Raynaud's Phenomenon

Raynaud's phenomenon is an episodic, reversible constriction of the small blood vessels supplying the fingers and toes — and sometimes the ears, nose, and nipples — triggered by cold exposure or emotional stress. The result is a dramatic color change in the affected digits that can be alarming the first time you see it. The condition ranges from a harmless nuisance in otherwise healthy young women to an early warning sign of serious autoimmune disease — and knowing which type you have changes everything about treatment. Maurice Raynaud, a French physician, first described the condition in Paris in 1862.

  1. Overview — What Is Raynaud's Phenomenon?
  2. Primary vs. Secondary Raynaud's — A Critical Distinction
  3. Causes of Secondary Raynaud's
  4. Clinical Presentation — The Triphasic Color Change
  5. Nailfold Capillaroscopy — The Key Diagnostic Tool
  6. Diagnosis and Laboratory Workup
  7. Treatment — Lifestyle and Medications
  8. Treatment of Secondary Raynaud's and Digital Ulcers
  9. Prognosis
  10. Research Papers
  11. Connections
  12. Featured Videos

Overview — What Is Raynaud's Phenomenon?

At its core, Raynaud's is an exaggerated vasomotor response. In a normal person exposed to cold, the body tightens small blood vessels in the extremities to conserve heat for the vital organs — a sensible survival mechanism. In Raynaud's, this response is dramatically amplified. The arterioles and small arteries supplying the fingers go into intense spasm (vasospasm), effectively cutting off blood flow to the fingertips. The same response can be triggered not just by cold air but by handling a cold drink, reaching into a refrigerator, air conditioning, swimming in cold water, or even acute emotional stress (because the sympathetic nervous system, which drives the fight-or-flight response, uses many of the same pathways as cold-induced vasoconstriction).

The fingers — and less commonly the toes, ears, nose, and nipples — are the most affected areas because they are the most distal from the heart and have the least thermal mass to protect them.

The triphasic color change is the hallmark of Raynaud's and reflects what is happening at the vascular level:

Not every patient shows all three phases. A biphasic change (white then red, skipping the blue) is common. Some patients only notice white and blue without the red flush. A typical episode lasts anywhere from a few minutes to an hour, resolving completely once the hands are warmed. In primary Raynaud's, there is no lasting tissue damage between episodes.

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Primary vs. Secondary Raynaud's — A Critical Distinction

This distinction is arguably the most important thing to understand about Raynaud's. The two types look similar from the outside but have completely different implications for your health.

Primary Raynaud's (Raynaud's Disease)

Primary Raynaud's has no identifiable underlying cause — the vasospasm is the disease itself, driven by genetic predisposition to vasomotor instability. It is extraordinarily common: roughly 10% of young women have some degree of it. Key features:

Secondary Raynaud's (Raynaud's Phenomenon)

Secondary Raynaud's is caused by an identifiable underlying disease. The term "Raynaud's phenomenon" (rather than "disease") technically refers to this secondary form. It is clinically far more important because the underlying disease — not the vasospasm itself — may be the real threat to your health. Key features:

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Causes of Secondary Raynaud's

Connective Tissue Diseases (Most Important Category)

Scleroderma (systemic sclerosis, SSc) is the connective tissue disease most closely associated with Raynaud's — 90 to 95% of SSc patients have it. Crucially, Raynaud's is often the very first symptom of scleroderma, preceding the skin thickening, lung fibrosis, and other manifestations by months to years. When a young person presents with new-onset Raynaud's and abnormal nailfold capillaroscopy, scleroderma must be actively excluded. In SSc, the vessel wall itself becomes fibrotic and narrowed (not just vasospasm), which is why digital ulcers and pitting scars develop. Specific antibodies: anti-Scl-70 (topoisomerase-I) is associated with diffuse cutaneous SSc; anti-centromere antibody is associated with limited cutaneous SSc (the old "CREST syndrome").

