Researchers ID 3 genes that were significantly dysregulated in SSc patients
Written by Steve Bryson, PhD | January 27, 2026

Abnormal fatty acid metabolism may play a role in the development of systemic sclerosis (SSc), according to a gene activity analysis.

Researchers identified three genes involved in fatty acid metabolism that were significantly dysregulated in SSc patients. These changes correlated with markers of fat metabolism and disease complications, including lung involvement, the data suggested.
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These findings indicate that “dysregulated fatty acid metabolism may be implicated in the [development] of SSc,” which may provide “potential targets for metabolic intervention,” researchers wrote in the study, “Expression and clinical significance of fatty acid metabolism–related genes in PBMCs of SSc patients,” which was published in Clinical Rheumatology.

Study finds treatment may help reduce skin scarring in patients
Written by Marisa Wexler, MS | January 20, 2026

​Carbon dioxide ablative fractional laser (CO2-AFL) therapy, a treatment that’s long been used to remove wrinkles, may help reduce skin scarring in people with localized scleroderma, according to a new study.

“Overall, CO2-AFL treatment appears to have good therapeutic effects in patients with [localized scleroderma], especially patients who are unresponsive to conventional treatments. Furthermore, most of the adverse effects related to this treatment were mild and manageable, indicating the favorable safety profile of CO2-AFL treatment,” researchers wrote.
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The study, “Efficacy and Safety of Ablative Fractional CO2 Laser Therapy for Localized Scleroderma: A Comprehensive Bench-to-Bedside Approach,” was published in Dermatologic Therapy.

Study links antibody levels with pain, physical limits, and disease burden
Written by Patricia Inácio, PhD | January 13, 2026

Lower blood levels of immunoglobulin G (IgG), an antibody measured through routine blood tests, were linked to poorer health-related quality of life in people with systemic sclerosis (SSc), including greater pain, reduced physical function, and higher overall disease burden, a study reports.

These findings suggest that blood IgG levels could serve as a “reliable biomarker of patient-perceived disease burden,” the researchers wrote, an area where reliable measures have long been lacking.
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The study, “Lower total serum Immunoglobulin G is associated with impaired patient-reported health-related quality of life in systemic sclerosis: a prospective cross-sectional study,” was published in Rheumatology International.

Study suggests isolated anti-SSA antibodies could help guide closer monitoring
Written by Andrea Lobo, PhD | January 6, 2026

Having anti-SSA antibodies, without other common scleroderma-related antibodies present, is linked to shorter survival and faster disease progression in people with systemic sclerosis (SSc), according to a recent study from Japan.

“These findings support the inclusion of anti-SSA in routine serologic [blood] assessment and underscore the potential utility of ‘isolated’ anti-SSA seropositivity as a marker of higher-risk [scleroderma],” the researchers wrote.

​The study, “Isolated Anti-SS-A Antibody Seropositivity as a Poor Prognostic Factor in Systemic Sclerosis: Insights From a Cohort of 307 Cases,” was published in The Journal of Dermatology.

Corticosteroid had similar effect on T-cells derived from SSC patients
Written by Andrea Lobo, PhD | December 16, 2025

Dexamethasone, a type of corticosteroid, reduced skin thickening, inflammation, and the activity of genes that induce fibrosis (scarring) in a mouse model of systemic sclerosis (SSc), according to a study.

The study also demonstrated that dexamethasone reduced the levels of pro-inflammatory molecules produced by certain T-cells derived from SSc patients. In SSc, these immune cells can become excessively active, releasing pro-inflammatory molecules that contribute to the development of fibrosis.
“In summary, [dexamethasone] showed immunomodulatory and antifibrotic effects in SSc, evidencing its actions in treating the disease,” researchers wrote.
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The study, “Dexamethasone modulates cytokine and chemokine secretion by CD4 + T cells from SSc patients and exerts antifibrotic effects in HOCl-induced SSc mice,” was published in Inflammopharmacology.

Study finding may show 'growing confidence' in strategy's safety, effectiveness
Written by Andrea Lobo, PhD | December 9, 2025

​Using combination therapy for pulmonary arterial hypertension (PAH) improves survival in people with systemic sclerosis (SSc), according to the results of a large study in Australia.

The study also demonstrated that the choice between a single medication or a combination of therapies did not vary significantly when comparing participants with more or fewer coexisting conditions, or comorbidities, or individuals with or without heart or lung issues.

“The findings are in line with current recommendations from the [World Symposium of Pulmonary Hypertension] to deploy upfront treatment with combination therapy in PAH, regardless of [a patient’s] comorbidity status,” the researchers wrote. “This prescribing pattern may reflect growing confidence in the safety and efficacy of combination therapy.”
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Titled “Impact of Comorbidities on Treatments and Outcomes of Systemic Sclerosis–Associated Pulmonary Arterial Hypertension,” the study was published in the Canadian Respiratory Journal.

Study: Biggest benefits seem when drugs started simultaneously, after short gap by Patricia Inácio, PhD | December 2, 2025

Combining rituximab and mycophenolate mofetil was significantly more effective than using either drug alone at reducing skin thickness and improving lung function after one year in people with systemic sclerosis (SSc), according to a large French study.

The safety profile of the combination therapy was similar to that of either drug alone. The greatest benefits were observed when both therapies were started simultaneously or after a short gap.

