Scleroderma: Symptoms, Causes, Diagnosis, Treatment & Prevention
PACE Hospitals
Written by: Editorial Team
Medically reviewed by: Dr. Shweta Bhardwaj - Consultant Rheumatologist and Clinical Immunologist
Overview | Prevalence | Types | Symptoms | Causes | Risk Factors | Complications | Diagnosis | Treatment | Prevention | Scleredema vs scleroderma | FAQs | When to consult a Doctor
Scleroderma definition
Scleroderma is a rare, chronic autoimmune connective tissue disorder in which the body's immune system causes excessive collagen production, leading to hardening and tightening of the skin and internal organs. Common symptoms include skin thickening and stiffness, shiny or tight skin on fingers, hands, or face, Raynaud's phenomenon (fingers turn white or blue in cold), joint pain, fatigue, difficulty swallowing, shortness of breath, and digestive problems (acid reflux, bloating, or constipation).
The exact cause of this disease is not known. However, it is believed to be a combination of genetic predisposition, immunological dysfunction, and environmental triggers. If not treated on time, it may lead to pulmonary hypertension, kidney crisis, digestive dysfunction, and restricted mobility.
A rheumatologist, a doctor specialised in autoimmune and connective tissue disorders, can accurately diagnose and provide the correct treatment for scleroderma.
Scleroderma meaning
The word scleroderma originates from the two Greek words
- “skleros” meaning hard
- “derma” meaning skin.
Together, scleroderma literally means “hard skin”, reflecting the hallmark feature of the disease, thickening and hardening of the skin due to excessive collagen deposition.
Scleroderma Incidence
Scleroderma incidence Worldwide
Incidence rates for scleroderma vary significantly worldwide, but recent global estimates suggest an overall systemic sclerosis (SSc) incidence of approximately 1.4 to 8.64 new cases per 100,000 people per year. A 2023 study estimated the global annual SSc incidence at 8.64 per 100,000 person-years and the global prevalence at 18.87 cases per 100,000 people.
Scleroderma incidence in India
Incidence data for scleroderma in India are limited, but a study from 2025 reported an incidence rate of 15.1 cases per 100,000 individuals as of 2016. However, significant geographical variations in clinical presentation and serological profiles have been observed in different regions of the country.
Types of Scleroderma
Scleroderma is a rare connective tissue condition characterized by skin hardening and tightness. It can affect only the skin or involve internal organs as well. The disease is classified into different types of scleroderma based on the extent and areas of involvement. Scleroderma classification is as follows:
- Localised scleroderma
- Circumscribed morphea
- Linear scleroderma
- Generalized scleroderma
- Systemic scleroderma
- Limited cutaneous scleroderma
- Diffuse cutaneous systemic scleroderma
- Systemic sclerosis sine scleroderma
Localized Scleroderma
Localised scleroderma affects the skin and underlying tissues, such as fat, muscle, or bone, without involving internal organs. It is generally less severe than systemic forms and often occurs in children or young adults. Localised scleroderma subtypes are:
- Circumscribed morphea: This form, also called plaque morphea, presents as one or more oval or round patches of hardened, thickened skin that may appear ivory or purple in colour. The lesions are generally confined to specific body areas, most commonly the trunk or limbs. Over time, these plaques may soften but can leave behind areas of pigmentation or scarring.
- Linear scleroderma: This is identified by a band or line of hard skin that runs down the face, arm, or leg in a linear pattern. It also affects deeper tissues, like muscles and bones, causing growth abnormalities or deformities, particularly in children. A subtype known as "en coup de sabre" affects the forehead and scalp and resembles a scar from a sword stroke.
- Generalised scleroderma: This type of scleroderma involves multiple widespread morphea lesions that merge together, covering large areas of the skin. Although internal organs are usually not affected, this form can cause significant skin tightening and restricted movement, making it more disabling than localised forms like plaque or linear morphea.
Systemic Scleroderma (systemic sclerosis)
Systemic scleroderma affects not only the skin but also internal organs, including the lungs, heart, kidneys, and gastrointestinal tract, due to abnormal collagen buildup. It is an autoimmune disease with variable severity and prognosis.
- Limited cutaneous scleroderma: Limited cutaneous systemic scleroderma mainly involves skin thickening of the face, hands, and forearms. It progresses slowly and is often associated with the CREST syndrome, calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia. Internal organ involvement, such as pulmonary hypertension, can occur later in the disease course.
