Buerger's disease medical therapy: Difference between revisions

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==Overview==
==Overview==
There is no treatment for Buerger's disease. In order to prevent progression and control symptoms smoking cessation is crucial. Smoking cessation does not reverse damage already caused. Pharmacologic medical therapies for Buerger's disease include smoking cessation, palliative treatments, prostaglandin analogs and phosphodiesterase inhibitors, calcium channel blockers, endothelin receptor anatagonists, compression therapy and some experimental therapies. It should be noted, however, that these therapies are purely palliative and do not reverse previous damage caused.  
There is no treatment for Buerger's disease. In order to prevent progression and control symptoms, [[smoking cessation]] is crucial. [[Smoking cessation]] does not reverse damage already caused. Pharmacologic medical therapies for Buerger's disease include [[smoking cessation]], [[palliative treatment]]<nowiki/>s, [[prostaglandin analogs]] and [[phosphodiesterase inhibitors]], [[Calcium channel blocker|calcium channel blockers]], [[Endothelin receptor antagonist|endothelin receptor antagonists]], [[compression therapy]] and some experimental therapies. It should be noted, however, that these therapies are purely palliative and do not reverse previous damage caused. [[Analgesic|Analgesics]] including [[Non-steroidal anti-inflammatory drug|NSAIDs]] and [[acetaminophen]] may be used to provide pain relief.
 


==Medical Therapy==
==Medical Therapy==
Pharmacologic medical therapies for Buerger's disease include smoking cessation, palliative treatments, prostaglandin analogs and phosphodiesterase inhibitors, calcium channel blockers, endothelin receptor anatagonists, compression therapy and some experimental therapies. It should be noted, however, that these therapies are purely palliative and do not reverse previous damage caused.
Pharmacologic medical therapies for Buerger's disease include [[smoking cessation]], [[Palliative treatment|palliative treatments]], [[prostaglandin analogs]] and [[phosphodiesterase inhibitors]], [[Calcium channel blocker|calcium channel blockers]], [[Endothelin receptor antagonist|endothelin receptor antagonists]], [[compression therapy]] and some experimental therapies. It should be noted, however, that these therapies are purely palliative and do not reverse previous damage caused.<ref name="pmid10995867">{{cite journal |vauthors=Olin JW |title=Thromboangiitis obliterans (Buerger's disease) |journal=N. Engl. J. Med. |volume=343 |issue=12 |pages=864–9 |date=September 2000 |pmid=10995867 |doi=10.1056/NEJM200009213431207 |url=}}</ref><ref name="pmid2225420">{{cite journal |vauthors=Olin JW, Young JR, Graor RA, Ruschhaupt WF, Bartholomew JR |title=The changing clinical spectrum of thromboangiitis obliterans (Buerger's disease) |journal=Circulation |volume=82 |issue=5 Suppl |pages=IV3–8 |date=November 1990 |pmid=2225420 |doi= |url=}}</ref><ref name="pmid14718836">{{cite journal |vauthors=Ohta T, Ishioashi H, Hosaka M, Sugimoto I |title=Clinical and social consequences of Buerger disease |journal=J. Vasc. Surg. |volume=39 |issue=1 |pages=176–80 |date=January 2004 |pmid=14718836 |doi=10.1016/j.jvs.2003.08.006 |url=}}</ref>


