Of Oral Ulcers and Papules in the Skin


New this week in the nonspecialty journals: Tattoos and sarcoidosis, oral ulcers and autoimmunity, gout and heart disease, and a review about a gene that affects autoimmune inflammation.

Last week's articles on rheumatology topics in the major nonspecialty journals.

Autoimmune Blistering Diseases

Case 22-2013 - A 51-Year-Old Woman with Epistaxis and Oral Mucosal UlcersNew England Journal of Medicine, July 18, 2013.

A middle-aged woman had a 3-year history of epistaxis, sore throat, fullness in the ears, lower gastrointestinal tract ulcers, and painful oral ulcers that responded to glucorticoids. Immune-mediated disorders (granulomatosis with polyangiitis, aphthous ulcers, Behets, erythema multiforme and lichen plantus) were ruled out. The oral lesions seemed to suggest autoimmune blistering diseases, particularly pemphigus vulgarus or mucous-membrane pemphigoid. The case study reviews how to distinguish these conditions and their autoimmune targets.


Granulomatous tattoo reaction in a young manLancet, July 20, 2013.

Tattoos sometimes cause sarcoidosis. In this case, small erythematous papules and plaques  appeared under a 12-year-old tattoo on a 37-year-old man’s right leg, followed by muscle ache in both legs, pain and swelling of both ankles, fever, fatigue and night sweats. Sarcoidosis was diagnosed. The patient became symptom-free after oral prednisone, which was tapered off.


Association of plasma uric acid with ischaemic heart disease and blood pressure: mendelian randomisation analysis of two large cohortsBMJ, July 18, 2013.

A prospective cohort study of 70,000 participants in Denmark found no causal association between uric acid and ischemic heart disease. However, higher body mass index (BMI) caused increased uric acid level and hyperuricemia. Every four-unit increase in BMI increased uric acid by 0.03 mmol/L and increased risk for hyperuricemia by 7.5%.



The Autoimmunity-Associated Gene PTPN22 Potentiates Toll-like Receptor-Driven, Type 1 Interferon-Dependent ImmunityImmunity, July 18, 2013

A variant in the gene PTPN22 confers increased risk for human autoimmune and infectious disease. Now researchers have figured out why. Viral pathogens engage toll-like receptors in myeloid immune cells, such as dendritic cells and macrophages, which activates a pathway that produces type 1 interferons. PTPN regulates that pathway, promoting interferon response to viral infection but suppressing interferon-mediated inflammation in autoimmune disease (such as colitis and arthritis), through an ubiquitination mechanism. The PTPN22 variant fails to promote ubiquitination.


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