These findings support the need for additional studies assessing the combo therapy as a first-line treatment in SSc, researchers said.
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The study, “Evaluation of the mycophenolate mofetil–rituximab combination in systemic sclerosis: a French retrospective multicenter study (MycRiSSc),” was published in the Journal of Autoimmunity.

Difficulty getting to sleep has been the worst side effect of mycophenolate by Tomisa Starr | November 26, 2025

​Note: This column describes the author’s own experiences with mycophenolate. Not everyone will have the same response to treatment. Consult your doctor before starting or stopping a therapy.

I’ve been taking mycophenolate for nine months now. An immunosuppressant, it is used to treat interstitial lung disease and scleroderma.

Scleroderma is an autoimmune disease that’s caused by an overactive immune response. Immunosuppressants help dampen the immune system, which can slow disease progression and help prevent the damage that scleroderma causes. But treatment must begin early, before organ involvement becomes advanced, as untreated scleroderma can result in damage to the lungs, heart, kidneys, and gastrointestinal tract.
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I went without immunosuppressant therapy until this year, after being diagnosed with scleroderma in 1993, because insurance maintained that there was no medical necessity for treatment. By the time I was able to access an immunosuppressant, I had developed lung and gastrointestinal involvement.
The medication seems to be really helping my symptoms, but I have experienced some side effects from it, namely intestinal upset and difficulty sleeping. It’s the difficulty sleeping that has really bothered me.

Are you newly diagnosed? Have someone close to you recently diagnosed and "don't understand" what Scleroderma is? This article will help you. 

Scleroderma is a chronic disease that affects the skin and connective tissue, the tissue that supports and holds organs together, and is also found in the joints.

The hallmark of scleroderma is thick and hardened skin caused by excessive production of collagen, a protein that is the main component of scar tissue. This scar tissue can accumulate in and damage organs, including the heart and blood vessels, and the lungs, stomach, and kidneys.

Females are about four times more likely to develop scleroderma than males. Disease onset typically occurs between ages 35 and 50, though people of all ages can be affected.

Causes
Scleroderma is an autoimmune disease, meaning it is caused by an overactive immune system that mistakenly attacks the body’s own tissues. The resulting excessive inflammation damages the skin and affected organs.

It is a complex condition, and the underlying disease process is not well understood. It is thought that the disease results from a combination of genetic and environmental factors. Scleroderma is not contagious, infectious, or cancerous.

Symptoms
Symptoms of scleroderma vary among patients, and can range from very mild to life-threatening depending on which parts of the body are affected and the extent of organ involvement. A mild case can become serious if not treated properly.

Characteristic symptoms, besides patches of thick and hardened skin, include contractures when skin stiffens over joints, skin ulcers (sores), calcinosis — when lumps of calcium form under the skin — and Raynaud’s phenomenon, in which the fingers and toes feel numb, prickly, or frigid in response to cold temperatures or emotional distress.

Manifestations affecting internal organs include damage to muscle and bone tissue, shortness of breath, an abnormal heart rhythm, a burning sensation in the chest (heartburn), difficulty swallowing, blurred vision.
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A scleroderma renal crisis is possible in some systemic scleroderma (mentioned below) patients. This renal, or kidney, crisis is a serious disorder characterized by a sudden onset of high blood pressure, progressive kidney failure, hypertensive encephalopathy (brain dysfunction or damage due to high blood pressure), and/or microangiopathic hemolytic anemia, or anemia due to the red blood cells being sheared (ripped apart) as they pass through small blood vessels.

Study: Inhibitor treatments could help mitigate fibrosis in multiple disorders by Marisa Wexler, MS | November 18, 2025

The molecular signaling pathway EGFR-STAT1 is key for driving fibrosis (scarring) in scleroderma, according to a new study.

The findings suggest that treatments designed to inhibit this pathway could be used to help mitigate fibrosis in scleroderma and other disorders that are characterized by excessive scarring. The study, “EGFR-STAT1 pathway drives fibrosis initiation in fibroinflammatory skin diseases,” was published in Nature Communications.

Inhibiting EGFR-STAT1 pathway could help control fibrosis in scleroderma
Scleroderma is characterized by inflammation and scarring, which can affect the skin and various other organs throughout the body. Inflammation and scarring are closely linked, but they don’t always occur simultaneously. Some disorders, such as scleroderma, are marked by both inflammation and fibrosis, while others are characterized by inflammation but not fibrosis.

In this study, scientists sought to better understand why fibrosis is a feature of some inflammatory skin diseases but not others. The scientists conducted in-depth analyses of cellular activity using samples from people with several different diseases, including disorders that cause scarring, such as scleroderma and lupus, as well as non-fibrotic diseases like atopic dermatitis and psoriasis.

“Treatments for fibrosis are an enormously unmet need,” Richard Flavell, PhD, co-senior author of the study at Yale University School of Medicine, said in a university news story. “Better understanding these conditions will likely yield new medicines to help patients.”
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The researchers found that a signaling protein called STAT1 was substantially more active in patients with fibrotic diseases. Further tests showed that EGFR (epidermal growth factor receptor), a signaling protein that’s previously been implicated in driving fibrosis, is able to activate STAT1, leading to changes in cellular activity that ultimately promote the formation of scar tissue.