Lupus (SLE) causes Raynaud's in 30 to 40% of patients. It is usually milder than in scleroderma and rarely leads to digital ulcers in isolation, though the overall vascular disease of lupus can complicate the picture.

Sjögren's Syndrome carries approximately 30% Raynaud's prevalence — often an underappreciated association. Patients with dry eyes and dry mouth who also have Raynaud's should be tested for Sjögren's.

Mixed Connective Tissue Disease (MCTD) has one of the highest Raynaud's rates of any CTD — up to 85% of patients. The hallmark antibody is anti-U1-RNP.

Dermatomyositis and Polymyositis both carry Raynaud's in a subset of patients, particularly those with anti-synthetase antibodies (anti-Jo-1 and related).

Rheumatoid Arthritis is associated with Raynaud's less commonly than the above, but the association is real and should not be overlooked in someone with joint disease and episodic finger color changes.

Arterial and Mechanical Causes

Buerger's disease (thromboangiitis obliterans) causes inflammatory occlusion of medium and small vessels in young smokers, producing ischemia of the digits that can be mistaken for Raynaud's but is actually fixed arterial obstruction combined with vasospasm.

Atherosclerotic peripheral artery disease (PAD) occurs in older patients with cardiovascular risk factors. The digital ischemia is driven by fixed vessel stenosis rather than vasospasm, though the two can coexist.

Thoracic outlet syndrome involves compression of the subclavian artery (or brachial plexus) by a cervical rib, an abnormal muscle (scalene or pectoralis minor), or post-traumatic scarring. Raynaud's-like symptoms are provoked or worsened by elevating the arm. Doppler ultrasound and provocative maneuvers (Adson's test, elevated arm stress test) can identify this.

Vibration white finger (hand-arm vibration syndrome, HAVS) is an occupational disease in workers who use vibrating tools — chain saws, jackhammers, grinders — for years. Chronic vibration damages both the vessel wall and the peripheral nerves, causing vasospasm alongside numbness. It is a legally recognized occupational injury in many countries.

Hypothenar hammer syndrome causes Raynaud's-like symptoms in the ring and little fingers due to thrombosis of the ulnar artery from repetitive palm trauma (common in carpenters, mechanics, baseball catchers). Ulnar artery occlusion can be confirmed with Allen's test and Doppler ultrasound.

Drug-Induced Raynaud's

Beta-blockers — especially non-selective agents like propranolol — block beta-2 receptors in peripheral blood vessels, leaving alpha-1 vasoconstrictor activity unopposed. Even a patient with only mild underlying Raynaud's tendency can develop severe episodes on a beta-blocker. Avoid non-selective beta-blockers in patients with Raynaud's; if a beta-blocker is clinically necessary, use a cardioselective agent (metoprolol, bisoprolol) at the lowest effective dose.

Ergotamine (used for migraines) causes intense vasoconstriction of peripheral vessels as a side effect of its activity at serotonin and alpha-adrenergic receptors. Even therapeutic doses can provoke severe Raynaud's in susceptible individuals.

Sympathomimetics — decongestants (pseudoephedrine), amphetamines, cocaine — directly stimulate alpha-adrenergic receptors, causing peripheral vasoconstriction. Cocaine, in particular, can cause catastrophic digital ischemia.

Chemotherapy agents — bleomycin and fluorouracil (5-FU) are the most recognized offenders; they cause direct vascular endothelial damage that leads to vasospasm and can persist long after chemotherapy ends.

Cyclosporine, the immunosuppressant used in transplantation and autoimmune disease, causes Raynaud's through its effects on endothelin (a potent vasoconstrictor) and nitric oxide (a vasodilator).

Hematological Causes

Cryoglobulinemia — immunoglobulins (usually IgM rheumatoid factor against IgG) that precipitate in the cold, physically blocking small vessels. The most common cause is chronic hepatitis C infection. Cryoglobulins are best detected by drawing blood into a pre-warmed tube and keeping it warm until processed.