- Diffuse cutaneous systemic scleroderma: Diffuse cutaneous systemic scleroderma causes widespread skin hardening, including the trunk and proximal limbs, and often progresses rapidly. It has a higher risk of early internal organ involvement, particularly affecting the lungs, kidneys, and heart. Because of its aggressive course, early diagnosis and management are crucial to prevent complications.
- Systemic sclerosis sine scleroderma: Sine sclerosis is a type of systemic scleroderma that affects internal organs but does not cause noticeable skin thickness. Even when there are no skin symptoms, patients can develop Raynaud's phenomenon, lung fibrosis, or gastrointestinal problems, making diagnosis more difficult.
Scleroderma Symptoms
Scleroderma causes a wide range of clinical features that vary depending on the severity and type of the disease. Symptoms can affect the skin, blood vessels, and internal organs, often developing gradually. Recognising these symptoms early is important for timely diagnosis and management.
The most common scleroderma signs and symptoms are:
- Skin thickening and hardening
- Raynaud's phenomenon
- Skin discolouration
- Small white calcium deposits
- Sores and pitted scars
- Joint pain, stiffness, and swelling,
- Skin temperature changes
- Heartburn and acid reflux
- Dysphagia (difficulty swallowing)
- Bowel problems
- Shortness of breath
- Abnormal heartbeat
- Scleroderma renal crisis
Skin thickening and hardening: In scleroderma, immune system dysfunction causes fibroblasts to produce excessive collagen, leading to fibrosis. This results in thick, tight, and hardened skin, particularly on the fingers, hands, and face, and sometimes on the trunk and limbs. The fibrosis reduces skin elasticity and limits movement in affected areas.
Raynaud's phenomenon: This occurs because the disease damages the small blood vessels and disrupts normal blood flow, particularly in fingers and toes. In response to cold or stress, these vessels constrict excessively, causing colour changes (white, blue, red), numbness, and pain.
Skin discoloration: The abnormal collagen deposition disrupts normal skin pigmentation. This can cause patches of lighter or darker skin due to damage to pigment cells and changes in blood supply.
Small white calcium deposits: This is also known as calcinosis; these deposits form under the skin in response to chronic inflammation and tissue damage. They appear as hardened lumps, sometimes painful, and can break through the skin, causing ulcers or infections.
Sores and pitted scars: Poor blood supply, combined with skin fibrosis and calcinosis, can cause ulcers or wounds on the fingertips and toes, leading to pitting scars. These are slow to heal due to impaired circulation.
Joint pain, stiffness, and swelling: In scleroderma, fibrosis can extend into the connective tissues around joints and tendons, causing reduced mobility. This can lead to joint discomfort, edema, and stiffness. Over time, the skin and nearby tissues may become tighter, this can lead to joint contractures, which limit movement and function even more.
Skin temperature changes: Vascular damage can impair the ability to regulate blood flow and temperature, leading to cold and pale extremities or alternating hot and cold sensations.
Heartburn and acid reflux: Scleroderma involvement of the esophagus causes muscle dysfunction and weakened sphincter control, allowing stomach acids to reflux into the esophagus, causing discomfort and damage.
Dysphagia (difficulty swallowing): Choking, aspiration risk, and nutritional deficiencies result from swallowing difficulties caused by esophageal smooth muscle fibrosis and motility disruption.
Bowel problems: Fibrosis of intestinal muscles disrupts normal bowel movements, leading to symptoms such as bloating, diarrhea, constipation, and bacterial overgrowth. Gastrointestinal problems are a major cause of discomfort and health decline because impaired absorption can result in malnutrition.
Shortness of breath: Scleroderma can cause lung fibrosis and pulmonary arterial hypertension, both of which impair oxygen exchange and blood flow. These changes lead to progressive breathlessness, especially with activity, and reduce overall function and survival.
Abnormal heartbeat: Cardiac involvement can cause scarring of the heart muscle or its conducting system, leading to irregular heart rhythms, reduced cardiac output, or heart failure.
Scleroderma renal crisis: Scleroderma renal crisis is a fatal condition caused by the sudden narrowing of renal blood arteries, which results in severe
hypertension and rapid
kidney failure. It reflects acute vascular injury and fibrosis in renal arteries.
Scleroderma Causes
The cause of scleroderma is not fully understood, but it is believed to result from a complex interaction of immune, genetic, and environmental factors that lead to abnormal collagen buildup in tissues.
