Síndrome de hipermovilidad articular / Joint hypermobility syndrome

Resumen: El síndrome de hipermovilidad articular es un desorden hereditario con patrón autosómico dominante; se caracteriza por hiperlaxitud articular y dolores musculoesqueléticos. El término hipermovilidad se refiere al incremento en los movimientos activos o pasivos de las articulaciones con base en sus rangos normales. El síndrome de hipermovilidad articular presenta además síntomas gastrointestinales, trastornos de sueño, fibromialgia, trastornos sicológicos, cefalea migrañosa, oftálmicos, autonómicos, entre otros. Para diagnosticar el síndrome de hipermovilidad, en general son aceptados los criterios de Brighton, los cuales fueron publicados en 1998. También se le conoce como síndrome de hipermovilidad articular benigno. El término benigno se utiliza para distinguirlo de otras condiciones más severas como Ehler-Danlos (tipo clásico o vascular), síndrome de Marfan y osteogénesis imperfecta. El tratamiento con fisioterapia y medidas farmacológicas ayudan a mejorar la calidad de vida de los pacientes.

Abstract: Joint hypermobility syndrome is an inherited disorder with autosomal dominant pattern; is characterized by joint hyperlaxity and musculoskeletal pains. Thermal hypermobility refers to the increase in active or passive movements of joints based on their normal ranges. Joint hypermobility syndrome also has gastrointestinal symptoms, sleep disorders, fibromyalgia, psychological disorders, migraine headache, ophthalmic, autonomic, among others. To diagnose hypermobility syndrome, Brighton's criteria are generally accepted and published in 1998. This criteria also known as benign joint hypermobility syndrome. The term benign is used to distinguish it from other more severe conditions such as Ehler-Danlos (classic or vascular type), Marfan syndrome, and imperfect osteogenesis. Treatment with physiotherapy and pharmacological means help improve patients' quality of life.

[Joint hypermobility syndrome]. / Síndrome de hipermovilidad articular.

Joint hypermobility syndrome is an inherited disorder with autosomal dominant pattern; is characterized by joint hyperlaxity and musculoskeletal pains. Thermal hypermobility refers to the increase in active or passive movements of joints based on their normal ranges. Joint hypermobility syndrome also has gastrointestinal symptoms, sleep disorders, fibromyalgia, psychological disorders, migraine headache, ophthalmic, autonomic, among others. To diagnose hypermobility syndrome, Brighton's criteria are generally accepted and published in 1998. This criteria also known as benign joint hypermobility syndrome. The term benign is used to distinguish it from other more severe conditions such as Ehler-Danlos (classic or vascular type), Marfan syndrome, and imperfect osteogenesis. Treatment with physiotherapy and pharmacological means help improve patients' quality of life.

El síndrome de hipermovilidad articular es un desorden hereditario con patrón autosómico dominante; se caracteriza por hiperlaxitud articular y dolores musculoesqueléticos. El término hipermovilidad se refiere al incremento en los movimientos activos o pasivos de las articulaciones con base en sus rangos normales. El síndrome de hipermovilidad articular presenta además síntomas gastrointestinales, trastornos de sueño, fibromialgia, trastornos sicológicos, cefalea migrañosa, oftálmicos, autonómicos, entre otros. Para diagnosticar el síndrome de hipermovilidad, en general son aceptados los criterios de Brighton, los cuales fueron publicados en 1998. También se le conoce como síndrome de hipermovilidad articular benigno. El término benigno se utiliza para distinguirlo de otras condiciones más severas como Ehler-Danlos (tipo clásico o vascular), síndrome de Marfan y osteogénesis imperfecta. El tratamiento con fisioterapia y medidas farmacológicas ayudan a mejorar la calidad de vida de los pacientes.

Seroprevalence of Trypanosoma cruzi in kidney transplant donors and recipients in Mexico City.

Infectious diseases are common causes of morbidity and mortality among kidney transplant recipients. Chagas disease (CD) has been recognized as an emerging infectious complication of transplantation caused by the parasite Trypanosoma cruzi. CD is prevalent in Mexico, particularly in the southern coastal region. The impact on Mexican kidney transplant programs has not been previously studied prospectively. From 2009 through 2010, serum samples from 59 kidney transplant donors and 405 renal transplant recipients were screened for antibodies against T. cruzi. Serum was initially screened using a locally developed ELISA test; positive results were confirmed by an indirect immunofluorescense test, in accordance with Panamerican Health Organization/World Health Organization guidelines. None of the donors were seropositive for T. cruzi, while 8 (1.97%) kidney transplant recipients were confirmed to be seropositive for T. cruzi. None of them have developed clinical manifestations of CD, although specific screening of recipients was not performed. A prospective study is planned to define the epidemiology and outcome of CD among kidney transplant donors and recipients in Mexico more thoroughly.

Immune response after rabies vaccine in a kidney transplant recipient.

A 48-year-old male kidney-transplant recipient was bitten by a rabid dog. His immunosuppressive treatment consisted of cyclosporine 60 mg b.i.d., mycophenolate mofetil (MMF) 250 mg t.i.d., and prednisone 5 mg. After wound care, he received 5 doses of purified vero cell rabies vaccine on days 0, 3, 7, 14, and 28, and human rabies immunoglobulin, according to international guidelines. Adequate levels of rabies virus neutralizing antibodies were observed after the administration of the third vaccine dose. However, a decrease of antibody titer was detected by day 28. Immunosuppressive medication was minimized, withdrawing MMF and reducing the dose of cyclosporine. Booster doses of the same vaccine were administered on days 38, 41, 45, 52, and 66. Adequate neutralizing antibody response was recovered during the ensuing 12 months, under reduced immunosuppression. Nineteen months after the incident, the patient remains with good graft function and is asymptomatic for rabies. It remains to be determined whether the attained immune response was either the result of the booster vaccinations or the reduction of immunosuppression alone. Nevertheless, such an outcome would have been possible only with the combined management strategy implemented.