Polycythemia vera causes hyperviscosity of blood, slowing flow through small vessels and making them more susceptible to vasospasm and occlusion in the cold.

Cold agglutinins and paraproteinemia (as in multiple myeloma or Waldenström's macroglobulinemia) can cause similar vessel obstruction in the cold.

Hypothyroidism

This is often overlooked. Thyroid hormone regulates vascular tone and sympathetic reactivity. Hypothyroid patients have reduced cardiac output, lower metabolic rate, and increased peripheral vascular resistance — all of which worsen Raynaud's. Correcting hypothyroidism with thyroid hormone replacement may substantially reduce Raynaud's episodes. A simple TSH should be part of every Raynaud's workup.

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Clinical Presentation — The Triphasic Color Change

Understanding the triphasic color change in detail helps patients recognize their episodes and communicate them to their doctor, and helps clinicians distinguish Raynaud's from other causes of cold hands.

Phase 1: Pallor (White)

An attack begins with sudden, sharply demarcated whitening of the digits. The onset can be almost instantaneous — reaching into a freezer, stepping outside on a cold morning, or even a moment of acute anxiety can trigger it. The fingers feel cold, numb, and in some cases painful. The whiteness is striking because it is sharply bordered: the vasospasm typically starts at a definite line partway up the finger rather than fading gradually. This sharp demarcation is diagnostically important — it distinguishes Raynaud's from the non-specific, diffusely cold hands that nearly everyone experiences in the cold.

During this phase, the tissues are ischemic — they are not receiving enough oxygenated blood. If you press a white finger and release it, the capillary refill is dramatically delayed.

Phase 2: Cyanosis (Blue/Purple)

As the vasospasm continues, the small amount of blood trapped in the vessels becomes deoxygenated as the tissues extract what little oxygen is available. The hemoglobin turns from oxyhemoglobin (red) to deoxyhemoglobin (blue), and the fingers take on a dusky blue or purple hue. The numbness usually continues; some patients experience a deeper aching pain during this phase.

Phase 3: Erythema (Red)

When the vasospasm releases — on entering a warm room, running warm (not hot — too sudden can be uncomfortable) water over the hands, or simply waiting long enough — the vessels dilate rapidly and blood floods back into the previously starved tissue. This reactive hyperemia causes the fingers to turn bright red. The sudden return of blood is often accompanied by a burning, throbbing, or tingling sensation that can be quite uncomfortable. Some patients find the rewarming phase more painful than the ischemic phase.

Triggers

Distribution

Attacks typically start at the fingertips and can spread to involve the whole digit or multiple fingers simultaneously. In primary Raynaud's, the involvement is bilateral and roughly symmetric. Toes are involved in about 40% of patients. Ear tips, the tip of the nose, and nipples are affected in a smaller proportion. Asymmetric involvement — one hand dramatically worse than the other, or only certain fingers on one hand — suggests secondary Raynaud's with a unilateral cause such as thoracic outlet syndrome or hypothenar hammer syndrome.

In secondary Raynaud's, episodes may be more severe (longer duration, more complete blood flow cutoff), more frequent, and may not resolve completely with rewarming if there is a fixed vessel obstruction superimposed on the vasospasm.

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Nailfold Capillaroscopy — The Key Diagnostic Tool

Nailfold capillaroscopy is one of the most underused and most powerful bedside tests in medicine for evaluating Raynaud's. It is inexpensive, non-invasive, takes only a few minutes, and can immediately distinguish primary from secondary Raynaud's in many patients — and even predict which autoimmune disease may be present years before it becomes clinically apparent.

How It Is Done

A drop of immersion oil is placed at the base of the fingernail, and the capillaries in the nailfold skin (the skin that runs along the base of the nail) are examined with a dermatoscope, a widefield microscope, or in specialized centers a video capillaroscope at 200x magnification. The ring finger and middle finger are most commonly examined (they have the most consistent capillary patterns). A normal exam takes only a minute per hand.

