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Available data suggest a possible link between abnormal vitamin D level and abnormal glucose homeostasis, two of the most common chronic medical conditions. Both conditions are associated with inflammation, and the exact mechanism for role of either on the other is not well clear. Literature investigating the link between vitamin D and either pre-diabetic states or diabetes is reviewed. Vitamin D deficiency is detrimental to insulin synthesis and secretion in animal and human studies. In humans, it has been shown by majority of observational studies, that vitamin D is positively correlated with insulin sensitivity and its role is mediated both by direct mechanism through the availability of vitamin D receptors in several tissues and indirectly through the changes in calcium levels. Large number of, but not all, variable samples cross sectional human trials have demonstrated an inverse relation between vitamin D status and impaired glucose tolerance, insulin resistance or diabetes. To compliment this conclusively, evidence from intervention studies is critically warranted before we can frankly state that vitamin D plays a role in diabetes prevention or treatment. Absence of both sizable prospective observational trials utilizing 25(OH)D as the main variable and the non-availability of randomized studies specifically designed to assess the effects of vitamin D on pre-diabetes and diabetes states, are the main obstacles to draw solid and conclusive relationships. 相似文献
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Walker AS; Peto TE; Babiker AG; Darbyshire JH 《QJM : monthly journal of the Association of Physicians》1998,91(6):423-438
The Concorde trial compared immediate (Imm) with deferred (Def) AZT
monotherapy in asymptomatic HIV-positive participants. Haematological and
immunological markers and weight were measured throughout, and correlated
with clinical endpoints. Markers associated with disease progression (CD4
lymphocyte count and percentage, platelets, p24 antigen and beta 2
microglobulin favoured Imm: those associated with toxicity (haemoglobin,
neutrophils and white cell count) favoured Def. CD8 and total lymphocyte
count did not differ significantly between groups. In multivariate
analysis, the combination of baseline CD4, p24 antigen and beta 2m was the
best baseline predictor of disease. Including change in CD4 and beta 2m at
12 weeks, or changes over follow- up in these markers significantly
improved the fit. Markers were also incorporated into the definition of
'clinical' endpoints. Hazard ratio estimates from end-points that included
CD4 < 50 and CD4 < 25 were closest to those for AIDS or death alone,
but added very few extra events. Use of other landmark CD4 counts (100 or
greater) or relative decreases in counts (25% or more) increased the number
of events, but overestimated the effect of immediate AZT. Although AZT had
a beneficial effect on the surrogate markers of efficacy evaluated, these
changes did not predict clinical outcome, nor could the markers be usefully
incorporated into an endpoint definition.
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MATÍAS PÉREZ-PAREDES FRANCISCO PICÓ-ARACIL RAFAEL FLORENCIANO JOSÉ G. SÁNCHEZ-VILLANUEVA JOSÉ ANTONIO RUIZ ROS JUAN A. RUIPÉREZ 《Pacing and clinical electrophysiology : PACE》1999,22(8):1173-1178
This study was designed to examine the "true sensitivity" of a specific head-up tilt (HUT) testing protocol using clinical findings. The HUT protocol used 45 minutes at 60 degrees for the baseline portion and intermittent boluses of 2, 4, and 6 micrograms of isoproterenol in the second phase. Eighty-eight patients (40 men and 48 women; mean age of 33.8 +/- 16 years) with recurrent syncope and high pretest likelihood of neurally mediated syncope were included. The following were considerated as high pretest likelihood criteria: (1) at least two syncopal episodes; (2) no structural heart disease and normal baseline ECG; (3) age < 65 years; (4) a typical history of neurally mediated syncope, triggering factors plus premonitory signs; and (5) short duration of symptoms and fast recovery without neurological sequelae. Fifty-four patients (61%) had a positive tilt test (34/88 baseline [39%] and 20/50 with isoproterenol [40%]). The shorter time interval between the last syncopal episode and baseline HUT test was the only predictor for a positive response (P < 0.003). Conversely, this time interval was not predictor of positive responses during isoproterenol-tilt testing. In conclusion: (1) we claim a "sensitivity" for this combined protocol of 61%; and (2) our results indicate that patients with syncope of unknown origin must be tilted nearest as possible to the last syncope to increase the positive responses of HUT test. 相似文献
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