===Smoking cessation===
===Smoking cessation===
*Smoking cessation is crucial to the management of Buerger's disease. Not only does smoking cessation halt progression but also controls pain symptoms and decreases the risk of amputation.
*[[Smoking cessation]] is crucial to the management of Buerger's disease. Not only does [[smoking cessation]] halt progression but also controls [[pain]] symptoms and decreases the risk of [[amputation]].<ref name="pmid10995867">{{cite journal |vauthors=Olin JW |title=Thromboangiitis obliterans (Buerger's disease) |journal=N. Engl. J. Med. |volume=343 |issue=12 |pages=864–9 |date=September 2000 |pmid=10995867 |doi=10.1056/NEJM200009213431207 |url=}}</ref><ref name="pmid2225420">{{cite journal |vauthors=Olin JW, Young JR, Graor RA, Ruschhaupt WF, Bartholomew JR |title=The changing clinical spectrum of thromboangiitis obliterans (Buerger's disease) |journal=Circulation |volume=82 |issue=5 Suppl |pages=IV3–8 |date=November 1990 |pmid=2225420 |doi= |url=}}</ref><ref name="pmid14718836">{{cite journal |vauthors=Ohta T, Ishioashi H, Hosaka M, Sugimoto I |title=Clinical and social consequences of Buerger disease |journal=J. Vasc. Surg. |volume=39 |issue=1 |pages=176–80 |date=January 2004 |pmid=14718836 |doi=10.1016/j.jvs.2003.08.006 |url=}}</ref>
*The patient may, however, still suffer from intermittent cluadication or Reynaud's phenomenon.
*The patient may, however, still suffers from intermittent [[claudication]] or [[Raynaud's phenomenon|Raynaud phenomenon]].
*Complete abstinence from smoking is a must as Buerger's disease in susceptible individuals can be triggered by a single cigarette.
*Complete abstinence from [[smoking]] is a must as Buerger's disease in susceptible individuals can be triggered by a single cigarette.
*Any anti-smoking aid containing nicotine such as transdermal patches or gum must be avoided as they may also trigger the disease.
*Any anti-smoking aid containing [[nicotine]] such as transdermal patches or gum must be avoided as they may also trigger the disease.
*Anti-smoking aids such as bupropion or varenicline may be of use and do not contribute to disease progression.
*Anti-smoking aids such as [[bupropion]] or [[varenicline]] may be of use and do not contribute to disease progression.
*A patient that claims to have stopped smoking but continues to suffer symptoms of active disease should be tested for urinary nicotine and cotinine.  
*A patient that claims to have stopped smoking but continues to suffer symptoms of active disease should be tested for urinary [[nicotine]] and [[cotinine]].  
*Previous studies have demonstrated that only 50% of patients with Buerger's disease are able to quit smoking. In these patients, nicotine dependence treatment may be sought.
*Previous studies have demonstrated that only 50% of patients with Buerger's disease are able to quit smoking. In these patients, nicotine dependence treatment may be sought.


===Iloprost===
===Iloprost===
*Iloprost is a prostaglandin analog and is available in an IV and oral form.
*[[Iloprost]] is a [[Prostaglandin analogs|prostaglandin analog]] and is available in an [[IV|intravenous]] and oral forms.<ref name="pmid9610341">{{cite journal |vauthors= |title=Oral iloprost in the treatment of thromboangiitis obliterans (Buerger's disease): a double-blind, randomised, placebo-controlled trial. The European TAO Study Group |journal=Eur J Vasc Endovasc Surg |volume=15 |issue=4 |pages=300–7 |date=April 1998 |pmid=9610341 |doi= |url=}}</ref><ref name="pmid1689791">{{cite journal |vauthors=Fiessinger JN, Schäfer M |title=Trial of iloprost versus aspirin treatment for critical limb ischaemia of thromboangiitis obliterans. The TAO Study |journal=Lancet |volume=335 |issue=8689 |pages=555–7 |date=March 1990 |pmid=1689791 |doi= |url=}}</ref><ref name="pmid16763533">{{cite journal |vauthors=Bozkurt AK, Köksal C, Demirbas MY, Erdoğan A, Rahman A, Demirkiliç U, Ustünsoy H, Metin G, Yillik L, Onol H, Cinar B, Karaçelik M, Erdinç I, Bolcal C, Sayin AG |title=A randomized trial of intravenous iloprost (a stable prostacyclin analogue) versus lumbar sympathectomy in the management of Buerger's disease |journal=Int Angiol |volume=25 |issue=2 |pages=162–8 |date=June 2006 |pmid=16763533 |doi= |url=}}</ref>
*Iloprost is especially effective in the intravenous form at reducing pain symptoms, better than low dose aspirin or lumbar sympathectomy.
*[[Iloprost]] is expensive and not available in the USA.
*Iloprost can facilitate smoking cessation and may be used to manage resting pain symptoms in those patients with critical limb ischemia.  
*[[Iloprost]] is especially effective in the intravenous form at reducing pain symptoms, better than low dose [[aspirin]] or lumbar [[sympathectomy]].
*Iloprost may also hasten ulcer healing.
*[[Iloprost]] can facilitate [[smoking cessation]] and may be used to manage resting pain symptoms in those patients with critical [[limb ischemia]].  
*[[Iloprost]] may also hasten [[ulcer]] healing.


