Relación entre la prolactina y la retinopatía diabética / Relation between prolactin and diabetic retinopathy

La retinopatía diabética, como forma de microangiopatía, se caracteriza por la pérdida de los pericitos y de las células endoteliales, lo que conlleva a una alteración de la permeabilidad de los capilares retinianos. El factor de crecimiento del endotelio vascular estimula directamente el desarrollo de la vasculatura interna y externa del ojo, y actúa además como un factor de permeabilidad vascular. Por lo general, en condiciones naturales, existe un equilibrio entre las moléculas promotoras y las inhibidoras de la angiogénesis; sin embargo, cuando estas condiciones son alteradas, como sucede durante los episodios de hipoxia o inflamación, este equilibrio se rompe, e inclina la balanza hacia la formación de vasos anormales que se extienden y sangran dentro del vítreo, y pueden provocar el desprendimiento de la retina, con la consiguiente pérdida de la visión. Se han desarrollado algunos medicamentos antiangiogénicos que reducen la expresión del factor de crecimiento del endotelio vascular y del factor de crecimiento del tejido conectivo en las células del epitelio retiniano expuestas al estrés oxidativo. Se ha avanzado también en el desarrollo de otros medicamentos con acción antiangiogénica, con gran efectividad en su uso, solos o combinados con fotocoagulación láser y cirugía, pero son muy costosos, solo disponibles en centros muy especializados, y la vía de administración es intravítrea. En la actualidad se conoce que la hormona hipofisaria prolactina, puede prevenir la progresión y promover la regresión de la retinopatía diabética a través de su conversión proteolítica a vasoinhibinas, en particular, la fracción de menor peso molecular (16 kDa-Prolactina), con importante acción antiangiogénica, bloqueando la estimulación de la angiogénesis inducida por varios factores, como el factor de crecimiento del endotelio vascular, y el factor de crecimiento fibroblástico en la proliferación de las células endoteliales, lo cual abre la esperanza de nuevos medicamentos para el tratamiento de la retinopatía proliferativa, aspectos sobre los que trata la presente revisión(AU)

Diabetic retinopathy, as a form of microangiopathy, is characterized by loss of pericytes and of endothelial cells, which causes alteration of the permeability of the retinal capillaries. The growth factor of the vascular endothelium directly stimulates the development of the internal and external vasculature of the eye, and additionally acts as a vascular permeability factor. In general, under natural conditions, there is a balance of promoting and inhibitory cells of angiogenesis. However, if these conditions are changed -as it happens during the hypoxia or inflammation episodes- this balance breaks and this tips the balance in favor of the formation of abnormal vessels that spread over and bleed into the vitreous, an event that may cause the retinal detachment and the resulting loss of vision. Some antiangiogenic drugs have been developed to reduce the expression of the vascular endothelium growth factor and of the connective tissue growth factor in the retinal epithelium cells under oxidative stress. Advances have also been made in the development of other antiangiogenic drugs of high effectiveness when they are used alone or combined with laser photocoagulation and surgery, but they are very expensive, available only in highly specialized centers and with intravitreal administration. Nowadays, it is known that hyphophysial hormone called prolactin can prevent the progress and encourage the regression of diabetic retinopathy through its proteolytic conversion to vasoinhibins, particularly, the lowest molecular weight fraction (16 kDa-prolactin). This fraction has an important antiangiogenic action since it blocks the stimulation of angiogenesis induced by several factors such as the vascular endothelium growth factor and the fibroblastic growth factor in the proliferation of the endothelial cells, all of which brings the possibilities of new drugs for the treatment of proliferative retinopathy. These are the aspects addressed in the present review(AU)

Diagnostic potential of 16 kDa (HspX, α-crystalline) antigen for serodiagnosis of tuberculosis.

Background & objectives: Tuberculosis (TB) is a public health problem worldwide. Rapid and accurate diagnosis of tuberculosis is crucial to facilitate early treatment of infectious cases and to reduce its spread. The present study was aimed to evaluation of 16 kDa antigen as a serodiagnostic tool in pulmonary and extra-pulmonary tuberculosis patients in an effort to improve diagnostic algorithm for tuberculosis. Methods: In this study, 200 serum samples were collected from smear positive and culture confirmed pulmonary tuberculosis patients, 30 tubercular pleural effusions and 21 tubercular meningitis (TBM) patients. Serum samples from 36 healthy, age matched controls (hospital staff), along with 60 patients with non-tubercular respiratory diseases were also collected and evaluated. Humoral response (both IgG and IgA) was looked for 16 kDa antigen using indirect ELISA. Results: Sensitivity of detection in various categories of pulmonary TB patients ranged between 73.8 and 81.2 per cent. While in the extra-pulmonary TB samples the sensitivity was 42.8 per cent (TBM) and 63.3 per cent (tubercular pleural effusion). The test specificity in both the groups was high (94.7%). All of the non-disease controls were negative. Among non-tubercular disease controls, five patients gave a positive humoral response against 16 kDa. Interpretation & conclusions: Serodiagnostic tests for TB have always had drawbacks of suboptimal sensitivity and specificity. The antigen used in this study gave encouraging results in pulmonary TB only, while in extra-pulmonary TB (tubercular meningitis and tubercular pleural effusion), this has shown a limited role in terms of sensitivity. Further work is required to validate its role in serodiagnosis of TB especially extra-pulmonary TB.