- Genetic predisposition
- Immune system factors
- Environmental and occupational triggers
Genetic predisposition: Certain genetic variations raise the risk of developing scleroderma. Research indicates that it can run in families, particularly among people who carry specific HLA (human leukocyte antigen) genes and non-HLA genes (e.g., PTPN22, STAT4) that influence immunological response. However, the condition is not directly inherited.
Immune system factors: In scleroderma, abnormal immune activation triggers chronic inflammation and collagen overproduction, leading to fibrosis of the skin and organs. Key immune mediators, such as transforming growth factor-beta (TGF-β) and interleukin-6 (IL-6), worsen tissue damage, while autoantibodies and vascular injury further drive disease progression.
Environmental and occupational triggers: Exposure to some environmental factors can cause the disease in genetically predisposed people. This includes:
- Silica dust (in miners and stoneworkers)
- Organic solvents
- Certain chemotherapeutic medicines
- Viral infections (such as cytomegalovirus, Epstein–Barr virus) have also been suggested as potential triggers.
Scleroderma Risk Factors
Risk factors for scleroderma include a combination of genetic and environmental factors, along with certain demographic traits. While the exact cause is unknown, these factors can increase a person's risk of developing the condition.
These factors are:
- GenderS
- Age
- Genetic background
- Race and ethnicity
- Smoking
- Coexisting autoimmune conditions
- Environmental exposure
Gender: Scleroderma is significantly more common in women than men, with approximately a 7:1 female predominance. Hormonal factors are thought to increase autoimmune activation and fibrosis, making women more susceptible. However, when men develop scleroderma, the disease tends to be more severe and diffuse, with higher anti–Scl-70 antibody levels and poorer survival.
Age: Most cases of scleroderma appear between the ages of 30 and 50, though localised forms can affect children. With age, the immune system undergoes regulatory changes, which may trigger autoimmune reactions in genetically predisposed individuals. Early-onset cases tend to be milder (localised), while later-onset forms often have more systemic and internal organ involvement.
Genetic background: Certain gene variants, especially in immune-related loci such as the HLA complex and cytokine regulators, increase susceptibility to scleroderma. Familial clustering of autoimmune diseases suggests heritable components that influence immune dysregulation and fibrosis pathways, although the diseases are not directly inherited.
Race and ethnicity: Ethnic background affects both the likelihood and severity of scleroderma. African Americans have a higher incidence and tend to develop more diffuse and severe forms, often with lung or kidney complications. Native Americans (particularly the Choctaw tribe) also show higher prevalence.
Smoking: Cigarette smoking is an environmental risk factor that worsens vascular damage and immune dysfunction, both central in scleroderma pathogenesis. Smoking can aggravate Raynaud’s phenomenon, delay wound healing and increase fibrosis by enhancing oxidative stress and endothelial injury.
Coexisting autoimmune conditions: Patients with coexisting or other autoimmune diseases, like systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA), have an increased risk of overlapping scleroderma features. Shared immune dysregulation may predispose individuals to multiple connective tissue disorders.
Environmental exposure: Exposure to some environmental toxins has been linked to scleroderma-like conditions. These include:
- Silica dust (among miners, stonecutters, and construction workers)
- Organic solvents
- Vinyl chloride (used in plastic manufacture)
These compounds can harm the vascular endothelium and cause abnormal immune responses and altered collagen synthesis, resulting in the development of scleroderma or the aggravation of its symptoms.
Scleroderma Complications
Scleroderma can cause widespread fibrotic, autoimmune, and vascular problems that damage the skin and internal organs, resulting in severe impairment and morbidity. The major complications involve the skin, lungs, heart, kidneys, gastrointestinal tract, musculoskeletal system, and oral structures. The following are the complications of scleroderma:
- Cardiac system
- Cor pulmonale
- Pericardial effusion
- Infiltrative cardiomyopathy
- Gastrointestinal system
- Gastric antral vascular ectasia
- Aspiration events
- Renal system
- Scleroderma renal crisis
- Neurologic system
- Carpal tunnel syndrome
- Sensory neuropathies
Cor pulmonale: In scleroderma, pulmonary arterial hypertension (PAH) and interstitial lung disease cause increased pressure in the pulmonary arteries. This increases the workload on the right ventricle, leading to right ventricular enlargement and failure, commonly referred to as cor pulmonale.
Pericardial effusion: Inflammation and scarring (fibrosis) of the pericardium can cause fluid to build up around the heart. This fluid buildup, called pericardial effusion, can lead to chest pain, make it harder for the heart to fill properly, and may cause heart failure.
