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Systemic Lupus Erythematosus and Its Effects on the Foot
Posted: Jul 12, 2025
Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease characterized by widespread inflammation and tissue damage across multiple organ systems. The condition arises from the immune system attacking healthy tissues, leading to a variety of symptoms that can affect virtually any part of the body, including the musculoskeletal system. While SLE is commonly associated with joint pain, skin rashes, and systemic complications, its impact on the foot is often underrecognized despite being a significant source of morbidity. This essay explores how SLE affects the foot, focusing on its biomechanical, vascular, neurological, and dermatological manifestations, as well as diagnostic challenges, clinical implications, and management strategies.
Overview of Systemic Lupus Erythematosus
SLE is a complex autoimmune disorder with a prevalence of approximately 20–150 cases per 100,000 people, predominantly affecting women of childbearing age. The disease is characterized by periods of flares and remission, with symptoms ranging from mild to life-threatening. The American College of Rheumatology criteria for SLE diagnosis include clinical and immunological features such as malar rash, photosensitivity, arthritis, and positive antinuclear antibodies. The foot, as a weight-bearing structure, is particularly vulnerable to the inflammatory, vascular, and neurological changes induced by SLE, which can significantly impair mobility and quality of life.
Biomechanical and Musculoskeletal Effects
One of the most common manifestations of SLE in the foot is musculoskeletal involvement, particularly arthritis and tenosynovitis. Lupus arthritis is typically non-erosive, symmetrical, and polyarticular, affecting small joints such as those in the foot. The metatarsophalangeal joints (MTPJs) and proximal interphalangeal joints (PIPJs) are frequently involved, leading to pain, swelling, and stiffness. Unlike rheumatoid arthritis, lupus arthritis rarely causes joint destruction, but chronic inflammation can result in deformities such as hallux valgus or hammertoes due to synovitis and ligamentous laxity.
Tenosynovitis, inflammation of the tendon sheaths, is another common feature in SLE and can affect tendons in the foot, such as the tibialis posterior or peroneal tendons. This condition leads to pain and functional limitations, particularly during weight-bearing activities. For example, tibialis posterior tenosynovitis can contribute to pes planus (flatfoot), altering foot biomechanics and increasing stress on surrounding structures. These changes may exacerbate symptoms during gait, leading to compensatory movements and secondary issues like plantar fasciitis or Achilles tendinopathy.
Muscle weakness and myalgia, though less common, can also affect the foot in SLE. Inflammatory myopathy may weaken intrinsic foot muscles, compromising arch support and stability. This can result in fatigue, altered gait patterns, and increased risk of overuse injuries. In severe cases, joint and tendon involvement can lead to significant functional impairment, making walking or standing painful and challenging.
Vascular and Circulatory Complications
SLE is associated with vascular complications that can profoundly affect the foot. Raynaud’s phenomenon, a common feature in SLE, is characterized by vasospasm of small blood vessels in response to cold or stress, leading to color changes, numbness, and pain in the toes. In the foot, Raynaud’s can cause discomfort during cold weather, impairing circulation and increasing the risk of tissue ischemia. Chronic or severe episodes may lead to digital ulcers or gangrene, particularly in patients with coexisting antiphospholipid syndrome, which increases the risk of thrombosis.
Antiphospholipid syndrome, present in approximately 30–40% of SLE patients, predisposes individuals to microvascular and macrovascular thrombosis. In the foot, this can manifest as ischemic lesions, ulcerations, or even osteonecrosis of bones such as the talus or metatarsals. Osteonecrosis, also known as avascular necrosis, results from disrupted blood supply to the bone, leading to pain, structural collapse, and impaired foot function. These vascular complications underscore the importance of monitoring peripheral circulation in SLE patients, as foot involvement can significantly impact mobility.
Neurological Manifestations
Neurological involvement in SLE, often referred to as neuropsychiatric lupus, can also affect the foot. Peripheral neuropathy, reported in up to 20% of SLE patients, may present as sensory or motor deficits in the lower extremities. In the foot, this can manifest as numbness, tingling, or burning sensations, particularly in a distal distribution. These symptoms can mimic diabetic neuropathy, complicating diagnosis in patients with overlapping conditions. Sensory neuropathy increases the risk of unnoticed injuries, such as cuts or blisters, which may become infected due to impaired immune responses in SLE.
