Grado de conocimiento de la osteoporosis en mujeres posmenopáusicas / No disponible

En enfermedades asintomáticas como la osteoporosis es especialmente importante que las pacientes conozcan la enfermedad, sus tratamientos y las pautas de vidanecesarias para prevenir de ese modo las posibles fracturas y sus consecuencias. En un estudio observacional, prospectivo, multicéntrico, comparativo y abierto de 12 meses de duración para evaluar el cumplimiento, como objetivo secundario del estudio se analizó el grado de conocimiento de la enfermedad mediante la prueba de Batalla, modificada para la osteoporosis. Los resultaron mostraron que, globalmente, el 49,3% de las pacientes tenía un conocimientoaceptable de la enfermedad, el 14,3% medianamente aceptable y en un 36,5% era inaceptable. Por tanto, si bien el grado de conocimiento de la osteoporosisen mujeres posmenopáusicas españolas fue aceptable, el conocimiento de esta enfermedad es todavía deficiente en más del 50%, por lo que es necesario continuaraumentando el conocimiento de la enfermedad en esta población

In asymptomatic diseases such as osteoporosis, it is especially important for the patients to know about the disease, its treatment and the life guidelines necessaryto prevent this method of possible fractures and their consequences. In an observational, prospective, multicenter, comparative and open label 12 monthlong study to evaluate compliance, as a secondary objective of the study, grade of knowledge of the disease was evaluated to study compliance using theBatalla test, modified for osteoporosis. The results showed that, overall, 49.3% of the patients had acceptable knowledge about the disease, 14.3% somewhatacceptable and 36.5% unacceptable knowledge. Thus, although the grade of knowledge on osteoporosis in postmenopausal Spanish women was accepted,knowledge on osteoporosis is still deficient in more than 50%. Thus, it is necessary to continue to increase knowledge about the disease in this population

Pseudohipertrofia muscular asociada a hipotiroidismo (síndrome de Hoffmann) / Muscle pseudohypertrophy associated with hypothyroidism (Hoffman´s syndrome)

No disponible

[Cryptococcosis of the central nervous system. A report of five cases]. / Criptococosis del sistema nervioso central. A propósito de cinco casos.

INTRODUCTION: Since the 1980s, in relation to the spread of AIDS, there has been an enormous increase in cryptococcosis, a mycotic disorder which usually affects the central nervous system (CNS). This disease is caused by Cryptococcus neoformans, a microorganism acquired by inhalation of bird excrement. This germ produces a capsule which protects it from phagocytosis, can synthesize melanin which acts as an antioxidant of the cytotoxic lymphocytes and can reproduce at body temperature. Clinically it may show as chronic or subacute meningitis and/or encephalitis, as endocranial hypertension or as an intracranial space occupying lesion (crytococcoma). To establish the diagnosis, Chinese ink, culture and the latex agglutination test are useful. Treatment is with amphotericin B associated or not with fluocytokine and fluconazole, the protocol used depending on the clinical form. OBJECTIVE: To review the most up-to-date literature on cryptococcosis of the CNS to study the condition in relation to five cases. CLINICAL CASES: We report five patients with cryptococcosis of the CNS diagnosed and treated in the Instituto Nacional de Neurología y Neurocirugia de la Habana, Cuba, showing an increase in the frequency of the occurrence of cases not related to HIV infection, great variety of clinico-humoral presentation and the characteristics of the treatment given. CONCLUSION: Cryptococcosis can be cured completely when the condition is diagnosed early; without treatment it is invariably fatal.

Criptococosis del sistema nervioso central. A propósito de cinco casos / Cryptococcosis of the central nervous system. A report of five cases