Normal Pattern (Primary Raynaud's)

Normal nailfold capillaries form regular, evenly spaced U-shaped hairpin loops arranged in parallel rows. Density is uniform — there are no gaps where capillaries are absent. No hemorrhages (small red dots from broken capillaries). This pattern is seen in people without underlying connective tissue disease, and its presence strongly supports a primary Raynaud's diagnosis.

Scleroderma Pattern (Secondary Raynaud's, Especially SSc)

The following abnormalities, alone or in combination, constitute the "scleroderma pattern" and indicate secondary Raynaud's — most often systemic sclerosis or another connective tissue disease:

An "early scleroderma pattern" — enlarged loops only, without dropout yet — may precede the diagnosis of systemic sclerosis by years. This is why capillaroscopy is recommended in all patients with Raynaud's at their first specialist visit: finding the early pattern allows close monitoring and early treatment before organ damage occurs.

Any scleroderma pattern on capillaroscopy, regardless of antibody status, warrants an aggressive workup for underlying connective tissue disease.

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Diagnosis and Laboratory Workup

The diagnosis of Raynaud's itself is clinical — made from the history and description of the triphasic color change in response to cold or stress. The workup is designed to determine whether the Raynaud's is primary or secondary.

History and Physical Examination

Key questions include: age at onset; sex; whether episodes are bilateral and symmetric; whether there has been any tissue loss (ulcers, pitting scars); what the specific triggers are; complete medication list (beta-blockers, ergotamines, chemotherapy); occupational history (vibrating tools, repetitive palm trauma); and any symptoms of connective tissue disease (dry eyes, dry mouth, rash, joint swelling, skin thickening, shortness of breath, swallowing difficulty).

On examination, assess for digital ulcers or pitting scars (immediate red flag for secondary Raynaud's), skin tightening, joint inflammation, and the asymmetry of involvement. Perform nailfold capillaroscopy at the bedside.

Nailfold Capillaroscopy

As described above, this is the single most informative non-blood test for distinguishing primary from secondary Raynaud's. A normal result strongly supports primary Raynaud's; an abnormal scleroderma pattern mandates further investigation.

Blood Tests

Vascular Studies

Doppler/duplex ultrasound of the upper limb vessels is useful when fixed arterial occlusion is suspected (asymmetric symptoms, absent pulses, suspicion of thoracic outlet syndrome or hypothenar hammer syndrome). It can quantify flow in the radial, ulnar, and digital arteries and detect aneurysm formation at the ulnar artery hook (hypothenar hammer syndrome).

Medication Review

A careful review of all current medications is essential. Stopping a causative drug (beta-blocker, ergotamine) may resolve or substantially reduce Raynaud's without any other treatment.

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Treatment — Lifestyle and Medications

Lifestyle Measures (The Cornerstone of Treatment)

For primary Raynaud's, lifestyle measures alone are often sufficient. For secondary Raynaud's, they are an important adjunct to medical treatment.

Keep the whole body warm, not just the hands. This is the most important and most counterintuitive lifestyle principle. When core body temperature drops even slightly, the body responds with sympathetic activation and peripheral vasoconstriction — the hands then cool down even if they are wearing gloves. Wearing a hat (which prevents significant heat loss), layering the torso with an insulated vest or thermal underlayer, and warming the core first is more effective than gloves in isolation. Chemical hand warmers in gloves or pockets provide supplemental local heat.

Avoid cold triggers systematically. This means: wearing gloves when reaching into the refrigerator or freezer (not just outdoors); requesting that air conditioning be moderated in workplaces; carrying a light cardigan for air-conditioned restaurants and cinemas; using insulated cups for cold drinks; and selecting jobs that minimize cold exposure if Raynaud's is severe.

