Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 5 de 5
Filter
1.
Rev. chil. reumatol ; 31(4): 234-238, 2015. tab
Article in Spanish | LILACS | ID: lil-790582

ABSTRACT

Chikungunya fever is an emerging infection in our country due to travelers to endemic areas. It presents acutely with high fever, fatigue, headache, myalgia, skin rash and arthritis, usually as a symmetric polyarthritis compromising the interphalangeal and metacarpophalangeal joints, wrist, elbow, ankle and knee. While most of the symptoms last about a week, arthralgias may become chronic and generate significant functional impairment. Chikungunya has been postulated as a triggering factor for rheumatoid arthritis because of the presence of positive rheumatoid factor. We present the three confirmed cases in Almirante Nef Naval Hospital with the review of the published literature...


La fiebre de Chikungunya es una infección novedosa en nuestro país pues su contagio se produce por viajeros en zonas endémicas. Se presenta generalmente en forma aguda con fiebre alta, astenia, cefalea, mialgia, rash cutaneo y artritis, mayoritariamente como poliartritis simétrica comprometiendo las articulaciones interfalángicas, metacarpofalángicas, muñecas, codos, tobillo y rodillas. Si bien la mayoría de los síntomas duran aproximadamente una semana, las artralgias pueden hacerse crónicas y generar un importante deterioro funcional. Se ha postulado que podría ser un factor gatillante de artritis reumatoide ante la presencia de factor reumatoideo positivo. A continuación se presentan los tres casos confirmados del Hospital Naval Almirante Nef junto a la revisión de la literatura publicada hasta el momento...


Subject(s)
Humans , Male , Adult , Arthritis/virology , Chikungunya Fever/complications , Chikungunya Fever/epidemiology , Arthralgia/virology , Chile , Clinical Evolution , Diagnosis, Differential , Chikungunya Fever/therapy , Immunoglobulin G , Retrospective Studies
2.
Rev. chil. reumatol ; 26(4): 298-301, 2010.
Article in Spanish | LILACS | ID: lil-574192

ABSTRACT

Se presenta el caso de una mujer de 53 años con historia de aumento de volumen y dolor articular, pérdida de peso y síntomas sicca. El estudio de laboratorio mostró VHS elevada, anemia, linfopenia, hipocomplementemia y autoanticuerpos contra SSA/Ro y SSB/La, compatibles con un síndrome de Sjõgren (SS). Además, la radiografía de tórax mostró múltiples nódulos pulmonares, lo que fue confirmado por una TAC de tórax. El estudio histológico de los nódulos, plasmocitosis y proliferación linfocitaria atípica no demostró linfoma. Es ampliamente conocido que el SS confiere un mayor riesgo de desarrollar sindromes linfoproliferativos, lo que aumenta cuando hay presencia de vasculitis, hipo-complementemia y linfopenia. En este caso clínico el diagnóstico diferencial de la etiología de los nódulos pulmonares fue particularmente difícil. Dado lo anterior, se discute y revisa la literatura disponible acerca de compromiso pulmonar en SS.


We report the case of a 53-year old woman with a history of joint swelling and pain, weight loss and sicca symptoms. The laboratory showed a high ESR, anemia, lymphopenia, low complements and circulating auto-antibodies against SSA/Ro and SSB/La consistent with Sjõgren´s Syndrome (SS). Interestingly, the chest x-ray revealed multiple nodules in both lungs, which were corroborated by CT scan. The histological study of the pulmonary nodules showed plasmocytosis and atypical lymphocytes, but failed to demonstrate lymphoma. It is widely acknowledged that SS confers a high risk of developing lymphoproliferative syndromes, which is increased when vasculitis, low complements and lymphopenia are present. In this case, it was particularly difficult to elucidate the differential diagnosis of lung nodules. Accordingly, we discuss and review the available literature regarding pulmonary involvement in SS.


Subject(s)
Humans , Female , Middle Aged , Lung Diseases/etiology , Pseudolymphoma/etiology , Sjogren's Syndrome/complications , Lymphoma/etiology , Lung Neoplasms/etiology
3.
Rev. chil. infectol ; 26(3): 265-269, jun. 2009. ilus
Article in Spanish | LILACS | ID: lil-518465

ABSTRACT

Tungiasis is a cutaneous ectoparasitosis caused by the female sand flea Tunga penetrans whose higher prevalence occurs in Sub-Saharan África, South América and the Caribbean. We report a case of a 23 year old chilean male who presented dermal lesions suggestive of tungiasis on his return from Brazil. The diagnosis was confirmed by biopsy, identifying the arthropod and an egg from one of the lesions. The natural history, co-morbidities and treatment options were reviewed.


