I've had several friends on Sjogren's lists who also joined a Schleroderma list. Each disease has it's own set of problems. Perhaps someone here is in the same boat and can offer some insights.

What is Scleroderma? Is it a separate autoimmune disorder or part of the same one sjs?

Scleroderma is often related to Sjorgren's. Normally it affects the skin - thickening it. But in some cases it affects internal organs or what-not. It's not clear if I mainly have Scleroderma and Sjogren's secondary or t'other way around. My symptoms seem more like Sjogren's - dry mouth facial pain and aching joints mostly in the back and neck. I imagine the Rhumy will have to sort out what the tests mean in light of my symptoms.

I did a little research quickly and I certainly hope if you have it it is just a mild case. It seems it can be more systemic in adults than children.

I truly hope you do not have it. Good luck with this. As far as I know at this point I just have Primary sjs along with advanced Osteoarthritis and as far as I'm concerned that is more than enough for me, but I know just having sjs makes me more suseptible to other autoimmune disorders down the road sooner or later.

Take care

Here is some info on homocysteine and Scleroderma. Notice the researchers say they believe homocysteine"may worsen injury of the endothelium." The endothelial cells line all of the body's blood vessels, from the smallest capillary to the largest vessel. I will find another study to show the massive damage homocysteine causes to the endothelial cells.

Homocysteine Plasma Concentration Is Related to Severity of Lung Impairment in
Scleroderma
Caramaschi, P., N. Martinelli, D. Biasi, A. Carletto, G. Faccini, A. Volpe, M. Ferrari, C. Scambi, L.M. Bambara.
2003. J Rheumatol 30(2):298-304.
Objective: To investigate the correlation between plasma concentration of total homocysteine and
pulmonary involvement in patients with limited or diffuse scleroderma (systemic sclerosis, SSc).
Conclusion: High level of homocysteinemia is associated with an increased risk of pulmonary disease
in patients with scleroderma. We hypothesize that hyperhomocysteinemia may worsen injury of the
endothelium, a key lesion in scleroderma disease, favoring the development of lung involvement. Our data
support the hypothesis that homocysteine could be involved in the pathogenetic process of scleroderma
pulmonary involvement. (J Rheumatol 2003;30:298-304).

Here is a study on the damage homocysteine does to the endolithial cells. Homocysteine causes them to commit mass suicide.

Homocysteine Induces Programmed Cell Death in Human Vascular Endothelial Cells
Through Activation of the Unfolded Protein Response
Zhang, C, Y. Cai, M.T. Adachi, S. Oshiro, T. Aso, R.J. Kaufman, S. Kitajima. 2001. J Biol Chem 276(38):35867-74.
Severe hyperhomocysteinemia is associated with endothelial cell injury that may contribute to an increased
incidence of thromboembolic disease. In this study, homocysteine induced programmed cell death in human
umbilical vein endothelial cells as measured by TdT-mediated dUTP nick end labeling assay, DNA ladder
formation, induction of caspase 3-like activity, and cleavage of procaspase 3. Homocysteine-induced cell
death was specific to homocysteine, was not mediated by oxidative stress, and was mimicked by inducers
of the unfolded protein response (UPR), a signal transduction pathway activated by the accumulation of
unfolded proteins in the lumen of the endoplasmic reticulum. Dominant negative forms of the endoplasmic
reticulum-resident protein kinases IRE1alpha and -beta, which function as signal transducers of the UPR,
prevented the activation of glucose-regulated protein 78/immunoglobulin chain-binding protein and C/EBP
homologous protein/growth arrest and DNA damage-inducible protein 153 in response to homocysteine.
Furthermore, overexpression of the point mutants of IRE1 with defective RNase more effectively suppressed
the cell death than the kinase-defective mutant. These results indicate that homocysteine induces apoptosis
in human umbilical vein endothelial cells by activation of the UPR and is signaled through IRE1. The studies
implicate that the UPR may cause endothelial cell injury associated with severe hyperhomocysteinemia.

If anyone would like, I can show how elevated levels of homocysteine are directly related to SjS, arthritis or other autoimmune diseases.