Autonomic neuropathy, though less common, can disrupt sweat gland function and skin integrity, leading to dry, cracked skin on the feet. This increases susceptibility to infections, particularly in patients with compromised immune systems due to immunosuppressive therapy. In rare cases, mononeuritis multiplex—a condition involving multiple peripheral nerves—can cause focal weakness or sensory loss in the foot, further impairing gait and balance.
Dermatological Effects
The skin of the foot is frequently affected in SLE due to the disease’s propensity for cutaneous manifestations. Lupus-specific skin lesions, such as acute cutaneous lupus erythematosus, may present as erythematous, scaly patches on the dorsum of the foot or toes, often exacerbated by sun exposure. Subacute cutaneous lupus, characterized by psoriasiform or annular lesions, can also occur in the foot, causing discomfort and cosmetic concerns. There is also Chilblain Lupus Erythematosus
Chronic discoid lupus lesions, though less common in the foot, may lead to scarring and skin atrophy, particularly in weight-bearing areas like the heel. Vasculitic lesions, such as palpable purpura or livedo reticularis, can also affect the foot, reflecting underlying small vessel inflammation. These dermatological changes not only cause pain but also increase the risk of secondary infections, especially in patients with poor wound healing due to vascular or immunosuppressive factors.
Diagnostic Challenges
Diagnosing SLE-related foot involvement requires a multidisciplinary approach, as symptoms may overlap with other conditions such as rheumatoid arthritis, gout, or peripheral vascular disease. A thorough clinical history and physical examination are essential, focusing on joint swelling, skin changes, and neurological symptoms. Laboratory tests, including antinuclear antibodies, anti-double-stranded DNA, and complement levels, support the diagnosis of SLE but are not specific to foot involvement.
Imaging modalities, such as X-rays, ultrasound, or magnetic resonance imaging (MRI), can assess joint inflammation, tenosynovitis, or osteonecrosis. For example, ultrasound is particularly useful for detecting synovitis and tendon pathology, while MRI can identify early osteonecrosis. Vascular studies, such as Doppler ultrasound, may be indicated in patients with suspected Raynaud’s or thrombosis. Skin biopsies of suspicious lesions can confirm lupus-specific dermatological changes.
Clinical Implications and Management
The impact of SLE on the foot has significant implications for patient mobility, quality of life, and overall disease management. Pain and deformity in the foot can limit physical activity, contributing to deconditioning and exacerbating systemic symptoms. Furthermore, foot complications increase the risk of infections and hospitalizations, particularly in patients on immunosuppressive therapies such as corticosteroids or biologics.
Management of SLE-related foot involvement is multifaceted, focusing on controlling systemic inflammation, alleviating symptoms, and preventing complications. Pharmacological treatment includes nonsteroidal anti-inflammatory drugs (NSAIDs) for mild arthritis, corticosteroids for acute flares, and disease-modifying antirheumatic drugs (DMARDs) such as hydroxychloroquine or methotrexate for long-term control. Biologics, such as belimumab, may be considered in refractory cases.
Non-pharmacological interventions are equally important. Custom orthotics and supportive footwear can alleviate biomechanical stress, improve gait, and reduce pain in patients with arthritis or flatfoot deformity. Physical therapy, including exercises to strengthen foot muscles and improve joint mobility, is beneficial for maintaining function. For patients with Raynaud’s, keeping the feet warm with insulated socks and avoiding cold exposure are critical preventive measures.
Dermatological management involves topical corticosteroids or calcineurin inhibitors for localized skin lesions, along with strict sun protection to prevent exacerbations. Wound care is essential for ulcerations or infections, particularly in patients with neuropathy or vascular compromise. In cases of osteonecrosis or severe deformity, surgical interventions such as joint fusion or osteotomy may be required, though these are rare.
Conclusion
Systemic Lupus Erythematosus profoundly affects the foot through its musculoskeletal, vascular, neurological, and dermatological manifestations. These effects can lead to pain, deformity, and functional impairment, significantly impacting patients’ quality of life. Early recognition and comprehensive management are crucial to mitigate complications and preserve mobility. By addressing both systemic and localized aspects of the disease, clinicians can improve outcomes for SLE patients with foot involvement. Ongoing research into the mechanisms of SLE and its peripheral manifestations will further enhance our understanding and treatment of this complex condition, ensuring better care for those affected.
About the Author
Craig Payne is a University lecturer, runner, cynic, researcher, skeptic, forum admin, woo basher, clinician, rabble-rouser, blogger and a dad.
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