===Calcium channel blockers===
===Calcium channel blockers===
Calcium channel blockers are frequently used to manage vasospasm associated with the Raynaud phenomenon. When significant vasospasm is present in patients with thromboangiitis obliterans, calcium channel blocking agents such as nifedipine, nicardipine or amlodipine may similarly be used [4] (See "Initial treatment of the Raynaud phenomenon", section on 'Calcium channel blockers'.)
*[[Calcium channel blocker|Calcium channel blockers]] are used in patients whose main complaint is [[Raynaud's phenomenon|Raynaud phenomenon]].<ref name="pmid10995867">{{cite journal |vauthors=Olin JW |title=Thromboangiitis obliterans (Buerger's disease) |journal=N. Engl. J. Med. |volume=343 |issue=12 |pages=864–9 |date=September 2000 |pmid=10995867 |doi=10.1056/NEJM200009213431207 |url=}}</ref>
 
*[[Calcium channel blocker|Calcium channel blockers]] that prevent [[vasospasm]] include the [[Dihydropyridine|dihydropyridines]] such as, [[nifedipine]], [[nicardipine]] and, [[amlodipine]].
===Intermittent pneumatic compression===  
===Intermittent pneumatic compression===  
 
*[[Intermittent pneumatic compression]] (IPC) is used in patients whose main complaint is that of poor circulation and healing in the extremities.<ref name="pmid9790203">{{cite journal |vauthors=Labropoulos N, Watson WC, Mansour MA, Kang SS, Littooy FN, Baker WH |title=Acute effects of intermittent pneumatic compression on popliteal artery blood flow |journal=Arch Surg |volume=133 |issue=10 |pages=1072–5 |date=October 1998 |pmid=9790203 |doi= |url=}}</ref>
Application of intermittent pneumatic compression (IPC) to the foot and calf augments popliteal artery flow through a sharp decrease in peripheral arterial resistance manifested by increases in peak systolic and end diastolic flow velocities on Doppler ultrasound [73].
*IPC is a therapy that is able to increase the flow of blood through the arteries by decreasing the peripheral arterial resistance.  
 
Intermittent pneumatic compression enhances calf inflow in patients with intermittent claudication or critical limb ischemia. In one study, complete healing of ischemic ulcers was demonstrated in patients with small vessel occlusive diseases such as scleroderma, CREST and thromboangiitis obliterans [74]. We utilize this therapy in patients with painful ulcerations when there is no viable revascularization option. It is useful in decreasing pain even before complete ulcer healing occurs. While there are limited studies, specifically in thromboangiitis obliterans, studies have demonstrated efficacy in small vessel occlusive disease of many etiologies. (See 'Revascularization' below.)


===Experimental therapies===
===Experimental therapies===
====Therapeutic angiogenesis====
*Patients with ischemic pain or non-healing ulcers may benefit from therapeutic [[angiogenesis]] that uses grow factors, such as intramuscular [[vascular endothelial growth factor]], or through the introduction of a Kirschner wire placed in the medullary canal of the tibia (distraction osteogenesis) in order to promote the generation of blood vessels.<ref name="pmid9845647">{{cite journal |vauthors=Isner JM, Baumgartner I, Rauh G, Schainfeld R, Blair R, Manor O, Razvi S, Symes JF |title=Treatment of thromboangiitis obliterans (Buerger's disease) by intramuscular gene transfer of vascular endothelial growth factor: preliminary clinical results |journal=J. Vasc. Surg. |volume=28 |issue=6 |pages=964–73; discussion 73–5 |date=December 1998 |pmid=9845647 |doi= |url=}}</ref> <ref name="pmid17652224">{{cite journal |vauthors=Saito S, Nishikawa K, Obata H, Goto F |title=Autologous bone marrow transplantation and hyperbaric oxygen therapy for patients with thromboangiitis obliterans |journal=Angiology |volume=58 |issue=4 |pages=429–34 |date=2007 |pmid=17652224 |doi=10.1177/0003319706292015 |url=}}</ref><ref name="pmid15694801">{{cite journal |vauthors=Inan M, Alat I, Kutlu R, Harma A, Germen B |title=Successful treatment of Buerger's Disease with intramedullary K-wire: the results of the first 11 extremities |journal=Eur J Vasc Endovasc Surg |volume=29 |issue=3 |pages=277–80 |date=March 2005 |pmid=15694801 |doi=10.1016/j.ejvs.2004.12.011 |url=}}</ref><ref name="pmid21886930">{{cite journal |vauthors=Kulkarni S, Kulkarni G, Shyam AK, Kulkarni M, Kulkarni R, Kulkarni V |title=Management of thromboangiitis obliterans using distraction osteogenesis: A retrospective study |journal=Indian J Orthop |volume=45 |issue=5 |pages=459–64 |date=September 2011 |pmid=21886930 |pmc=3162685 |doi=10.4103/0019-5413.83954 |url=}}</ref>
*Therapeutic [[angiogenesis]] has also demonstrated that it may reduce the occurrence of nocturnal resting pain.