Introducción. Desde la década de los 80 ha existido, en relación con la generalización del sida, un incremento vertiginoso de la criptococosis, enfermedad micótica que con mayor frecuencia afecta el sistema nervioso central (SNC). Esta enfermedad es producida por el Criptococcus neoformans, un microrganismo que se adquiere por inhalación desde las heces de aves. Dicho germen produce una cápsula que lo protege de la fagocitosis, es capaz de sintetizar melanina que actúa como antioxidante ante los linfocitos citotóxicos y puede reproducirse a la temperatura corporal. Clínicamente puede manifestarse como una meningitis y/o encefalitis subaguda o crónica, como una hipertensión endocraneal o proceso ocupativo intracraneal (criptococoma). Para establecer el diagnóstico es muy útil la tinción con tinta china, el cultivo y la prueba de aglutinación en látex. El tratamiento consiste en la administración de anfotericina B asociado o no a fluocitocina y fluconazol, con diferentes esquemas en función de la forma clínica. Objetivo. Revisar la literatura más actualizada sobre la criptoccosis del SNC con el objetivo de profundizar en el conocimiento de esta entidad, a propósito de cinco pacientes.Casos clínicos. Se presentan cinco pacientes con criptococosis del SNC diagnosticados y tratados en el Instituto Nacional de Neurología y Neurocirugía de la Habana, Cuba, que muestran un aumento en la frecuencia de aparición de los casos no relacionados con la infección por VIH, la multivariedad en la presentación clínico-humoral y las particularidades del tratamiento empleado. Conclusión. La criptococosis es una enfermedad perfectamente curable con un diagnóstico temprano; sin tratamiento, es inevitablemente fatal (AU)

A platelet activating factor receptor antagonist prevents the development of chronic arthritis in mice.

OBJECTIVE: To examine the effect of treatment with the platelet activating factor (PAF) receptor antagonist BN 50730 on the clinical and morphological evolution of collagen induced arthritis in mice. METHODS: Mice with collagen induced arthritis were treated with BN 50730 (0.3, 1, 3 mg/kg) or vehicle (0.1% Tween-20 in saline) once a day, from 3 days before the induction of the arthritis to 70 days after. Disease evolution was followed daily by inspection of inflammatory signs and measurement of the knee joint diameter on Days 0, 40, and 70. At the end of the treatment period, the morphological evaluation of the synovial membrane, the immunodetection of fibronectin, and the content of cartilage proteoglycans were studied. RESULTS: On Day 40, mice receiving the highest dose of BN 50730 (3 mg/kg) showed a reduction in the knee joint diameter in comparison with untreated (2.1 +/- 0.2 vs 2.8 +/- 0.4 mm, p < 0.01). On Day 70, animals receiving 1 and 3 mg/kg had a normal knee diameter, while it remained enlarged in the untreated ones. In BN 50730 treated mice (3 mg/kg) we also observed a significant reduction of the inflammation score (0.1 +/- 0.1 vs 2.5 +/- 0.2 in the untreated) and deposition of fibronectin. Depletion of cartilage proteoglycans was also reversed with BN 50730. CONCLUSION: The beneficial effects in this model of joint injury after administration of the PAF antagonist BN 50730 suggest that PAF could be implicated in the pathogenesis of chronic arthritis.

Tenidap decreases IL-8 and monocyte chemotactic peptide-1 (MCP-1) mRNA expression in the synovial tissue of rabbits with antigen arthritis and in cultured synovial cells.

Since IL-8 and MCP-1 are chemoattractant proteins that participate in the recruitment of inflammatory cells into the arthritic joint, we examined the effects of tenidap, a new anti-inflammatory drug of the oxindole family, on IL-8 and MCP-1 expression in the joints of rabbits with acute antigen arthritis. The model was induced by injecting 5 mg/ml ovalbumin into the knees of 20 preimmunized rabbits. Animals were randomized into two groups: treated with tenidap (15 mg/kg per 12 h), or untreated. The effect of tenidap treatment was evaluated on chemokine production in synovial membranes of rabbits with arthritis and in cultured monocytic and synovial cells (SC). By immunoperoxidase staining, chemokines were localized in the synovial tissue. Chemokine messenger RNA levels in the synovial membranes and in cultured cells were analysed by reverse transcription-polymerase chain reaction (RT-PCR). At the end of the study, tenidap significantly reduced neutrophil infiltration into the joint cavity (27+/-4 x 10(6) cells/ml versus 45+/-6 x 10(6) cells/ml in untreated; P<0.05), and synovial effusion (134+/-15 microl versus 236+/-19 microl in untreated; P<0.005). Untreated rabbits showed synovial membrane up-regulation in mRNA expression of IL-8 and MCP-1 (11- and seven-fold versus healthy rabbits, respectively) that was markedly decreased by tenidap (two- and three-fold versus healthy rabbits, respectively). IL-8 and MCP-1 were localized in the synovial tissue in a perivascular pattern and areas of the interstitium and lining, mostly coinciding with cell infiltration. Tenidap also reduced the accumulation of IL-8 and MCP-1 proteins. In cultured synovial and monocytic cells, tumour necrosis factor-alpha (TNF-alpha) elicited an increase in gene expression of IL-8 (four- and nine-fold, respectively) and MCP-1 (nine- and four-fold, respectively) that was significantly reversed in both cell types by 10 microM tenidap. These results suggest that the beneficial effect of tenidap in acute antigen arthritis could be related to the down-regulation in gene expression and synthesis of IL-8 and MCP-1, two key chemokines involved in the recruitment of inflammatory cells.

