Showing 1 – 20 of 4095
Relevance | Newest | Oldest |
  • JAMA May 10, 2016

    Figure 3: Time to First Digital Ulcer Complication Up to End of Treatment in DUAL-1 and DUAL-2

    Digital ulcer complications were defined as any of the following (resulting from digital ulcer worsening): (1) critical ischemic crisis necessitating hospitalization; (2) gangrene, (auto) amputation; (3) failure of conservative management: surgical and chemical sympathectomy, vascular reconstructions, or any unplanned surgery in the management of hand systemic sclerosis manifestations; (4) use of parenteral prostanoids; (5) use of endothelin receptor antagonists; (6) required class 2, 3, or 4 narcotics or a >50%-increase in the existing dose compared with baseline; (7) initiation of systemic antibiotics for the treatment of infection attributed to digital ulcers.A, Treatment effect for macitentan, 3 mg vs placebo: hazard ratio (HR), 0.77 (95% CI, 0.38-1.57); log-rank P = .47; for macitentan, 10 mg vs placebo: HR, 1.12 (95% CI, 0.58-2.15); log-rank P = .74. The median duration (Q1, Q3) of treatment exposure was 41.4 weeks (22.1, 59.9) in the macitentan, 3-mg group, 37.4 weeks (18.3, 63.5) in the macitentan, 10-mg group, and 43.1 weeks (22.9, 65.1) in the placebo group.B, Treatment effect of macitentan, 3 mg vs placebo: HR, 1.19 (95% CI, 0.61-2.33); log-rank P = .62; for macitentan, 10 mg vs placebo: HR, 1.08 (95% CI, 0.4-2.15); log-rank P = .84. The median duration (Q1, Q3) of treatment exposure was 40.5 weeks (17.7, 61.7) in the macitentan, 3-mg group, 38.6 weeks (15.0, 62.1) in the macitentan, 10-mg group, and 37.4 weeks (17.0, 58.1) in the placebo group.
  • JAMA June 16, 2015

    Figure: Recurrent Oral Ulcers

    Round, symmetric ulcer, measuring approximately 8 mm × 8 mm, with pseudomembrane and erythematous halo on the left lateral surface of the tongue.
  • JAMA December 3, 2014

    Figure: Example of Relationship of Risk Factors With Lifetime Benefit of Colorectal Cancer Screening With Colonoscopy

    CRC indicates colorectal cancer; RR, relative risk.aIndividuals are classified as having moderate comorbidity if diagnosed with an ulcer, rheumatologic disease, peripheral vascular disease, diabetes, paralysis, or cerebrovascular disease and in case of a history of acute myocardial infarction; as having severe comorbidity if diagnosed with chronic obstructive pulmonary disease, congestive heart failure, moderate or severe liver disease, chronic renal failure, dementia, cirrhosis and chronic hepatitis, or AIDS; and as having no comorbidity if none of these conditions is present.bThe range of the background risk for CRC is based on the National Cancer Institute’s Colorectal Cancer Risk Assessment Tool. In white women, the minimum background risk for CRC is 0.5, the maximum background risk in the absence of a family history of CRC is 1.8, and the maximum risk in the presence of a family history of CRC is 3.5.
  • JAMA September 24, 2014

    Figure: Nasal Erythema and Crusting After a Trip to the Venezuelan Rainforest

    Left, Erythematous plaque with crusting on the right side of the neck. No ulceration was noted. Right, Pronounced erythema, swelling, and crusting of the left nasal ala, extending to the infratip lobule and left alar rim.
  • JAMA June 25, 2014

    Figure: Risk Ratios for Complete Venous Leg Ulcer Healing Among Patients Treated With Systemic or Topical Antimicrobial Agent vs Usual Care

    Source: Data adapted with permission from Wiley. Risk ratio estimates were plotted on a log scale. Control treatment was most often usual care (cleansing, dressings, and bandages without antimicrobial therapy).aNo mention or unclear report of ulcer infection at baseline.bEligible patients had clinically infected ulcers at baseline.cEligible patients had ulcers described as “critically colonized.”dPatients using systemic antibiotics were excluded.
  • Ulcer Insights

    Abstract Full Text
    JAMA. 2012; 307(1):24-24. doi: 10.1001/jama.2011.1906
  • JAMA December 10, 2008

    Figure 1: Presentation of Patient With Sickle Cell Disease

    A, The patient had a left medial ankle ulcer of 17 years' duration. B, One day after hospital admission with vaso-occlusive pain crisis, the patient developed a pulmonary infiltrate, encephalopathy, and renal insufficiency. Induced sputum demonstrated lipid-laden macrophages by oil red O stain (magnification × 1000), which is indicative of fat embolus to the lung from infarcted marrow. C, Approximately 2 weeks later, the patient presented with acute dysarthria and right-hand weakness. Diffusion-weighted magnetic resonance imaging (MRI) showed a bright signal in the left hemisphere (left image, arrowhead), indicating acute edema and new stroke. Additional images at the same time using the FLAIR technique (fluid-attenuated inversion recovery) demonstrated right frontal lobe cavitation (right image, left [blue] arrowhead) and chronic watershed zone infarcts (right image, right [yellow] arrowhead) from previously unsuspected ischemic strokes. Magnetic resonance angiography revealed nearly absent flow in the internal carotid arteries (not shown).
  • Nobels Honor Research on Ulcer Microbe, “Green” Drug Production Method

    Abstract Full Text
    JAMA. 2005; 294(18):2289-2290. doi: 10.1001/jama.294.18.2289
  • JAMA October 2, 2002