Stop smoking. Nicotine directly constricts peripheral blood vessels. Even in primary Raynaud's — where the blood vessels are otherwise healthy — smoking significantly increases the frequency and severity of attacks. There is no safe level of smoking for someone with Raynaud's.

Biofeedback and relaxation techniques. Because emotional stress can trigger attacks through sympathetic activation, biofeedback (learning to consciously raise peripheral finger temperature using a thermal feedback device) has shown genuine benefit in controlled trials. Mindfulness, progressive muscle relaxation, and cognitive behavioral approaches to stress management are reasonable adjuncts.

Medication review. Any drug that could be causing or worsening Raynaud's should be stopped or substituted: replace non-selective beta-blockers with cardioselective agents or an alternative antihypertensive (ACE inhibitor, calcium channel blocker, or ARB); stop ergotamine if alternative migraine prophylaxis is available; review stimulants and decongestants.

Calcium Channel Blockers (First-Line Pharmacotherapy)

Calcium channel blockers (CCBs) are the best-evidenced and most widely used drugs for Raynaud's. They work by relaxing the smooth muscle in the walls of blood vessels, preventing the vasospasm that causes episodes.

Nifedipine extended-release (30–60 mg once daily) has the strongest evidence base. Multiple randomized controlled trials show it reduces the frequency and severity of Raynaud's attacks by approximately 50%. It is taken daily as a preventive medication, not just during acute attacks. Side effects include headache, facial flushing, ankle edema, and hypotension — most common in the first few weeks and often improving with time. The extended-release formulation is better tolerated than immediate-release.

Amlodipine (5–10 mg once daily) and felodipine (5–10 mg once daily) are alternatives with equivalent efficacy and once-daily dosing, which aids adherence. Some patients tolerate one dihydropyridine CCB better than another, so switching within the class is a reasonable strategy if side effects are troublesome.

Phosphodiesterase Type 5 (PDE5) Inhibitors

PDE5 inhibitors — best known as erectile dysfunction drugs — promote vasodilation through the cyclic GMP/nitric oxide pathway in blood vessel walls. They are particularly effective in secondary Raynaud's, especially the scleroderma-related form.

Sildenafil (25–50 mg twice daily) and tadalafil (20 mg daily) both have evidence from randomized trials in SSc-related Raynaud's. They reduce the frequency and severity of attacks, and in some studies have been shown to reduce digital ulcer healing time and help prevent new ulcers. Side effects include headache, flushing, and in men, visual changes at higher doses. They can be combined with iloprost infusion for severe disease.

Topical Vasodilators

Glyceryl trinitrate (GTN, nitroglycerin) gel or patch releases nitric oxide locally, relaxing vessel smooth muscle in the area where it is applied. Critically, it should be applied to the forearm (not directly to the fingertips — the concentration would be too high and cause intense headache and paradoxical irritation). A 0.5% GTN gel (available commercially or compounded by a pharmacy) applied to the forearm before anticipated cold exposure significantly reduces attack frequency. The major limiting side effect is headache, which affects the majority of users and limits long-term adherence.

Alpha-1 Adrenergic Blockers

Prazosin (0.5–1 mg twice daily, titrating slowly to reduce hypotension risk) reduces sympathetic vasoconstrictor tone. It is a second-line option for patients who do not respond to or tolerate CCBs. First-dose hypotension and dizziness are the main side effects — the first dose should be taken lying down at night.

Selective Serotonin Reuptake Inhibitors (SSRIs)

Fluoxetine has modest evidence in primary Raynaud's, likely through reduction of serotonin-mediated vasoconstriction (serotonin causes constriction of peripheral vessels). Its role is modest compared to CCBs, but it may be useful in patients who also have anxiety or depression — treating both conditions simultaneously.