Infiltrative cardiomyopathy: Scleroderma causes patchy myocardial fibrosis due to repeated ischemia from microvascular dysfunction and immune-mediated inflammation. This fibrosis stiffens the heart muscle, impairs diastolic relaxation and conduction, and causes arrhythmias and cardiomyopathy.
Gastric antral vascular ectasia (GAVE): This is also called "watermelon stomach." GAVE arises when mucosal blood vessels in the stomach antrum become dilated and fragile, leading to chronic bleeding and anemia. Fibrosis and vascular abnormalities in scleroderma disrupt the normal gastric vasculature, leading to GAVE.
Aspiration events: Esophageal dysmotility and impaired lower esophageal sphincter function lead to gastroesophageal reflux and aspiration of gastric contents into the lungs. This aggravates pulmonary fibrosis and increases the risk of infection.
Scleroderma renal crisis (SRC): An acute, severe complication characterised by the sudden onset of malignant hypertension and rapidly progressive kidney failure. It results from intimal proliferation and narrowing of renal arterioles due to endothelial injury and fibrosis, causing ischemic injury to the kidneys.
Carpal tunnel syndrome: Thickening and fibrosis of connective tissue in the wrist can compress the median nerve, causing pain, numbness, and tingling in the hand. This is frequent due to skin and soft tissue involvement.
Sensory neuropathies: Nerve damage can occur due to vascular insufficiency and fibrosis around nerves, leading to numbness, burning, or pain in peripheral nerves.
Scleroderma Diagnosis
Scleroderma diagnosis is primarily clinical, supported by specific laboratory and imaging tests that confirm disease involvement and exclude other conditions. The current best practice combines clinical criteria with autoantibody testing and organ-specific evaluations. Below are the steps involved in the diagnosis of scleroderma:
- Medical history
- Physical examination
- Laboratory evaluation
- Complete blood count (CBC)
- Kidney function test
- 24-hour urine protein or urine protein creatinine ratio
- Inflammatory markers (ESR and CRP)
- Muscle enzymes
- Autoantibody tests
- Antinuclear antibody (ANA)
- Scleroderma-specific antibody testing
- Ancillary & radiographic evaluation
- X-ray
- Musculoskeletal ultrasound
- Electromyography (EMG)/nerve conduction studies
- Muscle biopsy
- High-resolution computed tomography (HRCT)
- Pulmonary function tests (PFTs)
- Right heart catheterisation
- Electrocardiography (ECG) and Holter monitoring
- Nail-fold capillary microscopy
- Cardiac magnetic resonance imaging
- Transthoracic echocardiography
- Gastrointestinal studies
- Upper endoscopy
- Esophageal manometry
- 24-hour pH monitoring
- Computed tomography (CT) scan
Scleroderma Treatment
There is no permanent cure for scleroderma, but early detection and treatment can reduce disease progression, regulate symptoms, and prevent complications. The treatment aims to relieve symptoms, protect organs, and regulate the immune system. Scleroderma management includes the following:
Non-pharmacological management
- Patient education
- Regular exercise
- Healthy diet and lifestyle
- Emotional support
- Routine monitoring of organ involvement
Pharmacological management
- Immunosuppressive agents
- Corticosteroids
- Organ-specific medications
- Raynaud phenomenon: Calcium channel blockers, prostacyclin analogues, phosphodiesterase type 5 inhibitors (PDE5 inhibitors), endothelin receptor antagonists
- Pulmonary involvement: Tyrosine kinase inhibitors, supplemental oxygen, diuretics, anticoagulants
- Gastrointestinal symptoms: PPIs, H2 blockers, prokinetic agents, antibiotics for SIBO
- Scleroderma renal crisis: ACE inhibitors
- Supportive medications
- Antihistamines and topical agents for pruritus
- Moisturisers for skin care
- Analgesics
Surgical intervention
- Digital sympathectomy
- Debridement/ amputation
- Hand surgery
- Removal of calcinotic deposits
- Surgical fundoplication
- Laser ablation /excision
- Gastric antrectomy
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Scleroderma Prevention
Preventing scleroderma itself is currently not possible, as it is an autoimmune disease with complex, multifactorial causes. However, prevention efforts focus mainly on reducing risk factors and preventing disease complications through lifestyle and supportive ways:
- Avoiding environmental triggers
- Stopping smoking
- Protecting against cold
- Reducing stress
- Practising regular exercise
- Ensuring skin care
- Vaccinations
- Early detection
Avoiding environmental triggers: Exposure to substances such as silica dust, organic solvents, and epoxy resins is associated with an increased risk of developing scleroderma. Avoiding or minimizing contact with these occupational or environmental toxins decreases immune activation and vascular injury that can initiate the disease process.
