Treatment of vasospastic disease with prostaglandin E1.

Clifford, P. C.; Martin, M. F. R.; Sheddon, E J; Kirby, John D.; Baird, R. N.; Dieppe, P A

doi:10.1136/bmj.281.6247.1031

Cited by 99 publications

(24 citation statements)

References 18 publications

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“…Effi cacy has been documented in multiple randomised trials [64 -70] and has also been demonstrated in systematic reviews and meta-analyses [30,71]. Whereas the evidence is excellent for the effi cacy of the prostacyclin (prostaglandin I2; PGI2) analogue iloprost, the situation is less clear for alprostadil (prostaglandin E1; PGE1) [66,67]. Usually, iloprost is administered intravenously at an infusion rate of 0.5 -2.0 ng/kg/minute over six hours on at least fi ve subsequent days.…”

Section: Intravenous Prostanoidsmentioning

confidence: 99%

Raynaud’s phenomenon and digital ischaemia - pharmacologic approach and alternative treatment options

Linnemann

Erbe

2016

Vasa

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Summary:The primary goal of therapy is to reduce the frequency and intensity of Raynaud's attacks and to minimize the related morbidity rather than to cure the underlying condition. Treatment strategies depend on whether Raynaud's phenomenon (RP) is primary or secondary. All patients should be instructed about general measures to maintain body warmth and to avoid triggers of RP attacks. Pharmacologic intervention can be useful for patients with severe and frequent RP episodes that impair the patient's quality of life. Calcium channel blockers are currently the most prescribed and studied medications for this purpose. There has been limited evidence for the effi cacy of alpha-1-adrenergic receptor antagonists, angiotensin receptor blockers, topical nitrates or fl uoxetine to treat RP. The intravenously administered prostacyclin analogue iloprost can reduce the frequency and severity of RP attacks and is considered a second-line therapy in patients with markedly impaired quality of life, critical digital ischaemia and skin ulcers who are at risk for substantial tissue loss and amputation. Phosphodiesterase inhibitors (e.g., sildenafi l) can also improve RP symptoms and ulcer healing whereas endothelin-1 receptor antagonists (e.g., bosentan) are mainly considered treatment options in secondary prevention for patients with digital skin ulcers related to systemic sclerosis. However, their use in clinical practice has been limited by their high cost. Antiplatelet therapy with low-dose aspirin is recommended for all patients who suffer from secondary RP due to ischaemia caused by structural vessel damage. Anticoagulant therapy can be considered during the acute phase of digital ischaemia in patients with suspected vascular occlusive disease attributed to the occurrence of new thromboses. In patients with critical digital ischaemia, consideration should be given to hospitalisation, optimisation of medical treatment in accordance with the underlying disease and evaluation for a secondary, possibly reversible process that is causing or aggravating the clinical symptoms.

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Section: Intravenous Prostanoidsmentioning

confidence: 99%

Raynaud’s phenomenon and digital ischaemia - pharmacologic approach and alternative treatment options

Linnemann

Erbe

2016

Vasa

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“…Prostaglandin E1 (PGE1), a potent vasodilator and platelet aggregation inhibitor, is well known as a useful drug for peripheral arterial disease, such as Raynaud's and Burerger's diseases [59] , and diabetic neuropathy [60] . PGE1 has been reported to relax the contraction of vascular smooth muscle cells [61] and increase blood flow in peripheral arteries [62] , followed by improvement of endothelial function [63] .…”

Section: Effect Of Prostaglandin-e1 To Normal Nerve Root and Compressmentioning

confidence: 99%

Pathophysiology, diagnosis and treatment of intermittent claudication in patients with lumbar canal stenosis