A number of additional therapies have been studied or are under active clinical investigation [46]. Some of these are highlighted below:
====Autologous bone marrow mononuclear cell implantation====
*When traditional [[revascularization]] interventions have failed in those with severe [[Peripheral arterial disease|peripheral artery disease]], autologous bone marrow mononuclear cell implantation may be performed.<ref name="pmid9845647">{{cite journal |vauthors=Isner JM, Baumgartner I, Rauh G, Schainfeld R, Blair R, Manor O, Razvi S, Symes JF |title=Treatment of thromboangiitis obliterans (Buerger's disease) by intramuscular gene transfer of vascular endothelial growth factor: preliminary clinical results |journal=J. Vasc. Surg. |volume=28 |issue=6 |pages=964–73; discussion 73–5 |date=December 1998 |pmid=9845647 |doi= |url=}}</ref>
*Autologous bone marrow mononuclear cell implantation may be able to relieve ischemic pain symptoms and decrease ulcer size, whilst increasing walking distance.


●Therapeutic angiogenesis has been evaluated for treatment of peripheral artery disease and this therapy may improve the ischemic manifestations of thromboangiitis obliterans. Short-term results of therapeutic angiogenesis using growth factors or autologous bone marrow have been promising, but longer term studies are needed.
====Immunoabsorption therapy, bosentan and cilostazol====
*Immunoabsorption therapy and [[bosentan]] ([[endothelin receptor antagonist]]) have demonstrated that they are effective in improving pain intensity and ulcer healing.<ref name="pmid15365252">{{cite journal |vauthors=Kim HJ, Jang SY, Park JI, Byun J, Kim DI, Do YS, Kim JM, Kim S, Kim BM, Kim WB, Kim DK |title=Vascular endothelial growth factor-induced angiogenic gene therapy in patients with peripheral artery disease |journal=Exp. Mol. Med. |volume=36 |issue=4 |pages=336–44 |date=August 2004 |pmid=15365252 |doi=10.1038/emm.2004.44 |url=}}</ref> <ref name="pmid22333218">{{cite journal |vauthors=De Haro J, Acin F, Bleda S, Varela C, Esparza L |title=Treatment of thromboangiitis obliterans (Buerger's disease) with bosentan |journal=BMC Cardiovasc Disord |volume=12 |issue= |pages=5 |date=February 2012 |pmid=22333218 |pmc=3306190 |doi=10.1186/1471-2261-12-5 |url=}}</ref>
*[[Cilostazol]] ([[Phosphodiesterase inhibitors|phosphodiesterase inhibitor]]) is a suppressor of [[platelet aggregation]] and a direct arterial vasodilator, it is able to casue a reactive hyperemia and therefore, improve blood flow.<ref name="pmid4074434">{{cite journal |vauthors=Yasuda K, Sakuma M, Tanabe T |title=Hemodynamic effect of cilostazol on increasing peripheral blood flow in arteriosclerosis obliterans |journal=Arzneimittelforschung |volume=35 |issue=7A |pages=1198–200 |date=1985 |pmid=4074434 |doi= |url=}}</ref>


•In one trial of six patients with nonhealing wounds (>1 month), intramuscular vascular endothelial growth factor (VEGF) 165 was injected into seven affected limbs [75]. Ulcers completely healed in three of five limbs. In the other two patients, nocturnal rest pain was relieved, although both continued to have claudication. In all seven limbs, perfusion was improved on magnetic resonance imaging and newly visible collateral vessels were seen on contrast angiography.
===Analgesia===
 
