Talk:Systemic scleroderma

message: Heat is bad as is the cold for scleroderma. Heat causes excessive fatigue more so then you allready get with this disease. The harding of the skin can be very life threatening. I am not getting any blood to my rear end I can't stand the pain. Sleeping is very hard to do. It is hard to stand, sit or lie down. Because of the hard skin there is no blood flow along my skin between my two cheeks, it is raw and getting open sores much like the ones on fingers of others with scleroderma. We must get the word out about this disease, I did not know about it till I was told that I have it.
:I agree.  My mother has the disease and it took doctors years to arrive at this diagnosis.  she does not show very much of the characteristic skin hardening, but she makes up for it with the other symptoms.  --Morbid-o 12:44, 3 Jun 2005 (UTC)
replies: text: I agree that this article should be based on authoratitive sources, preferably a recent systematic review. Many medical articles are indeed updated frequently, but there is clearly nobody around who is willing to nurture this article. Instead of criticism, how about you put some work in to improve this article? JFW | T@lk 00:45, 17 November 2005 (UTC)

text: Coding system? It's Wiki markup and very easy to learn, see how to edit a page for more. JFW | T@lk 15:00, 22 November 2005 (UTC)

text: I'm unsure how scleroderma symptoms should impair Wikipedia editing more than any other form of typing. I did not intend to offend you. JFW | T@lk 14:04, 15 December 2005 (UTC)

text: This study laments the absence of well-designed trials of colchicine in scleroderma. There's a nice subject for your PhD! JFW | T@lk 23:38, 25 April 2006 (UTC)
thread_title: Heat

message: I wrote the pathogenesis section completely on the basis of Jimenez & Derk's excellent review. One wishes there were more systemic reviews of this type. Further sources would still be welcome. The review was in 2004. Has anything else come to the surface that is worth discussing? JFW | T@lk 23:38, 25 April 2006 (UTC)
replies: text: Nice additions.  The review article is quite good.  -- Samir   धर्म 21:07, 1 May 2006 (UTC)

text: Added a bit on complications.  -- Samir   धर्म 08:22, 14 May 2006 (UTC)
thread_title: Pathogenesis

message: If Scleroderma is a genetic diseases? my mother has the diseases, what are the chances that i will have it?(i mean is it dominant diseases?) what pecautions should i take to avoid the disease?
:There does appear to be a genetic component to the disease as suggested by the following abstract: 
::Assassi S, Tan FK. Genetics of scleroderma: update on single nucleotide polymorphism analysis and microarrays. Curr Opin Rheumatol. 2005 Nov;17(6):761-7. Review. . 
:I suggest you talk to your doctor. Nephron  T|C 08:34, 28 October 2006 (UTC)
replies: text: Having a member of the family with scleroderma increases the rate to 1.3% from a few in a million. Rates among identical twins are about 20% (if one gets it, the chance the other will is about 20%). JoshNarins (talk) 12:53, 2 July 2013 (UTC)
thread_title:  '''Scleroderma : help me''' 

message: This cannot be correct. Scleroderma reduces Lower Esophageal Sphincter(LES) pressure by reducing the ability of the muscles to contract, causing the GE junction to be slack, and allowing the regurgitation of stomach acid into the esophagus. This causes esophageal erosion, Barrett's Esophagus, and esophageal strictures. Strictures are not muscular, they are fibrous connective tissue bands caused by the corrosive scarring of the stomach acid. The treatment for strictures is by esophageal dilitation with a device called a Bouge (among others).
Botulinum Toxin, maybe the most potent toxin known to man, is a paralytic substance. There is no need to use a paralytic on an already slackened LES. Since esophageal strictures are fibrous bands and not muscular, they cannot be treated with a paralytic. In fact, BoTox is one of the treatments for Achalasia, which is the failure of the LES to relax; the exact OPPOSITE effect of Scleroderma.
I hope that it is Ok that I delete the Botulinum toxin reference from the GI effects section. 
Cochise11 00:01, 2 April 2007 (UTC)
thread_title: Deleted BoTox reference