Stopping smoking: While smoking is not definitively proven to cause scleroderma, it worsens vascular function and complications such as Raynaud's phenomenon and lung disease. Quitting smoking preserves vascular health, reduces oxidative stress, and lowers the progression risk of complications.
Protecting against the cold: Cold exposure triggers Raynaud’s attacks, causing blood vessel spasms and ischemia in extremities. Keeping warm prevents these spasms, reducing tissue injury and inflammation that contribute to disease progression.
Reducing stress: Managing emotional and physical stress is another important preventive step since stress can trigger vascular spasms and an immune imbalance. Techniques such as meditation and deep-breathing exercises helps in maintaining circulation and emotional stability.
Practicing regular exercise: Regular exercise, including walking, stretching, and swimming, helps keep joints flexible, strengthens muscles, improves circulation, and prevents stiffness and contractures.
Ensuring skin care: Proper skin care is important in scleroderma to prevent dryness, cracking, and secondary infections. Proper skin care alleviates one of the earliest manifestations and reduces exacerbation of skin fibrosis and ulcers.
Vaccinations: Infections can trigger immune activation and exacerbate autoimmune diseases. Staying updated on vaccinations reduces infectious risks, indirectly lowering disease flares and complications.
Early detection: Early detection of signs, including autoantibodies, skin abnormalities, or Raynaud's phenomenon, enables timely diagnosis and treatment to prevent or delay the progression of the disease and minimise permanent organ damage.
Difference between Scleredema and Scleroderma
scleredema vs scleroderma
Both scleroderma and scleredema are connective tissue disorders that cause the skin to become thick. They are distinct disorders, though, with their own causes, symptoms, and prognoses. Despite their apparent similarity, accurate diagnosis and treatment depend on knowledge of their underlying causes, associated disorders, and skin-related effects. Below are some of the parameters that help in differentiating scleredema and scleroderma:
| Parameters | Scleredema | Scleroderma |
|---|---|---|
| Definition | A rare connective tissue disorder characterised by non-pitting, diffuse thickening of the skin, usually over the upper body. | A chronic autoimmune disease causes hardening (fibrosis) of the skin and, in some cases, internal organ involvement due to excess collagen deposition. |
| Cause/etiology | Often follows infections (especially streptococcal infections), diabetes mellitus, or monoclonal gammopathy. | Autoimmune in origin, triggered by genetic, hormonal, and environmental factors (e.g., silica exposure, infection, drugs). |
| Onset and progression | Usually acute or subacute, it develops after infection and may resolve spontaneously over months or years. | Chronic and progressive, it may last lifelong with periods of worsening. |
| Areas affected | Commonly affects the neck, upper back, shoulders, and face; hands and feet are usually spared. | Often begins in fingers and hands (sclerodactyly) and may spread to the face and trunk; it may also involve internal organs (lungs, kidneys, heart, GI tract). |
| Systemic involvement | Usually absent; primarily a cutaneous condition. | Multisystem disease can involve lungs, kidneys, heart, and GI tract. |
| Treatment | Mainly supportive – control underlying cause (infection or diabetes), physiotherapy, phototherapy, and sometimes corticosteroids. | Immunosuppressants, vasodilators, ACE inhibitors, and anti-fibrotic therapy for organ protection and symptom control. |
Frequently Asked Questions (FAQs) on Scleroderma
Is scleroderma painful?
Yes, scleroderma can be painful. The pain mainly comes from skin tightening, joint stiffness, and inflammation of muscles and connective tissues. People often feel discomfort in the fingers, hands, or joints, especially during cold weather or movement. In some cases, nerve involvement or reduced blood flow can also cause burning or aching sensations.
Is scleroderma a form of arthritis?
Scleroderma is not a form of arthritis, but it can cause arthritis-like symptoms. It is an autoimmune disease that affects connective tissues, causing hardening of the skin and, in some cases, internal organs. However, inflammation of joints and muscles can occur, leading to pain, stiffness, and reduced movement similar to arthritis.
Does scleroderma affect the lungs?
Yes, scleroderma often affects the lungs. It can cause scarring (fibrosis) of lung tissue that leads to coughing, breathlessness, and difficulty exercising. Another common lung complication is pulmonary hypertension, which is high blood pressure in the vessels connecting the heart and lungs. This condition can cause swelling in the legs and feet and make breathing harder.