*[[Non-steroidal anti-inflammatory drug|Non-steroidal anti-inflammatory drugs]] may be used to relieve pain symptoms, including [[naproxen]],[[ibuprofen]], [[indomethacin]], [[diclofenac]], and ketofen.<ref name="pmid10995867">{{cite journal |vauthors=Olin JW |title=Thromboangiitis obliterans (Buerger's disease) |journal=N. Engl. J. Med. |volume=343 |issue=12 |pages=864–9 |date=September 2000 |pmid=10995867 |doi=10.1056/NEJM200009213431207 |url=}}</ref><ref name="pmid2225420">{{cite journal |vauthors=Olin JW, Young JR, Graor RA, Ruschhaupt WF, Bartholomew JR |title=The changing clinical spectrum of thromboangiitis obliterans (Buerger's disease) |journal=Circulation |volume=82 |issue=5 Suppl |pages=IV3–8 |date=November 1990 |pmid=2225420 |doi= |url=}}</ref>
•A second phase one trial tested the safety of intramuscular gene transfer by using naked plasmid DNA encoding the gene for VEGF in seven patients with thromboangiitis obliterans [76]. Ischemic pain in the affected limb was relieved or improved markedly in six of seven patients, and ischemic ulcers healed or improved in four of six patients.
*[[Acetaminophen]]<nowiki/>used alone, or with [[codeine]] or [[hydrocodone]], is also effective.  
 
●Cell-based therapy with autologous bone marrow mononuclear cell implantation has also been used with some degree of success [77]. A meta-analysis indicates that intramuscular autologous bone marrow cell therapy is a feasible, relatively safe and potentially effective therapeutic strategy for patients with severe peripheral artery disease who are not candidates for traditional revascularization [78]. The therapeutic angiogenesis by cell transplantation (TACT) trial, which included patients with thromboangiitis obliterans, randomly assigned patients to autologous bone marrow mononuclear cell injection versus placebo [79]. Significant improvements were seen in leg pain scale, ulcer size and pain-free walking distance that were maintained at two years after therapy. Other available small nonrandomized studies have shown similar short-term improvements [80-83]. A confounding factor for many of these studies is the fact that, in addition to receiving therapy, many of the patients stopped smoking.
 
●Immunoabsorption therapy was tested in a pilot study of 10 patients. The treatment was tolerated without side effects. Pain intensity decreased rapidly from a mean of 7.7/10.0 before treatment to 2.0/10.0 at the second day of five consecutive days of therapy [84]. One month after immunoabsorption, all patients were without pain, an effect that persisted over the follow-up period of six months. Healing of ischemic ulcerations was observed in all patients during follow-up. Six of the ten patients were studies were active smokers and smoking habits were reported not to change throughout the course of the study. Although the results are encouraging, the sample size of this observational study was quite small; a randomized trial would be needed to prove efficacy.
 
●Another method of stimulating angiogenesis using a Kirschner wire placed in the medullary canal of the tibia was used in six patients with thromboangiitis obliterans [85]. At a mean follow-up of 19 months, significant improvements were seen in symptoms with reduced rest pain, increased pain-free walking distance and ulcer healing. Most studies have not reported significant adverse events to angiogenic therapy; however, in one study, four of eight patients suffered significant clinical events underscoring the need for long-term monitoring [86].
 
●Bosentan, which is an endothelin receptor antagonist, was used to treat 12 patients with thromboangiitis obliterans and ischemic ulceration or rest pain [87]. An increase in distal flow was observed in 10 out of the 12 patients on magnetic resonance and digital subtraction arteriography and clinical improvement was observed in 12 of the 13 extremities; however, 2 extremities subsequently required amputation. In a separate series of 26 patients, a complete therapeutic response was achieved in 80 percent of patients, whereas a partial response was observed in 12 percent [88]. No significant differences were found for bosentan efficacy when comparing patients who gave up smoking with those who were unable to completely abstain from smoking during follow-up.
 
●Cilostazol is a phosphodiesterase inhibitor that suppresses platelet aggregation and is a direct arterial vasodilator [89]. It is often used in the treatment of peripheral artery disease. In one small study, flow improvements measured in response to reactive hyperemia were significantly increased after two weeks of cilostazol therapy [90]. Case reports treating patients with digital ischemia with cilostazol have reported improvements in digit pain and ulceration [91].


