerger's patients during a period of 18 years from 2002 to 2020.

In this cross-sectional study, 315 newly diagnosed Buerger patients in a period of 18 years (by Census sampling) were evaluated. Data included age, sex, cigarette smoking status, clinical presentation, the affected limb (right or left, upper or lower extremities), and the performed therapeutic procedures such as angiography of limb arteries, amputation, sympathectomy, and vascular bypass surgery, which were collected in a data sheet. Vascular reconstruction was done if there were suitable inflow and outflow arteries. Sympathectomy was performed for the patients who were unsuitable for revascularization. All analyzes were performed using SPSSV.18 software package (SPSS Inc., Chicago, IL). Data are presented as frequency, mean ± variance (SD).

The mean age of patients was 42.6±9 years old, ranging from (26-75). There were 309 (98.1%) males and 6 (1.9%) females. The most common symptom was ulcer 252 (80%), and the most commonly involved arteries were the dorsal pedis (N=231; 73.4%) and posterior tibialis (N=225; 71.5%). Vascular bypass surgery, sympathectomy, and amputation were performed for patients who met surgical indications. Aortofemoral (N=9) and femoropopliteal (N=24) bypass procedures were done in 2.8% and 7.6% of patients respectively. Of nine patients who underwent aorto-femoral bypass procedure, 6 cases presented with leg claudication, 3 with an ulcer, and 3 with the Raynaud phenomenon. The digital loss rate was 9.6% (N=9) in toes and 1% (N=3) in fingers.

As most of the Buerger patients have multi arterial involvement, bypass surgery or sympathectomy can’t help treat these patients more than cigarette smoking or pharmaceutical therapy.

Thromboangiitis obliterans (TAO) is a non-atherosclerotic inflammatory arthritis mainly involving small arteries and veins. Although it is closely related to the tobacco exposure, the general pathophysiology of the disease remains unclear. TAO mainly affects young male patients with ischemic ulcer, pain during rest, limping, chills in limbs, and migratory thrombophlebitis. However, some patients present joints swelling and pain as the first manifestations before the clinical manifestations above. They are easy to be misdiagnosed as rheumatic diseases, which is a challenge to the diagnosis and treatment of rheumatologists. Here we report a case in which TAO was misdiagnosed as Seronegative Spondyloarthritis (SpA) and eventually amputated.

The aim of this review was to assess several factors associated with Buerger’s disease or thromboangiitis obliterans (TAO), especially the immunological basis of this disease. We found that an established etiology for TAO has not been agreed on so far, but no one denies the strong association between TAO and tobacco consumption. Another possible etiology for this disease is bacterial infections such as Porphyromonas gingivalis and Rickettsia and their possible role via inflammatory processes. TAO was more common in low socioeconomic societies with poor hygiene. It may be attributable to the prevalence of Rickettsia infection because of the tick bite in these societies. In case of autoimmunity, it should be noted that T 17 cells keep the body away from autoimmune processes. The number of infiltrated CD4+ T cells in the arterial wall is higher than B cells. In fact, this may propose the significant role of T cells in the immunopathology of patients with TAO. The disease is also associated with tumor necrosis factor (TNF-α), interleukin (IL)-1β, IL-4, IL-17 and IL-23, as inflammatory cytokines. Antiphospholipid antibodies, anti-CL, anti-TLRVYK, anti-TLRIYT, anti-TLALYK, and anticardiolipin may also play a role in this disease. Further evidence is needed to shed light on the condition, especially in case of T cell lymphocytes’ role.

Buergerchr('39')s disease is a clot forming vasculitis which can lead to severe complications such as amputation of extremities. It is more prevalent in young male smokers and has a higher occurrence in eastern regions of the globe. The risk factors which raise the susceptibility to this condition include infection, tobacco consumption, and genetic factors. It is also hypothesized that the LPS of oral commensal bacteria can lead to various immune reactions that are seen in this disease. Several pathways have been proposed to be responsible for this disease, and the main pathways are through the innate and adaptive immune systems. One of the controversial aspects of the pathophysiology of this disease is its relation to the T cell immunity; histopathology findings have shown T cell infiltration in the arterial wall. In this literature review, our aim was to review the articles published in relation to Buerger’s disease, and the conclusion was that the T cell adaptive immunity might have a fundamental role in the disease pathophysiology, however, further investigation is needed.

Thromboangiitis obliterans (TAO), also known as Burger’s disease, is a devastating disease affecting the arteries and veins of the upper and lower distal limbs most commonly afflicting young male smokers of low socioeconomic status. The expression of human leukocyte antigen (HLA)-A, B and –DRB1 genes have been implicated in the pathogenesis of TAO. Our study aimed to examine the association of different HLA-A, B and –DRB1 genes in TAO patients in the Iranian population.

