ABSTRACT
We report a 68-year-old woman with a history of idiopathic pulmonary fibrosis, who had immediate skin reactions associated with the use of pirfenidone in two opportunities. In the evaluation by immunology, an allergy to pirfenidone was diagnosed. Given the urgent need for the drug, a desensitization procedure was started. The dose of the medication was increased progressively, previous premedication with cetirizine, ranitidine and montelukast. After this procedure the patient was able to tolerate the treatment with pirfenidone without cutaneous reactions.
ABSTRACT
The main treatment for patients with severe Covid-19 is to maintain adequate ventilatory support and monitor the possible progression of the disease. Therapeutic strategies such as High Flow Nasal Cannula, awake prone position, antithrombotic prophylaxis and the use of dexamethasone. There have improved the probability of not presenting complications and not requiring invasive mechanical ventilation. The use of convalescent plasma is still under investigation and is currently only recommended in clinical trials. Finding antivirals that allow treating the infection and clinically improving patients has led to mounting studies with different methodologies, and currently there are specific and limited indications for their routine use, as in the case of Remdesivir, which has been approved by the FDA as emergency treatment in severe cases. Immunomodulatory treatments are still under study. An example of this is Tocilizumab and Anakinra, which have shown promising results for the management of seriously ill patients. It should be noted that there are many therapies that are being tested and that every day the information about the results obtained is changing. (AU)
Subject(s)
Humans , Male , Female , COVID-19/therapy , Antiviral Agents/therapeutic use , Protease Inhibitors/therapeutic use , Antibodies, Monoclonal/therapeutic useABSTRACT
SARS-CoV-2 infection in the people has been characterized by great variability in the clinical manifestations, ranging from an asymptomatic infection in some individuals to a fatal disease in others. Recently, the importance of human genetics in determining clinical response has been highlighted. Within this context there are patients who don't become infected despite viral exposure and others who, being young without comorbidities, develop a severe disease. On the other hand, it's under constant investigation whether the presence of a concomitant primary or secondary immunodeficiency determines a different clinical course. (AU)
Subject(s)
Humans , SARS-CoV-2/immunology , SARS-CoV-2/pathogenicity , COVID-19/diagnosis , COVID-19/immunologyABSTRACT
La osteoartritis es una enfermedad de alto impacto que produce importante morbilidad y discapacidad en adultos sobre 60 años. Su proceso patológico se caracteriza por degeneración del cartílago articular, asociado a inflamación secundaria, lo que produce cambios proliferativos con la formación de osteofitos y esclerosis del hueso subcondral. Actualmente existe evidencia de la importancia del proceso inflamatorio subyacente, destacando la participación de polimorfismos genéticos que fomentan el proceso inflamatorio. Asociado a esto, se ha evidenciado un cambio en el fenotipo del condrocito, el cual produce mayor cantidad de IL-1-beta y TNF-alfa, las que activan el catabolismo del cartílago. Además, se postula que la sinovial actuaría como un potenciador de la inflamación, pues los fibroblastos ahí presentes son capaces de producir diversas sustancias proinflamatorias, tales como citoquinas, prostaglandinas y óxido nítrico. Por otra parte, alteraciones mecánicas y la obesidad pueden activar al condrocito, fomentado su cambio de fenotipo, lo que aumenta la producción de citoquinas proinflamatorias que aumentan el daño cartilaginoso. Sin embargo, aún no existe claridad sobre los gatillantes exactos del proceso inflamatorio en OA.
Osteoarthritis (OA) is a disease of high impact that produces significant morbidity and disability in adults over 60 years. His disease process is characterized by degeneration of articular cartilage, associated with secondary inflammation that produces proliferative changes with osteophyte formation and subchondral bone sclerosis. There is evidence of the importance of the underlying inflammatory process, highlighting the involvement of genetic polymorphisms that promote the inflammatory process. Associated with this has shown a change in chondrocyte phenotype which produces more IL-1-beta and TNF-alpha, which activate the catabolism of cartilage. Furthermore, it is postulated that synovial act as an enhancer of inflammation present there as fibroblasts are capable of producing various proinflammatory substances such as cytokines, prostaglandins and nitric oxide. Moreover, mechanical alterations and obesity can activate the chondrocyte phenotype promoted the change of increasing the production of proinflammatory cytokines that promote cartilage damage. However, even there is no clarity on the exact gatillantes the inflammatory process in OA.