===Management of ulcers===
===Management of ulcers===
Digit ulcerations are managed as with other ischemic wounds, debridement and moist dressing. Negative pressure wound therapy is becoming popular for the management of open wounds and has been used in the management of open wounds associated with thromboangiitis obliterans [64]. General considerations for the clinical assessment and management of open wounds are discussed in elsewhere. (See "Clinical assessment of wounds" and "Negative pressure wound therapy".)
*Digital ulcers may be treated with [[debridement]] and moist dressing.<ref name="pmid17980686">{{cite journal |vauthors=Canter HI, Isci E, Erk Y |title=Vacuum-assisted wound closure for the management of a foot ulcer due to Buerger's disease |journal=J Plast Reconstr Aesthet Surg |volume=62 |issue=2 |pages=250–3 |date=February 2009 |pmid=17980686 |doi=10.1016/j.bjps.2007.09.031 |url=}}</ref>
 
*[[Negative pressure wound therapy]] may be of benefit in open wounds.  


==References==
==References==

Latest revision as of 19:36, 1 May 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]

Overview

There is no treatment for Buerger's disease. In order to prevent progression and control symptoms, smoking cessation is crucial. Smoking cessation does not reverse damage already caused. Pharmacologic medical therapies for Buerger's disease include smoking cessation, palliative treatments, prostaglandin analogs and phosphodiesterase inhibitors, calcium channel blockers, endothelin receptor antagonists, compression therapy and some experimental therapies. It should be noted, however, that these therapies are purely palliative and do not reverse previous damage caused. Analgesics including NSAIDs and acetaminophen may be used to provide pain relief.

Medical Therapy

Pharmacologic medical therapies for Buerger's disease include smoking cessation, palliative treatments, prostaglandin analogs and phosphodiesterase inhibitors, calcium channel blockers, endothelin receptor antagonists, compression therapy and some experimental therapies. It should be noted, however, that these therapies are purely palliative and do not reverse previous damage caused.[1][2][3]

Smoking cessation

  • Smoking cessation is crucial to the management of Buerger's disease. Not only does smoking cessation halt progression but also controls pain symptoms and decreases the risk of amputation.[1][2][3]
  • The patient may, however, still suffers from intermittent claudication or Raynaud phenomenon.
  • Complete abstinence from smoking is a must as Buerger's disease in susceptible individuals can be triggered by a single cigarette.
  • Any anti-smoking aid containing nicotine such as transdermal patches or gum must be avoided as they may also trigger the disease.
  • Anti-smoking aids such as bupropion or varenicline may be of use and do not contribute to disease progression.
  • A patient that claims to have stopped smoking but continues to suffer symptoms of active disease should be tested for urinary nicotine and cotinine.
  • Previous studies have demonstrated that only 50% of patients with Buerger's disease are able to quit smoking. In these patients, nicotine dependence treatment may be sought.

Iloprost

Calcium channel blockers

Intermittent pneumatic compression

  • Intermittent pneumatic compression (IPC) is used in patients whose main complaint is that of poor circulation and healing in the extremities.[7]
  • IPC is a therapy that is able to increase the flow of blood through the arteries by decreasing the peripheral arterial resistance.

Experimental therapies

Therapeutic angiogenesis

  • Patients with ischemic pain or non-healing ulcers may benefit from therapeutic angiogenesis that uses grow factors, such as intramuscular vascular endothelial growth factor, or through the introduction of a Kirschner wire placed in the medullary canal of the tibia (distraction osteogenesis) in order to promote the generation of blood vessels.[8] [9][10][11]
  • Therapeutic angiogenesis has also demonstrated that it may reduce the occurrence of nocturnal resting pain.

Autologous bone marrow mononuclear cell implantation

  • When traditional revascularization interventions have failed in those with severe peripheral artery disease, autologous bone marrow mononuclear cell implantation may be performed.[8]
  • Autologous bone marrow mononuclear cell implantation may be able to relieve ischemic pain symptoms and decrease ulcer size, whilst increasing walking distance.