La tungiasis es una ectoparasitosis cutánea producida por la hembra de la pulga de arena Tunga penetrans, cuya mayor prevalencia ocurre en África Sub-sahariana, Sudamérica y el Caribe. Comunicamos el caso de un chileno de 23 años que viajó a Brasil y que a su regreso presentó lesiones dérmicas sugerentes de tungiasis. El diagnóstico fue confirmado por una biopsia identificando el artrópodo y un huevo en una de las lesiones. Se revisa la historia natural, las co-morbilidades asociadas y alternativas de tratamiento.


Subject(s)
Adult , Animals , Humans , Male , Ectoparasitic Infestations/parasitology , Siphonaptera , Travel , Brazil , Chile , Ectoparasitic Infestations/diagnosis
4.
Rev. chil. reumatol ; 24(4): 2006-211, 2008. graf
Article in Spanish | LILACS | ID: lil-532982

ABSTRACT

Los síndromes autoinflamatorios (SAI) se caracterizan por periodos recurrentes de inflamación no mediada por anticuerpos ni linfocitos T y sin desencadenantes conocidos. Investigaciones acerca de alteraciones en la regulación del inflamasoma, la producción anómala de interleukina-1 beta (IL - 1B) y el rol del factor de necrosis tumoral alfa (TNF-a) que ocurre en algunas de estas enfermedades, han permitido ampliar el conocimiento sobre los mecanismos de activación de la inmunidad innata y el uso de terapias biológicas como alternativas de tratamiento.


Autoinflammatory syndromes (AIS) are characterized by recurrent periods of inflammation, not mediated by antibody and T lymphocytes and without triggers known. Investigations about alterations in regulation of inflammasome, abnormal production of interleukin-1 beta (IL - 1b) and the role of tumor necrosis factor alpha (TNF-a) that occurs in some of these diseases, has improved knowledge about the mechanisms of activation of innate immunity and the use of biological therapies such as treatment options.


Subject(s)
Humans , Autoimmune Diseases/diagnosis , Autoimmune Diseases/immunology , Autoimmune Diseases/therapy , Inflammation/immunology , Carrier Proteins , Autoimmune Diseases/genetics , Familial Mediterranean Fever/genetics , Familial Mediterranean Fever/immunology , Familial Mediterranean Fever/therapy , Immunity, Innate , Immunoglobulin D , Receptors, Tumor Necrosis Factor , Syndrome
5.
Rev. méd. Chile ; 134(3): 391-394, mar. 2006. tab
Article in Spanish | LILACS-Express | LILACS | ID: lil-426110

ABSTRACT

Abstract: Previous trials have demonstrated that lowering low-density lipoprotein (LDL) cholesterol levels below currently recommended levels is beneficial in patients with acute coronary syndromes. We prospectively assessed the efficacy and safety of lowering LDL cholesterol levels below 100 mg per deciliter (2.6 mmol per liter) in patients with stable coronary heart disease (CHD). Methods: A total of 10,001 patients with clinically evident CHD and LDL cholesterol levels of less than 130 mg per deciliter (3.4 mmol per liter) were randomly assigned to double-blind therapy and received either 10 mg or 80 mg of atorvastatin per day. Patients were followed for a median of 4.9 years. The primary end point was the occurrence of a first major cardiovascular event, defined as death from CHD, nonfatal non-procedure-related myocardial infarction, resuscitation after cardiac arrest, or fatal or nonfatal stroke. Results: The mean LDL cholesterol levels were 77 mg per deciliter (2.0 mmol per liter) during treatment with 80 mg of atorvastatin and 101 mg per deciliter (2.6 mmol per liter) during treatment with 10 mg of atorvastatin. The incidence of persistent elevations in liver aminotransferase levels was 0.2 percent in the group given 10 mg of atorvastatin and 1.2 percent in the group given 80 mg of atorvastatin (P <0.001). A primary event occurred in 434 patients (8.7 percent) receiving 80 mg of atorvastatin, as compared with 548 patients (10.9 percent) receiving 10 mg of atorvastatin, representing an absolute reduction in the rate of major cardiovascular events of 2.2 percent and a 22 percent relative reduction in risk (hazard ratio, 0.78; 95 percent confidence interval, 0.69 to 0.89; P <0.001). There was no difference between the two treatment groups in overall mortality. Conclusions: Intensive lipid-lowering therapy with 80 mg of atorvastatin per day in patients with stable CHD provides significant clinical benefit beyond that afforded by treatment with 10 mg of atorvastatin per day. This occurred with a greater incidence of elevated aminotransferase levels.

SELECTION OF CITATIONS
SEARCH DETAIL