    Figure 2: Patient's Skin Biopsy Specimen

    Biopsy of the skin from the edge of an ulcer shows leukocytoclasis and fibrinoid necrosis in a medium-sized muscular artery situated at the junction of the deep dermis and subcutaneous fat (hematoxylin-eosin, original magnification × 400).
  • Effect of Therapeutic Footwear on Foot Reulceration in Patients With Diabetes: A Randomized Controlled Trial

    Abstract Full Text
    free access
    JAMA. 2002; 287(19):2552-2558. doi: 10.1001/jama.287.19.2552
  • Process of Care and Outcomes for Elderly Patients Hospitalized With Peptic Ulcer Disease: Results From a Quality Improvement Project

    Abstract Full Text
    free access
    JAMA. 2001; 286(16):1985-1993. doi: 10.1001/jama.286.16.1985
  • New Suppository for Ulcerative Proctitis

    Abstract Full Text
    JAMA. 2001; 285(9):1146-1146. doi: 10.1001/jama.285.9.1146-JFD10002-3-1
  • JAMA February 7, 2001

    Figure: Mechanisms in the Initiation and Progression of Atherosclerosis

    Chronic endothelial injury, inflammation, and oxidative stress are central to the development of atherosclerosis. Endothelial injury results from a variety of factors including tobacco use, hypercholesterolemia, interventional therapies with angioplasty or coronary stents, and from ulceration or fissuring of atherosclerotic plaques. At sites of endothelial injury, production of endothelial-derived substances (nitric oxide [NO], tissue plasminogen activator [tPA], and prostacyclin [PGI2]) is decreased, creating a prothrombotic environment characterized by increased platelet and leukocyte adhesion, increased permeability to plasma lipoproteins, myointimal hyperplasia, and vasoconstriction. Ulceration or fissuring of the atherosclerotic plaque results from degradation of collagen matrix in the fibrous cap by metalloproteases released from macrophages. Exposure of the subendothelium after plaque ulceration or fissuring leads to platelet adhesion and aggregation and local accumulation of largely platelet-derived mediators (thromboxane A2, serotonin, adenosine diphosphate [ADP], thrombin, platelet activating factor [PAF], oxygen-derived free radicals, tissue factor, and endothelin) that promote thrombus growth, fibroproliferation, and vasoconstriction. LDL indicates low-density lipoprotein.
  • JAMA September 27, 2000

    Figure: Peristomal Pyoderma Gangrenosum Following Relocation of a Stoma

    Patient 4 had a total proctocolectomy for ulcerative colitis 25 years prior to ulceration at the previous site of the ileostomy. A, This new ulcer developed 1 month after the relocation of her stoma and failed to respond to systemic antibiotics for a presumed wound infection. Note the ulcer's violaceous, overhanging, scalloped border. B, Healing of the lesion in the same patient following therapy with oral dapsone.
  • JAMA September 13, 2000

    Figure 2: Annualized Incidence of Upper Gastrointestinal Tract Ulcer Complications Alone and With Symptomatic Gastroduodenal Ulcers

    Numbers above bars indicate events per patient-years of exposure. NSAIDs indicates nonsteroidal anti-inflammatory drugs.
  • Gastrointestinal Toxicity With Celecoxib vs Nonsteroidal Anti-inflammatory Drugs for Osteoarthritis and Rheumatoid Arthritis: The CLASS Study: A Randomized Controlled Trial

    Abstract Full Text
    free access
    JAMA. 2000; 284(10):1247-1255. doi: 10.1001/jama.284.10.1247
  • JAMA September 13, 2000

    Figure 3: Patients With Decreases in Hematocrit and/or Hemoglobin at 6 Months

    Data are shown for patients with decreases from pretreatment levels in hematocrit of 10 percentage points or more, in hemoglobin of 20 g/L or more, or both. Results for the entire study population are shown on the left. On the right, results for all patients excluding those with an upper gastrointestinal (GI) ulcer complication, symptomatic ulcer, or other diagnosed GI disease are shown. NSAIDs indicates nonsteroidal anti-inflammatory drugs. Numbers above bars indicate the number of patients with the event per total number of patients in the treatment group.
  • A Rainbow From Joanne

    Abstract Full Text
    JAMA. 1999; 282(22):2101-2101. doi: 10.1001/jama.282.22.2101
  • JAMA November 24, 1999

    Figure: 12-Month Survival Analysis of Confirmed Upper Gastrointestinal (GI) Perforations, Symptomatic Ulcers, and Upper GI Bleeding by Combined Treatment Groups

    Relative risk with rofecoxib vs nonsteroidal anti-inflammatory drugs (NSAIDs) is 0.51 (95% confidence interval, 0.26-1.00; P = .046 by log-rank test).
  • JAMA November 24, 1999

    Figure 4: Incidence of Gastroduodenal Ulcers Over 12 Weeks of Treatment

    An ulcer was defined as any break in the mucosa at least 3 mm in diameter with unequivocal depth. For each patient there were 3 possible outcomes: known ulcer, known no ulcer, and unknown. Any endoscopic finding other than ulcer was categorized as unknown if the data were obtained before the 12-week visit. Naproxen-treated patients had a significantly greater incidence of gastroduodenal ulcers than did patients treated with either celecoxib or placebo (P<.001). The incidences of gastroduodenal ulcers in the celecoxib treatment groups were similar to that in placebo-treated patients (P>.40). Error bars indicate 95% confidence intervals. Asterisk indicates P<.001 vs all other treatments. Celecoxib and naproxen were both administered twice daily for all dosages.