Immunoabsorption therapy, bosentan and cilostazol

Analgesia

Management of ulcers

References

  1. ↑ 1.0 1.1 1.2 1.3 Olin JW (September 2000). "Thromboangiitis obliterans (Buerger's disease)". N. Engl. J. Med. 343 (12): 864–9. doi:10.1056/NEJM200009213431207. PMID 10995867.
  2. ↑ 2.0 2.1 2.2 Olin JW, Young JR, Graor RA, Ruschhaupt WF, Bartholomew JR (November 1990). "The changing clinical spectrum of thromboangiitis obliterans (Buerger's disease)". Circulation. 82 (5 Suppl): IV3–8. PMID 2225420.
  3. ↑ 3.0 3.1 Ohta T, Ishioashi H, Hosaka M, Sugimoto I (January 2004). "Clinical and social consequences of Buerger disease". J. Vasc. Surg. 39 (1): 176–80. doi:10.1016/j.jvs.2003.08.006. PMID 14718836.
  4. ↑ "Oral iloprost in the treatment of thromboangiitis obliterans (Buerger's disease): a double-blind, randomised, placebo-controlled trial. The European TAO Study Group". Eur J Vasc Endovasc Surg. 15 (4): 300–7. April 1998. PMID 9610341.
  5. ↑ Fiessinger JN, Schäfer M (March 1990). "Trial of iloprost versus aspirin treatment for critical limb ischaemia of thromboangiitis obliterans. The TAO Study". Lancet. 335 (8689): 555–7. PMID 1689791.
  6. ↑ Bozkurt AK, Köksal C, Demirbas MY, Erdoğan A, Rahman A, Demirkiliç U, Ustünsoy H, Metin G, Yillik L, Onol H, Cinar B, Karaçelik M, Erdinç I, Bolcal C, Sayin AG (June 2006). "A randomized trial of intravenous iloprost (a stable prostacyclin analogue) versus lumbar sympathectomy in the management of Buerger's disease". Int Angiol. 25 (2): 162–8. PMID 16763533.
  7. ↑ Labropoulos N, Watson WC, Mansour MA, Kang SS, Littooy FN, Baker WH (October 1998). "Acute effects of intermittent pneumatic compression on popliteal artery blood flow". Arch Surg. 133 (10): 1072–5. PMID 9790203.
  8. ↑ 8.0 8.1 Isner JM, Baumgartner I, Rauh G, Schainfeld R, Blair R, Manor O, Razvi S, Symes JF (December 1998). "Treatment of thromboangiitis obliterans (Buerger's disease) by intramuscular gene transfer of vascular endothelial growth factor: preliminary clinical results". J. Vasc. Surg. 28 (6): 964–73, discussion 73–5. PMID 9845647.
  9. ↑ Saito S, Nishikawa K, Obata H, Goto F (2007). "Autologous bone marrow transplantation and hyperbaric oxygen therapy for patients with thromboangiitis obliterans". Angiology. 58 (4): 429–34. doi:10.1177/0003319706292015. PMID 17652224.
  10. ↑ Inan M, Alat I, Kutlu R, Harma A, Germen B (March 2005). "Successful treatment of Buerger's Disease with intramedullary K-wire: the results of the first 11 extremities". Eur J Vasc Endovasc Surg. 29 (3): 277–80. doi:10.1016/j.ejvs.2004.12.011. PMID 15694801.
  11. ↑ Kulkarni S, Kulkarni G, Shyam AK, Kulkarni M, Kulkarni R, Kulkarni V (September 2011). "Management of thromboangiitis obliterans using distraction osteogenesis: A retrospective study". Indian J Orthop. 45 (5): 459–64. doi:10.4103/0019-5413.83954. PMC 3162685. PMID 21886930.
  12. ↑ Kim HJ, Jang SY, Park JI, Byun J, Kim DI, Do YS, Kim JM, Kim S, Kim BM, Kim WB, Kim DK (August 2004). "Vascular endothelial growth factor-induced angiogenic gene therapy in patients with peripheral artery disease". Exp. Mol. Med. 36 (4): 336–44. doi:10.1038/emm.2004.44. PMID 15365252.
  13. ↑ De Haro J, Acin F, Bleda S, Varela C, Esparza L (February 2012). "Treatment of thromboangiitis obliterans (Buerger's disease) with bosentan". BMC Cardiovasc Disord. 12: 5. doi:10.1186/1471-2261-12-5. PMC 3306190. PMID 22333218.
  14. ↑ Yasuda K, Sakuma M, Tanabe T (1985). "Hemodynamic effect of cilostazol on increasing peripheral blood flow in arteriosclerosis obliterans". Arzneimittelforschung. 35 (7A): 1198–200. PMID 4074434.
  15. ↑ Canter HI, Isci E, Erk Y (February 2009). "Vacuum-assisted wound closure for the management of a foot ulcer due to Buerger's disease". J Plast Reconstr Aesthet Surg. 62 (2): 250–3. doi:10.1016/j.bjps.2007.09.031. PMID 17980686.

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