Diagnosing reactive arthritis: Role of clinical setting in the value of serologic and microbiologic assays

2002 ◽  
Vol 46 (2) ◽  
pp. 319-327 ◽  
Author(s):  
Joachim Sieper ◽  
Martin Rudwaleit ◽  
J�rgen Braun ◽  
D�sir�e van der Heijde
1987 ◽  
Vol 12 (1) ◽  
pp. 55-97 ◽  
Author(s):  
Fran Carnerie

AbstractMany individuals develop a temporary state of cognitive and emotional impairment after being diagnosed with catastrophic illness. Thus, when crucial decisions about medical treatment are required, they are unable to assimilate information; or worse, the legal need to be informed can rival a psychological desire to not be informed. The Canadian informed consent doctrine is unresponsive to crisis and clinically impracticable, and so paradoxically compromises the integrity and autonomy it was designed to protect. Many aspects of the physician-patient relationship and clinical setting also undermine the philosophical values enshrined in this doctrine. This further jeopardizes the individual's integrity. The Article explores proposals for change such as delaying the informing and consenting, improving the concept of consent, and improving the role of the physician.


2018 ◽  
Vol 25 (6) ◽  
pp. 1396-1401 ◽  
Author(s):  
Charis G Durham ◽  
Deepthi Thotakura ◽  
Lauren Sager ◽  
Jennifer Foster ◽  
Jon D Herrington

Objective This study evaluated the role of cetirizine compared to diphenhydramine as premedications for patients receiving paclitaxel, cetuximab, and rituximab infusions. Historically, diphenhydramine has been linked with more sedation in comparison to cetirizine; however, it is unknown if cetirizine can replace diphenhydramine in the prevention of hypersensitivity reactions in patients receiving chemotherapy. Methods This is a retrospective study designed to assess infusion reactions occurring in patients receiving diphenhydramine or cetirizine premedication for rituximab, paclitaxel, or cetuximab therapies. Infusion reactions were defined as various symptoms such as flushing, itching, alterations in heart rate and blood pressure, and dyspnea plus the clinical setting of a concurrent or very recent infusion. Results A total of 207 patients were evaluated in this study with 83 patients receiving cetirizine and 124 diphenhydramine patients. Overall, the percentage of patients with at least one chemotherapy-related infusion event in the cetirizine group was 19.3% (95% CI 11.4–29.4) compared to diphenhydramine group 24.2% (95% CI 17.0–32.7), P = 0.40. Of the patients who received cetirizine and then experienced an event in the first cycle, 41.7% (95% CI 13.7–74.3) of the events were due to paclitaxel, 50.0% (95% CI 19.4–80.6) were due to rituximab, and 8.3% (95% CI 0.1–43.6) were due to cetuximab. Of the patients who received diphenhydramine and then experienced an event in the first cycle, 26.1% (95% CI 5.7–51.4) were due to paclitaxel, 73.9% (95% CI 48.6–94.3) were due to rituximab and none due to cetuximab. Conclusion Cetirizine appears to be a viable substitute for diphenhydramine for the prevention of infusions reactions with cetuximab, paclitaxel, and rituximab infusions in adults. Prospective studies are needed to determine the efficacy and safety of cetirizine compared with diphenhydramine in the prevention of chemotherapy-related infusion reactions.


PEDIATRICS ◽  
1988 ◽  
Vol 81 (6) ◽  
pp. 915-915
Author(s):  
MITCHELL S. CAIRO

In Reply.— The comments raised by Baley et al are well taken and bring up one of the most important variables in the role of granulocyte transfusion in neonatal sepsis. Most of the studies to date have involved small numbers of patients in single institutions. This has prevented us from accumulating a large enough population of patients to adequately assess the role of either buffy coat transfusions or leukapheresed transfusions in this clinical setting. My comments in the commentary suggested that, with only eight patients in a group of preterm infants with presumed sepsis and only five patients with presumed sepsis with birth weights greater than 1,500 g, the numbers are essentially too small to determine any statistical significance between the role of buffy coat transfusions or supportive care.


2019 ◽  
Vol 13 (2) ◽  
pp. 94-99 ◽  
Author(s):  
Catherine Henshall ◽  
Andrea Doherty ◽  
Helen Green ◽  
Liz Westcott ◽  
Helen Aveyard

2006 ◽  
Vol 61 (4) ◽  
pp. 223-227 ◽  
Author(s):  
Purvita Dam ◽  
Hasibul Hasan Shirazee ◽  
Sourendra Kanta Goswami ◽  
Sanghamitra Ghosh ◽  
Ashalatha Ganesh ◽  
...  

1988 ◽  
Vol 66 (15) ◽  
pp. 662-669 ◽  
Author(s):  
P. Gross ◽  
M. Ketteler ◽  
C. Hausmann ◽  
C. Reinhard ◽  
A. Schömig ◽  
...  

2014 ◽  
Vol 31 (3) ◽  
pp. 167-184 ◽  
Author(s):  
Marina Sleptsova ◽  
Gertrud Hofer ◽  
Naser Morina ◽  
Wolf Langewitz

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Animesh Singh ◽  
Sarah Karrar

Inflammatory arthritis is a condition which is characterised by recurrent episodes of joint pain and swelling. It encompasses a spectrum of disorders ranging from rheumatoid arthritis to ankylosing spondylitis. In these conditions, for reasons that are poorly understood, the immune system raises an inflammatory response within the joint space. In some cases, autoantigens have been identified (e.g., anticitrullinated peptides in rheumatoid arthritis), but the absence of these, in the seronegative arthritides, for example, raises question as to the underlying pathogenesis. Interest has, therefore, turned to host-pathogen interactions and whether aberrant immune responses to these could explain the development of arthritis. This has been most widely studied in reactive arthritis (ReA), where an infectious episode precedes the development of the joint symptoms. In this review, we present the evidence for the role of host-bacterial interactions in the pathogenesis of joint inflammation with particular emphasis on ReA. We discuss a range of possible mechanisms including molecular mimicry, persistent low grade infections, and abnormal host responses to common bacterial causes of reactive arthritis as well as discussing some of the clinical challenges that we face in making the diagnosis and in treatment of persistent symptoms.


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