Scleroderma is a group of autoimmune diseases that may result in changes to the skin, blood vessels, muscles, and internal organs. The disease can be either localized to the skin or involve other organs, as well. Symptoms may include areas of thickened skin, stiffness, feeling tired, and poor blood flow to the fingers or toes with cold exposure. One form of the condition, known as CREST syndrome, classically results in calcium deposits, Raynauds syndrome, esophageal problems, thickening of the skin of the fingers and toes, and areas of small, dilated blood vessels.The cause is unknown, but it may be due to an abnormal immune response. Risk factors include family history, certain genetic factors, and exposure to silica. The underlying mechanism involves the abnormal growth of connective tissue, which is believed to be the result of the immune system attacking healthy tissues. Diagnosis is based on symptoms, supported by a skin biopsy or blood tests.While no cure is known, treatment may improve symptoms. Medications used include corticosteroids, methotrexate, and non-steroidal anti-inflammatory drugs (NSAIDs). Outcome depends on the extent of disease. Those with localized disease generally have a normal life expectancy. In those with systemic disease, life expectancy can be affected, and this varies based on subtype. Death is often due to lung, gastrointestinal, or heart complications.About three per 100,000 people per year develop the systemic form. The condition most often begins in middle age. Women are more often affected than men.
Patients that have mutations in their potassium channel, improved their glucose levels with sulfonylurea regimen and glibenclamide showed successful results in managing glucose levels as well. A 2006 study showed that 90% of patients with a KCNJ11 mutation were able to successfully transition to sulfonylurea therapy. See also
Type 1 Diabetes
Type 2 Diabetes

References
Yorifuji, T; Kurokawa, K; Mamada, M; Imai, T; Kawai, M; Nishi, Y; Shishido, S; Hasegawa, Y; Nakahata, T (Jun 2004). "Neonatal diabetes mellitus and neonatal polycystic, dysplastic kidneys: Phenotypically discordant recurrence of a mutation in the hepatocyte nuclear factor-1beta gene due to germline mosaicism". The Journal of Clinical Endocrinology and Metabolism. 89 (6): 2905–8. doi:10.1210/jc.2003-031828. PMID 15181075. Edghill, EL; Bingham, C; Slingerland, AS; Minton, JA; Noordam, C; Ellard, S; Hattersley, AT (Dec 2006). "Hepatocyte nuclear factor-1 beta mutations cause neonatal diabetes and intrauterine growth retardation: support for a critical role of HNF-1beta in human pancreatic development". Diabetic Medicine. 23 (12): 1301–6. doi:10.1111/j.1464-5491.2006.01999.x. PMID 17116179. Works cited
Atkinson MA, Mcgill DE, Dassau E, Laffel L (2020). "Type 1 Diabetes Mellitus". In Melmed S, Auchus RJ, Goldfine AB, Koeng RJ, Rosen CJ (eds.). Williams Textbook of Endocrinology (14 ed.). Elsevier. pp. 1403–1437. De Franco E (December 2021). "Neonatal diabetes caused by disrupted pancreatic and β-cell development". Diabet Med. 38 (12): e14728. doi:10.1111/dme.14728. PMID 34665882. Garg M, Devaskar SU (2020). "Disorders of Carbohydrate Metabolism in the Neonate". In Martin RJ, Fanaroff AA, Walsh MC (eds.). Fanaroff and Martins Neonatal-Perinatal Medicine (11 ed.). Elsevier. pp. 1584–1610. ISBN 9780323567114. Katugampola H, Gevers EF, Dattani MT (2020). "Endocrinology of Fetal Development".