message: Sorry about this. When I deleted the BoTox reference, it caused the paragraph to not make sense. Additionally, there is no mention in the literature about the development of Megaesophagus from Sclreoderma. Megaesophagus is a sequele of Chaga's disease, and Achalasia. "Chagas' disease is associated with esophageal dysfunction that is indistinguishable from idiopathic achalasia and should be considered in patients from endemic regions (Central and South America); it is becoming more common in the southern United States." (McQuaid et al., 2007, p. 593) "The chronic stage is usually manifested by cardiac disease in the third and fourth decades of life, characterized by arrhythmias, congestive heart failure (often with prominent right-sided findings), ventricular aneurysms, and systemic or pulmonary embolization originating from mural thrombi. Valvular lesions are absent. Sudden cardiac arrest in young persons may occur and is attributed to ventricular fibrillation. Megacolon and megaesophagus, caused by damage to nerve plexuses in the bowel or esophageal wall, occur in some areas of Chile, Argentina, and Brazil; findings include dysphagia, regurgitation, constipation, sigmoid volvulus, bacterial overgrowth in the small intestine, and parotid gland hypertrophy. Megasyndromes can also affect the urinary tract."(Jacobs et al., 2007, p. 1497)
The bold part below is what doesn't make sense:
"Scleroderma can decrease motility anywhere in the gastrointestinal tract.[5] The most common source of motility involvement is the esophagus, which can also lead to difficulty swallowing or dysphagia, or to chest pain. The esophagus can become massively dilated (megaesophagus).[1] This can be treated with esophageal dilatation."
I'm going to make the bold part say: 
"The most common source of decreased motility involvement is the esophagus and the lower esophageal sphincter, leading to dysphagia and chest pain. As Scleroderma progresses, esophageal involvement from abnormalities in decreased motility may worsen due to progressive fibrosis (scarring). If this is left untreated, acid from the stomach can back up into the esophagus causing esophagitis, and GERD. Further scarring from acid damage to the lower esophagus many times leads to the development of fibrotic narrowing, also known as strictures which can be treated by dilitation, and Barrett's esophagus."
McQuaid, K. R. (2007). Esophageal Motility Disorders. In L. M. Tierney, Jr., S. J. McPhee, & M. A. Papadakis (Eds.), Current Medical Diagnosis and Treatment (pp. 592-595). San Francisco: McGraw-Hill Companies, Inc.
Jacobs, R. A. (2007). American Trypanosomiasis (Chaga's Disease). In L. M. Tierney, Jr., S. J. McPhee, & M. A. Papadakis (Eds.), Current Medical Diagnosis and Treatment (pp. 1496-1498). San Francisco: McGraw-Hill Companies, Inc
Cochise11 22:02, 5 April 2007 (UTC)
thread_title: Cleanup of my own mess

message: Localised scleroderma... does it needs its own article given that this article is presently mainly about systemic sclerosis?
 is another nice resource that summarises recent trial results.
 suggests bacterial overgrowth is rather common, and that rifaximin may be of benefit. JFW | T@lk 11:30, 11 May 2008 (UTC)
replies: text: http://pats.atsjournals.org/cgi/content/full/4/5/434 - management of lung disease. JFW | T@lk 11:57, 11 May 2008 (UTC)
replies: text:  - when to suspect watermelon stomach. JFW | T@lk 09:22, 25 May 2008 (UTC)

text: Agree. If no one objects, I'll move this article to "systemic scleroderma", and generate a stub for "localised scleroderma". --Arcadian (talk) 04:58, 17 February 2009 (UTC)
replies: text: *This plan sounds good to me.  Also, just so you are aware, there are some stubs on the various types of scleroderma (see Scleroderma#Types). kilbad (talk) 12:44, 17 February 2009 (UTC)
thread_title:  Some issues 

message: I'm particularly interested in Pulmonary Hypertension secondary to Scleroderma. I can provide references and will keep everything according to current resources. The field is changing daily but since there is so little published here, I see it as an opportunity share what I have learned by necessity. I'm a former medical researcher, no longer able to do lab work. If I put up a suggested outline I hope other scientists would give me feedback and editors would help me learn how to do the article properly. The first decision would be what to put under scleroderma, and what to put under pulmonary hypertension. Jo47phox (talk) 19:48, 7 June 2008 (UTC)
thread_title:  I'd like to help 

message: I'm not a professional and I'm not American either so I don't want to mess with the article, but I was told by a rheumatologist that in the UK use of the CREST definition is falling out of favour and it is not longer used as an official classification.  She told me that what would previously have been called CREST is now lumped in as limited cutaneous sclerosis.
Also, I understand that that subtype does have a significant incidence of pulmonary hypertension (so people with scleroderma get yearly echos and pulmonary function tests) and also renal crisis with malignant hypertension.  So you can't really say that people with CREST (which doesn't officially exist any more) don't get pulmonary and renal sequelae.  Most don't, but enough do that it is an important complication.
Whrrivers (talk) 22:52, 19 November 2008 (UTC)
replies: text: CREST is a form of limited SSc, that's right. The rate of death, I've read, is 1-4%/annum for CREST's, 7-10%/annum for diffuse SSc forms. It certainly isn't a fun disease, but the dSSc forms are far more deadly. CREST, the term, might go away, but this form of SSc is very specific. People who have the anti-centromere antibodies (ACA) have CREST's, and many patients express one of the 9 anti-bodies that distinguish the 9 disease sub-types (e.g. ACA, Scl-70, Anti-Topoisomerase, Anti-RNP III, Anti-Th/To). Incidences of the four, major, internal organ complications (PAH, pulmonary fibrosis, scleroderma renal crisis, and GI complications) are much worse in dSSc than CREST's. By the way, using lSSc has its own problems. CREST's and Anti-Th/To can be classified as lSSc, because of the limited skin involvement, but Anti-Th/To acts like the progressive dSSc in every other respect. CREST's really is in its own boat, and represents 2/3rds of annual SSc cases. JoshNarins (talk) 13:07, 2 July 2013 (UTC)
thread_title:  CREST 

message: I think that most medical sources refer to systemic scleroderma as systemic sclerosis.Therefore,to be consistent,i propose renaming the page systemic scleroderma systemic sclerosis.I am a bit reluctant to do it my self because i have little experience renaming pages.Immunize (talk) 16:15, 16 January 2010 (UTC)
thread_title:  systemic sclerosis 

message: I agree completely: This page should be named Systemic Sclerosis. Systemic Scleroderma is NOT a medical term.
Altes2009 (talk) 17:59, 1 February 2010 (UTC)
thread_title:  Systemic Sclerosis 

message: doi:10.1111/bjh.13201 JFW | T@lk 00:15, 12 November 2014 (UTC)
thread_title:  Stem cell transplants