Anti-inflammatory effect of a PAF receptor antagonist and a new molecule with antiproteinase activity in an experimental model of acute urate crystal arthritis.

Platelet activating factor (PAF) is a potent mediator of allergic and inflammatory reactions in different pathological conditions. During recent years there has been increasing evidence that PAF can play an important role in the pathogenesis of arthritis. The PMN proteinases make an important contribution to the final tissue joint destruction in arthritis. In a rabbit model of acute crystal arthritis, we have compared the anti-inflammatory effect of two new molecules: BN 50727 with anti-PAF activity, and BN 50548 an inhibitor of PMN proteinases. These molecules were administered dissolved in DMSO at doses of 6 mg/kg three times daily i.p., beginning 24 h before the induction of arthritis. Compared with the untreated animals those receiving the drugs, presented a significant diminution in: (1) the synovial fluid volume; (2) the amount of cells infiltrating the joint cavity and the synovial membrane; and (3) the PGE2 concentration. Furthermore, in both groups of treated rabbits there was a significant decrease in synovial IL-6 concentration and in C-reactive protein serum levels and an important decline of histopathological score. The treatment with BN 50548 induced a significant reduction of TNF levels in the synovial fluid vs DMSO-treated and untreated rabbits. These results further strengthen that in an acute experimental arthritis model, molecules with capacity to antagonize the in vivo action of PAF have an anti-inflammatory effect reflecting an important role for this mediator in the pathogenesis of arthritis. We have also seen that an inhibitor of proteinases is capable of improving the joint inflammation apparently through a decrease in tumor necrosis factor (TNF) and interleukin-6 (IL-6) synovial levels. Furthermore, the proteinase inhibitor treatment preserves the loss of articular proteoglycan content, in an acute arthritis model. In conclusion, BN 50727 and BN 50548, two compounds with PAF antagonist and antiproteinase activity, respectively exert an anti-inflammatory effect in an experimental model of acute urate crystal arthritis, probably due to a decrease in TNF alpha and IL-6 synthesis.

IL-1 beta and IL-6 stimulate the production of platelet-activating factor (PAF) by cultured rabbit synovial cells.

The aim of this study was to determine whether synovial cells are capable of producing PAF in the presence of cytokines such as IL-1 beta and IL-6 and other stimuli. Synovial cells were obtained from joints of healthy rabbits. PAF production was assayed by measurement of serotonin release in rabbit platelets and the incorporation of 3H-acetate into PAF. Synovial cells produced PAF after 5 min of incubation with ionophore A23187, reaching the maximal amount at 15 min (4.3 +/- 0.7 x 10(-3) pmol of PAF/mg protein, P < 0.005, n = 4), and declining afterwards. The treatment of synoviocytes with IL-1 beta and IL-6 induced synthesis of PAF after 5 min of stimulation, reaching the greatest production at 15 min with IL-6 and 30 min with IL-1 beta (3.6 +/- 1.1 x 10(-3) and 3.3 +/- 1.2 pmol of PAF/mg protein, respectively, P < 0.05, n = 4). The incubation of the cells with PMSF, an inhibitor of acetylhydrolase, before the addition of the stimuli, increased the incorporation rate of 3H-acetate, suggesting a rapid degradation of PAF by synoviocytes. These results demonstrate that synovial cells can produce PAF after stimulation with agonists, such as ionophore, and cytokines. Thus, PAF, acting alone or with other mediators, could amplify the inflammatory joint reaction.