For Patients

If you have scleroderma, you are not alone. The scleroderma community is made up of tens of thousands of patients and their loved ones worldwide. The SRF is here to help.

The first time many people hear about scleroderma is when they, a family member or friend are diagnosed with the disease. Scleroderma is a complex and surprisingly widespread illness, affecting as many people as more commonly recognized diseases such as multiple sclerosis and muscular dystrophy.

In addition to funding the most promising research aimed at improved therapies and a cure, the Scleroderma Research Foundation provides information that may help scleroderma patients better understand their disorder and more effectively manage its symptoms.

To learn more about the various forms and subtypes of scleroderma, please click here. This section of the Scleroderma Research Foundation’s Web site provides information for patients to educate themselves, as well as their caretakers and loved ones, about this serious disease.

Please remember, information provided on this Website and others is intended as a guide. Specific medical advice can only be provided by your health care professional.


AddThis Social Bookmark Button
 
 

Research News

Screening for PAH in Systemic Sclerosis: Does It Matter?

Author: Kevin Deane, MD
Date Published: February-2012
Source: Medscape Today

ulmonary arterial hypertension (PAH) is a leading cause of mortality in patients with systemic sclerosis (SSc).[1] Once commonly thought to be a late complication of SSc, support for PAH as an early manifestation of disease is growing. PAH is present within 5 years of the onset of the first non-Raynaud symptoms of SSc in approximately 50% of patients.

Stimulation of soluble guanylate cyclase reduces experimental dermal fibrosis

Author: C. Beyer, N. Reich, S. Schindler, et al
Date Published: January-2012
Source: Annals of the Rheumatic Diseases

Fibrosis and vascular disease are cardinal features of systemic sclerosis (SSc). Stimulators of soluble guanylate cyclase (sGC) are vasoactive drugs that are currently being evaluated in phase III clinical trials for pulmonary arterial hypertension.

Emerging patterns of genetic overlap across autoimmune disorders.

Author: Richard-Miceli C, Criswell LA.
Date Published: January-2012
Source: Genome Medicine

Most of the recently identified autoimmunity loci are shared among multiple autoimmune diseases. The pattern of genetic association with autoimmune phenotypes varies, suggesting that certain subgroups of autoimmune diseases are likely to share etiological similarities and underlying mechanisms of disease.

Gender and ethnicity differences in the prevalence of scleroderma-related autoantibodies.

Author: Krzyszczak ME, Li Y, Ross SJ, et al
Date Published: October-2011
Source: Journal of Cellular and Molecular Medicine

Autoantibodies to topoisomerase I (topo I), RNA polymerase III (RNAPIII), centromere, U3RNP/fibrillarin, Th, PM-Scl, and U1RNP found in scleroderma (SSc) are associated with unique clinical subsets. The effects of race and gender on autoantibody prevalence and clinical manifestations were examined.

Elevated expression of cav-1 in a subset of SSc fibroblasts contributes to constitutive Alk1/Smad1 activation.

Author: Haines P, Hant FN, Lafyatis R, Trojanowska M, Bujor AM.
Date Published: January-2012
Source: Journal of Cellular and Molecular Medicine

Previous studies have shown that the TGFβ/Alk1/Smad1 signaling pathway is constitutively activated in a subset of systemic sclerosis (SSc) fibroblasts and this pathway is a critical regulator of CCN2 gene expression. Caveolin-1 (cav-1), an integral membrane protein and the main component of caveolae, has also been implicated in SSc pathogenesis.

News for Patients

Screening for PAH in Systemic Sclerosis: Does It Matter?

Author: Kevin Deane, MD
Date Published: February-2012
Source: Medscape Today

ulmonary arterial hypertension (PAH) is a leading cause of mortality in patients with systemic sclerosis (SSc).[1] Once commonly thought to be a late complication of SSc, support for PAH as an early manifestation of disease is growing. PAH is present within 5 years of the onset of the first non-Raynaud symptoms of SSc in approximately 50% of patients.

Emerging patterns of genetic overlap across autoimmune disorders.

Author: Richard-Miceli C, Criswell LA.
Date Published: January-2012
Source: Genome Medicine

Most of the recently identified autoimmunity loci are shared among multiple autoimmune diseases. The pattern of genetic association with autoimmune phenotypes varies, suggesting that certain subgroups of autoimmune diseases are likely to share etiological similarities and underlying mechanisms of disease.

An Evaluation of Long-Term Survival From Time of Diagnosis in Pulmonary Arterial Hypertension From REVEAL.

Author: Benza RL, Miller DP, Barst RJ, et al
Date Published: January-2012
Source: Chest

The Registry to EValuate Early And Long-Term Pulmonary Arterial Hypertension Disease Management (REVEAL) was established to characterize the clinical course, treatment, and predictors of outcomes in patients with pulmonary arterial hypertension (PAH) in the US. To date, estimated survival based on time of patient enrollment has been established and reported.

Evidence of the contribution of the X chromosome to systemic sclerosis susceptibility: association with the functional IRAK1 196Phe/532Ser haplotype.

Author: Dieudé P, Bouaziz M, Guedj M, et al
Date Published: December-2011
Source: Arthritis & Rheumatism

Several autoimmune disorders, including systemic sclerosis (SSc), are characterized by a strong sex bias. To date, it is not known whether genes on the sex chromosomes influence SSc susceptibility. Recently, an IRAK1 haplotype that contains the 196Phe functional variant (rs1059702), located on Xq28, was found to confer susceptibility to systemic lupus erythematosus (SLE).

Mechanism, Potential Therapy for Scleroderma Lung Disease Uncovered

Author: NIAMS / Tourkina E, et al
Date Published: January-2012
Source: NIAMS Spotlight on Research 2012

Investigators, partially supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, have found that a deficiency in the protein caveolin-1 (cav-1) is linked to the development of interstitial lung disease, the scarring of lung tissue that causes disability and death in people with scleroderma.

Ways to Give

There are many ways that you can support the work of the Scleroderma Research Foundation. We are grateful for your commitment to helping the SRF fund research that will result in improved therapies and, ultimately, a cure.

» Click here for details