What causes scleroderma?
The exact cause of scleroderma remains unknown, but it is believed to involve a combination of genetic susceptibility, environmental triggers (for example, toxins or silica exposure), vascular injury (blood vessel damage), immune system activation, and fibrosis (collagen buildup in tissues).
What is the most common complication of scleroderma?
The most frequent serious complication in scleroderma is lung involvement, particularly when the condition affects the tissue between air sacs (interstitial lung disease) or causes high pressure in the lung’s blood vessels (pulmonary arterial hypertension). These lung complications are now the leading cause of death in this disease, and identifying them early is an important part of care.
Who is at high risk for scleroderma?
Certain people are at higher risk of developing scleroderma. These include:
- High-risk individuals are mostly middle-aged women aged 45 to 64 years.
- Environmental exposures like silica and organic solvents contribute to risk.
- Ethnic background influences risk; African-Americans in the US have a higher incidence and often more severe disease.
- Geographic location affects prevalence, with higher rates in parts of North America and Australia compared to Asia.
- Smoking and alcohol are not established risk factors for scleroderma.
What is systemic scleroderma and its symptoms?
Systemic scleroderma is a chronic autoimmune disease in which the immune system causes the skin and internal organs to become hard and tight due to excess collagen deposition. Common symptoms include thickened or shiny skin, Raynaud's phenomenon (when cold , fingers changing to white or blue ), joint stiffness, heartburn, shortness of breath, fatigue, and swelling in the hands or feet.
What is scleroderma renal crisis?
Scleroderma renal crisis is a serious kidney complication seen mostly in people with diffuse systemic scleroderma. It happens when blood pressure suddenly rises to critical levels due to the narrowing of the kidney blood vessels. If left untreated, it can lead to kidney failure.
Can limited scleroderma turn into diffuse?
Limited scleroderma usually remains a milder, slower-progressing form that mainly affects the skin of the hands, arms, and face. In most cases, it does not change into diffuse scleroderma. However, both forms belong to the same disease spectrum and may share similar immune mechanisms.
What is diffuse scleroderma?
Diffuse scleroderma is a serious type of systemic scleroderma. In this condition, skin thickening occurs rapidly and affects large areas of the body, such as the face, trunk, arms, and legs. It may also involve internal organs like the lungs, heart, kidneys, and digestive system. This form typically progresses more quickly than limited scleroderma and requires careful medical supervision.
Is scleroderma more serious than lupus?
Both scleroderma and lupus are autoimmune diseases. However, scleroderma can be more severe because it can lead to permanent skin tightening and damage to internal organs. Symptoms of lupus often vary widely and can be managed more flexibly. The seriousness of each disease depends on how far it has progressed and which organs are involved. Scleroderma can sometimes result in more life-threatening complications.
What are the neurological symptoms of scleroderma?
Neurological symptoms in scleroderma can involve both the central and peripheral nervous systems. Common issues include headaches, seizures, memory or thinking problems, and cognitive impairment. Peripheral nerve problems may cause numbness, tingling, burning sensations, or weakness in muscles. Some people experience carpal tunnel syndrome, nerve pain in the face (trigeminal neuropathy), or difficulties with movement.
What are the first signs of scleroderma?
The first signs of scleroderma include Raynaud’s phenomenon and changes in skin texture, such as thickening or swelling. Early symptoms may also include fatigue, joint pain, and swelling. These signs can be subtle and variable, sometimes leading to delays in diagnosis until more prominent features develop.
When to consult a doctor for scleroderma?
Consult a doctor for scleroderma if you experience persistent skin tightening, thickening, or colour changes in your fingers, especially when exposed to cold. Signs that indicate a need for medical assistance are:
- Tight, shiny, or hard skin on fingers, hands, or face
- Fingers turning white, blue, or red in cold or stress (Raynaud’s phenomenon)
- Joint stiffness, swelling, or pain
- Persistent heartburn, acid reflux, or difficulty swallowing
- Shortness of breath, dry cough, or fatigue
- Sores or ulcers on fingertips
- Unexplained weakness or weight loss
If these symptoms continue or worsen, it is best to see a scleroderma doctor for an accurate diagnosis and management plan. Seek emergency medical attention if you experience severe breathlessness and renal problems. A rheumatologist can provide the correct scleroderma treatment to manage symptoms and reduce long-term risks.
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