Successful use of rituximab for cutaneous vasculitis.
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Abdomen↗
Biomedical subjects
Lorinda Chung
Publications and source records attributed to Lorinda Chung.
A pilot trial of treprostinil for the treatment and prevention of digital ulcers in patients with systemic sclerosis.
We performed a pilot trial of subcutaneous treprostinil for the treatment of digital ulcers in scleroderma. Of the 5 patients completing therapy, ulcer size significantly decreased and no new ulcers occurred on continuous therapy. Although effective, the high rate of injection site reactions may limit the utility of this therapy.
Adult↗
Digital ulcers in patients with systemic sclerosis.
Digital ulcers (DU), defined as necrotic lesions located at distal digits or overlying bony prominences, occur in up to 50% of patients with limited or diffuse systemic sclerosis (SSc). These lesions are extremely painful and lead to substantial functional disability. The pathogenesis of DU differs depending on their location. DU located at distal aspects of digits are thought to be related to tissue ischemia from several processes, including vasospasm secondary to Raynaud's phenomenon, intimal fibro-proliferation, and thrombosis of digital arteries. DU located over bony prominences, such as the phalangeal joints and elbows, are thought to be due to repetitive microtrauma and difficulty healing due to atrophic, avascular tissue overlying the joints. Management of DU include non-pharmacologic and pharmacologic modalities. This review summarizes the current available and investigational therapies for the treatment and prevention of DU in patients with SSc.
Anticoagulants↗
Coronary artery disease in patients with systemic lupus erythematosus.
BACKGROUND: A 24-year-old woman with an 11-year history of systemic lupus erythematosus presented with exacerbation of chronic abdominal pain followed by substernal chest pain. She had a history of pericarditis secondary to systemic lupus erythematosus and of varicella-zoster reactivation secondary to immunosuppression. Long-term medications included prednisolone, hydroxychloroquine, aspirin, and mycophenolate mofetil. INVESTIGATIONS: Physical examination, mesenteric angiography, CT of the abdomen, esophagogastroduodenoscopy, colonoscopy, pelvic ultrasound, laboratory testing, serologic testing, cardiac echocardiography, electrocardiography and coronary angiography. DIAGNOSIS: Acute myocardial infarction secondary to severe multivessel atherosclerotic coronary artery disease. MANAGEMENT: Intra-aortic balloon pump followed by emergent four-vessel coronary artery bypass grafting. Aspirin, hydroxychloroquine, and mycophenolate mofetil were continued and a judicious tapering of prednisolone was initiated.
Adult↗
Antibodies in scleroderma: direct pathogenicity and phenotypic associations.
Scleroderma is an autoimmune disease involving endothelial cell damage and fibroblast overproduction of extracellular matrix. Several autoantibodies present in the sera of patients with scleroderma, including anti-endothelial cell, antifibroblast, anti-matrix metalloproteinase, and antifibrillin-1 antibodies, may directly contribute to disease pathogenesis. Scleroderma also is characterized by the presence of antinuclear and antinucleolar antibodies, which correlate with particular phenotypes. These include antitopoisomerase-I, anticentromere, antihistone, anti-polymyositis/scleroderma, anti-Th/To, anti-U3-small nucleolar ribonucleoprotein particle, anti-U1-small nuclear ribonucleoprotein particle, anti-RNA polymerase, and anti-B23 antibodies. Other antibodies classically associated with other autoimmune diseases, such as antiphospholipid, antineutrophil cytoplasmic, and antimitochondrial antibodies, also have been described in patients with scleroderma. This review will summarize the various autoantibodies associated with scleroderma, their putative pathogenic roles, and their phenotypic correlations.
Autoantibodies↗
Systemic and localized scleroderma.
Sclerosing conditions of the skin are manifested by a full spectrum of presentations that includes skin-limited forms as well as those which can involve internal organs and result in death. At this point, we are just beginning to understand the mechanisms of tissue fibrosis, and it is likely that the fibrotic processes are a heterogeneous group of disorders in which perturbation of multiple molecular pathways, including vascular and immunologically mediated pathways, can lead to fibrosis. We now have some moderately effective therapies for vascular aspects of systemic sclerosis (eg, bosentan for pulmonary arterial hypertension, calcium-channel blockers for Raynaud's, or angiotensin-converting enzyme inhibitors for renal crisis). We also are beginning to find treatments interrupting the immunologic pathways that manifest as systemic sclerosis (eg, methotrexate for the skin or cyclophosphamide for the lungs). The basic process of fibrosis, however, awaits proven, effective therapy.
Antipruritics↗