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Treatment of Secondary Raynaud's and Digital Ulcers

When Raynaud's is secondary to a connective tissue disease — particularly systemic sclerosis — the stakes are higher. Digital ulcers are painful, slow to heal, vulnerable to infection (including osteomyelitis of the fingertip bones), and in severe cases can lead to amputation. Specialist treatments beyond CCBs are used in this setting.

Iloprost Intravenous Infusion (Standard of Care for Severe SSc-Related Raynaud's)

Iloprost is a synthetic prostacyclin analog — prostacyclin is the body's most potent naturally occurring vasodilator and platelet aggregation inhibitor. Intravenous iloprost is the standard of care for severe Raynaud's and digital ulcers in systemic sclerosis.

It is administered as an inpatient infusion over three to five consecutive days, typically every three to six months (or more frequently if ulcers develop). A large multicenter randomized trial (Wigley et al., Ann Intern Med 1994) established that iloprost infusion significantly reduces the frequency and severity of Raynaud's attacks and promotes healing of existing digital ulcers compared to placebo. It does not cure the underlying disease but provides a meaningful period of improved perfusion. The main side effects are headache, flushing, nausea, and hypotension during the infusion — managed by slow titration of the infusion rate.

Bosentan (Endothelin Receptor Antagonist)

Bosentan is an oral drug that blocks endothelin — one of the body's most potent vasoconstrictors — at both endothelin receptor subtypes. The RAPIDS-2 trial (Matucci-Cerinic et al., Ann Rheum Dis 2011) was a large randomized double-blind placebo-controlled study showing that bosentan significantly reduced the number of new digital ulcers appearing in SSc patients over the treatment period. Importantly, it did not speed up healing of ulcers that were already present at the start of treatment. Bosentan is therefore most useful as a preventive treatment in patients who keep developing new ulcers despite other therapy. It is approved for this indication in Europe. Liver toxicity is the main risk — monthly liver function tests are required during treatment. It is also teratogenic (causes serious birth defects) and contraindicated in pregnancy.

Riociguat (Soluble Guanylate Cyclase Stimulator)

Riociguat works through the same nitric oxide/cGMP pathway as PDE5 inhibitors but at a different point in the chain — it stimulates the enzyme that produces cGMP directly, even without nitric oxide as a signal. Emerging evidence supports its use in SSc-related Raynaud's. It is already established in pulmonary arterial hypertension (which commonly complicates SSc) and may offer dual benefit in SSc patients with both pulmonary hypertension and severe Raynaud's.

Digital Sympathectomy (Surgical)

In patients with severe digital ischemia — ulcers, threatened amputation — refractory to all medical therapy, surgical digital sympathectomy (stripping the sympathetic nerve fibers that surround the digital arteries) can provide relief. The benefit is real but time-limited: sympathetic reinnervation occurs over months to years, and symptoms gradually return. It is a last resort when other treatments have failed and tissue loss is imminent or ongoing.

Wound Care for Digital Ulcers

Digital ulcers require careful wound management. The principles are: keep the wound clean and moist using non-adherent dressings; protect the ulcer from trauma with padding; monitor for signs of infection (increasing redness, warmth, purulent discharge, fever). If infection is present, treat with antibiotics covering Staphylococcus aureus — oral antibiotics for superficial infection, intravenous antibiotics and bone biopsy for suspected osteomyelitis of the distal phalanx. Aggressive surgical debridement should be avoided unless necrotic tissue is clearly demarcated and the risk of spreading infection outweighs the risk of healing disruption.

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Prognosis

Primary Raynaud's

The long-term outlook for primary Raynaud's is excellent. The vast majority of patients manage their condition well with a combination of lifestyle modifications and, where needed, a calcium channel blocker. There is no risk of tissue loss, organ damage, or shortened life expectancy from primary Raynaud's itself. Symptoms may fluctuate with the seasons (worse in winter, better in summer) and often improve with age. The condition does not in itself progress to a more serious disease.