A case-control study examining 55 Iranian patients with TAO and 500 healthy subjects was performed in Imam Reza hospital, Mashhad, Iran. The prevalence of major histocompatibility complex (MHC) class I (-A, -B) and class II (-DRB) alleles were determined for each participant.

Our results revealed the HLA-A*03 (odds ratio [OR]=5.394), HLA-A*24 (OR=5.143), HLA-A*31 (OR=4.251), HLA-A*11 (OR=3.034), HLA-B*27 (OR=6.680), HLA-B*15 (OR=3.959), HLA-B*07 (OR=3.698), HLA-B*51 (OR=3.370), HLA-B*44 (OR=3.326), HLA-DRB1*16 (OR=20.583), HLA-DRB1*04 (OR=8.960), HLA-DRB1*14 (OR=3.746), HLA-DRB1*03 (OR=2.303), and HLA-DRB1*15 (OR=2.111) alleles to occur at a significantly higher frequency in TAO patients compared to controls (p<0.05). The HLA-A*25, HLA-A*66, HLA-DRB1*08, HLA-DRB1*10, and HLA-DRB1*12 alleles resulted in infinite OR, and was associated with an increased risk of TAO. However, the alleles HLA-A*30, HLA-B*08, HLA-B*45, HLA-B*46, and HLA-B*53 were associated with a protective role against TAO with an OR = 0.

This is the first study examining the HLA pattern in patients with Burger’s disease in the Iranian population. Our findings have revealed an association between HLA class I and II alleles with TAO.

Thromboangiitis obliterans (TAO) is a thrombotic-occlusive as well as an inflammatory peripheral vascular disease with unknown etiology. Recent evidence has supported the immunopathogenesis of the disease, however, the factors contributing to the altered immune function and vascular tissue inflammation are still unclear. This review was intended to collate the more current knowledge on the regulatory molecules involved in TAO from an immunoreactive perspective. The homeostasis of the immune system as well as a variety of progenitor cell populations appear to be affected during TAO and these alterations are associated with intrinsic signaling defects that are directing to an improved understanding of the crosstalk between angiogenesis and the immune system, as well as the potential of new co-targeting strategies applying both immunotherapy and angiogenic therapy.

Until recently, a gene polymorphism in the promoter region of endothelial nitric oxide synthase has been suggested as a risk factor for thromboangiitis obliterans (TAO) development. The aim of this study was to compare the metabolites of nitric oxide (NO) and its backup, heme-oxygenase-1 (HMOX1), between TAO patients and those of a smoking control group matched by race, age, sex, and smoking habits.
Twenty-four male Caucasian TAO patients and 20 male Caucasian controls enrolled in the study. Their smoking habits were matched based on the serum cotinine levels of 17 of the TAO patients and the 20 controls. A colorimetric kit was used to measure NO, and an enzyme-linked immunosorbent assay kit was used to measure cotinine and HMOX1 levels.
The mean serum level of NO metabolites in the TAO group was significantly less than in the controls (p = 0.03) and also significantly less in the patients with below-knee amputations than in non-amputees (p= 0.018). Also, HMOX1 was significantly greater in the TAO patients than in the controls (p= 0.01). No significant correlation was found between NO and HMOX1 (p = 0.054).
Nitric oxide may play a pivotal role in TAO development and its outcome. However, the intact HMOX1 pathway may demonstrate the unique role of NO, which cannot be compensated for by HMOX1 and whose absence may make patients susceptible to developing TAO. In addition, another pathway besides NO, with influence on vascular tone and hemostasis, might be involved in TAO development, such as the autonomic nervous system. Further studies are suggested regarding these issues.

The mechanism underlying Buerger’s disease (BD) is still unknown. Recently, thrombophilic conditions predisposing to a hypercoagulable state have been hypothesized as triggers for BD. The aim of the study is to evaluate the prevalence of the hyperhomocysteinemia and level of the anticardiolipin antibodies, and the role of folic acid on the hyperhomocysteinemia and on the rate of the amputations in the patients with BD. In an experimental placebo-controlled double-blinded study, between 2004 and 2010, thirty patients with BD were randomly assigned into two groups (14 patients in a drug group and 16 patients in the placebo group). Drug or placebo was administered, and they were followed in 2 and 6 months for homocysteine, Anticardiolipin antibodies and the risk of amputations. At the beginning of the study homocysteine level was higher than normal in 19 patients (63%). There was a significant decrease in homocysteine level during 6 months in folic acid group (P < 0.001), but there was no change in the placebo group. None of our patients had elevated Anticardiolipin antibodies, and there was no change in the level of Anticardiolipin antibody during study. High level of homocysteine did not associate with more amputations during 6 months of study (P > 0.05). This study shows the hyperhomocysteinemia in BD, and the benefit of folic acid treatment in homocysteine lowering, but folic acid doesn’t inhibit the risk of major and minor amputation during 6 months of follow-up. Longer follow-up may reveal the role of folic acid in these patients.