Kobayashi

2014

WJO

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Spinal nerve roots have a peculiar structure, different from the arrangements in the peripheral nerve. The nerve roots are devoid of lymphatic vessels but are immersed in the cerebrospinal fluid (CSF) within the subarachnoid space. The blood supply of nerve roots depends on the blood flow from both peripheral direction (ascending) and the spinal cord direction (descending). There is no hypovascular region in the nerve root, although there exists a so-called water-shed of the bloodstream in the radicular artery itself. Increased mechanical compression promotes the disturbance of CSF flow, circulatory disturbance starting from the venous congestion and intraradicular edema formation resulting from the breakdown of the blood-nerve barrier. Although this edema may diffuse into CSF when the subarachnoid space is preserved, the endoneurial fluid pressure may increase when the area is closed by increased compression. On the other hand, the nerve root tissue has already degenerated under the compression and the numerous macrophages releasing various chemical mediators, aggravating radicular symptoms that appear in the area of Wallerian degeneration. Prostaglandin E1 (PGE1) is a potent vasodilator as well as an inhibitor of platelet aggregation and has therefore attracted interest as a therapeutic drug for lumbar canal stenosis. However, investigations in the clinical setting have shown that PGE1 is effective in some patients but not in others, although the reason for this is unclear.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved.Key words: Lumbar canal stenosis; Cauda equine; Nerve root; Prostaglandin E1; Blood flow Core tip: The radicular symptoms associated with degenerative disease of the lumbar spine are reported to be attributable to a combination of mechanical nerve root compression and resultant circulatory disturbance. Disturbance of blood flow in the cauda equina and nerve roots is reported to play an important role in the mechanism of intermittent claudication in patients with lumbar canal stenosis. Prostaglandin E1 (PGE1) is a potent vasodilator as well as an inhibitor of platelet aggregation and has therefore attracted interest as a therapeutic drug for lumbar canal stenosis with intermittent claudication. However, investigations in the clinical setting have shown that lipo-PGE1 is effective in some patients but not in others, although the reason for this is unclear.Kobayashi S. Pathophysiology, diagnosis and treatment of intermittent claudication in patients with lumbar canal stenosis. World

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“…PGE1 has strong peripheral vasodilating activity and platelet aggregation-inhibiting activity, and its usefulness has been con®rmed both for the treatment of chronic arterial obstruction and other ischemic diseases and for the maintenance of blood circulation after blood vessel reconstruction. 11,12 However, it is not yet clear whether PGE1 improves blood circulation in the cauda equina and nerve root of patients with lumbar spinal canal stenosis.…”

Section: Introductionmentioning

confidence: 99%

The effect of Lipo prostaglandin E1 on cauda equina blood flow in patients with lumbar spinal canal stenosis: myeloscopic observation

1999

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Study Design: Myeloscopic examination was performed to observe the cauda equina in patients with lumbar spinal canal stenosis before and after treatment with Lipo prostaglandin E1, a strong peripheral vasodilator. Objectives: The purpose of this study was to clarify the e ects of Lipo prostaglandin E1 on blood¯ow in the cauda equina in patients with lumbar spinal canal stenosis. Setting: Japan, Kagoshima Methods: We performed myeloscopic observations of morphological changes in blood vessels running along the cauda equina in 11 patients with lumbar spinal canal stenosis before and after treatment with Lipo prostaglandin E1. Results: In six of these patients, dilation of the running blood vessels was observed immediately after administration. In all of the patients who exhibited a dilation of vessels on the surface of the cauda equina, intermittent claudication and lower extremity pain and/or numbness lessened immediately after examination. However, none of the patients who exhibited no morphological changes in the vessels along the cauda equina after administration of Lipo prostaglandin E1 experienced any improvement of symptoms at the time of examination. Conclusion: Results of this study suggest that Lipo prostaglandin E1 may enhance blood ow in the cauda equina and improve clinical symptoms in some patients with lumbar spinal stenosis. Sponsorship: None

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Treatment of vasospastic disease with prostaglandin E1.

Cited by 99 publications

References 18 publications

Raynaud’s phenomenon and digital ischaemia - pharmacologic approach and alternative treatment options

Raynaud’s phenomenon and digital ischaemia - pharmacologic approach and alternative treatment options

Pathophysiology, diagnosis and treatment of intermittent claudication in patients with lumbar canal stenosis

The effect of Lipo prostaglandin E1 on cauda equina blood flow in patients with lumbar spinal canal stenosis: myeloscopic observation

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