The one important caveat: approximately 5 to 10% of patients initially classified as primary Raynaud's will eventually develop an underlying connective tissue disease — most often within the first five years after diagnosis, but sometimes later. This risk is higher in patients who have a positive ANA at first presentation (even with an otherwise normal workup) or who develop any abnormality on follow-up nailfold capillaroscopy. For this reason, a single follow-up visit one to two years after diagnosis is reasonable, even in apparently primary cases.

Secondary Raynaud's

The prognosis depends almost entirely on the underlying disease. Raynaud's associated with Sjögren's syndrome or MCTD tends to be milder and carries less risk of tissue loss. Raynaud's in systemic sclerosis carries significant morbidity from digital ulcers — estimates suggest that 30 to 50% of SSc patients with Raynaud's develop at least one digital ulcer over the course of their disease. Early treatment with iloprost infusions and bosentan has substantially reduced the rates of ulcer progression and amputation in specialist centers compared to historical controls.

Red Flags That Warrant Specialist Investigation

Any of these features should prompt referral to a rheumatologist for full evaluation even if the initial presentation appeared to be primary Raynaud's.

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Research Papers

  1. Wigley FM, Flavahan NA. Raynaud's Phenomenon. N Engl J Med. 2016;375(6):556–565. PMID: 27509103
  2. Garner R, Kumari R, Lanyon P, Doherty M, Zhang W. Prevalence, risk factors and associations of primary Raynaud's phenomenon: systematic review and meta-analysis of observational studies. BMJ Open. 2015;5(3):e006389. PMID: 25748464
  3. Herrick AL. The pathogenesis, diagnosis and treatment of Raynaud phenomenon. Nat Rev Rheumatol. 2012;8(8):469–479. PMID: 22782006
  4. Cutolo M, Sulli A, Smith V. How to perform and interpret capillaroscopy. Best Pract Res Clin Rheumatol. 2013;27(2):237–248. PMID: 23910558
  5. Matucci-Cerinic M, Denton CP, Furst DE, et al. Bosentan treatment of digital ulcers related to systemic sclerosis: results from the RAPIDS-2 randomised, double-blind, placebo-controlled trial. Ann Rheum Dis. 2011;70(1):32–38. PMID: 20833734
  6. Fries R, Shariat K, von Wilmowsky H, Böhm M. Sildenafil in the treatment of Raynaud's phenomenon resistant to vasodilatory therapy. Circulation. 2005;112(19):2980–2985. PMID: 16275884
  7. Baumhäkel M, Böhm M. Recent achievements in the management of Raynaud's phenomenon. Vasc Health Risk Manag. 2010;6:207–214. PMID: 20448800
  8. Thompson AE, Shea B, Welch V, Fenlon D, Pope JE. Calcium-channel blockers for Raynaud's phenomenon in systemic sclerosis. Arthritis Rheum. 2001;44(8):1841–1847. PMID: 11508435
  9. Cooke JP, Marshall JM. Mechanisms of Raynaud's disease. Vasc Med. 2005;10(4):293–307. PMID: 16444863
  10. Lambova SN, Müller-Ladner U. The role of capillaroscopy in differentiation of primary and secondary Raynaud's phenomenon in rheumatic diseases: a review of the literature and two case reports. Rheumatol Int. 2009;29(11):1263–1271. PMID: 19418041
  11. Chung L, Shapiro L, Fiorentino D, et al. MQX-503, a novel formulation of nitroglycerin, improves the severity of Raynaud's phenomenon: a randomized, controlled trial. Arthritis Rheum. 2009;60(3):870–877. PMID: 19248109
  12. Wigley FM, Wise RA, Seibold JR, et al. Intravenous iloprost infusion in patients with Raynaud phenomenon secondary to systemic sclerosis. A multicenter, placebo-controlled, double-blind study. Ann Intern Med. 1994;120(3):199–206. PMID: 8273988

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Connections

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