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Data is presented as mean s. Citation: European Journal of Endocrinology , 3; Neutrophil counts increased, whereas lymphocyte and monocyte counts all decreased significantly in a dose-dependent manner.
Eosinophil counts also decreased significantly, but a dose-dependent effect was not seen at the doses of prednisone administered Supplementary Table 1S , see section on supplementary data given at the end of this article. However, this correction did not qualitatively change the results. The values are presented as geometric mean percent change from baseline s.
The increases in fasting glucose were comparable for both days 1 and 7, although the increases in fasting insulin were at least twofold higher on day 7 compared with day 1. Fasting C-peptide was also higher on day 7 compared with day 1. All prednisone doses resulted in significantly increased insulin resistance compared with placebo, using the homeostatic model assessment of insulin resistance HOMA-IR 23 , Table 3.
Furthermore, this impairment appeared to be exacerbated with longer treatment. These effects appeared to be transient since the differences compared with placebo were not seen on day 7. Prednisone treatment decreased glucose tolerance in a dose-dependent manner as indicated by the glycaemic excursion observed during an OGTT, with corresponding increases in serum insulin Fig.
Of note, the increases were numerically greater on day 7 than day 1. Serum concentrations of the bone formation marker osteocalcin were rapidly and significantly reduced by all prednisone doses Fig. Significant increases in a marker of bone resorption, serum NTX, also occurred for the higher prednisone doses.
There was no discernible effect of prednisone on either day 1 or 7 data not shown. The aim of the present study was to evaluate several dose-responsive, anti-inflammatory efficacy biomarkers and to compare the time-course of these dose-dependent, anti-inflammatory changes with those observed for indicators of glucose tolerance and bone metabolism following short-term administration of the widely used GC, prednisone.
Prednisone doses were selected to be representative of the therapeutic dose range typically used in clinical practice. Supraphysiologic GC activity has long been established to suppress the hypothalamic—pituitary—adrenal HPA axis. As anticipated, all prednisone doses suppressed serum ACTH compared with placebo acutely.
To our knowledge, these acute dose-dependent differences between supraphysiologic prednisone doses on the HPA axis suppression have not been previously described. In addition, acute, dose-dependent changes in peripheral WBC count were observed following single and multiple doses of all prednisone doses studied, as shown previously 24 , 25 , However, it was unknown whether attenuation of the LPR was either dose-responsive or a sensitive biomarker of GC anti-inflammatory effects. The inability to demonstrate any significant effects on LPR size with lower prednisone doses suggests that the LPR may not be adequately sensitive to assess less potent anti-inflammatory effects.
A notable complication was the significant inter-subject variability observed in LPR response, which may have served to obscure detection of the effect, particularly for the lower prednisone doses. A post hoc analysis of the LPR data revealed several parameters which could be optimized to reduce the observed variability. Supraphysiologic GC activity leads to impaired glucose tolerance 1 , 2 , 3. It was recently demonstrated that low doses of prednisolone 7.
GC-induced insulin resistance certainly contributed to the glucose intolerance and was evident in the elevated fasting insulin and C-peptide concentrations noted on day 7 compared with day 1, and consistent with the HOMA-IR findings. It should be noted that although all enrolled subjects demonstrated normal glucose tolerance at baseline, they were required to demonstrate hypersensitivity to allergen and had received a cutaneous allergen challenge prior to glucose administration for the OGTT.
It is unknown what contribution this hypersensitive state may have had in exacerbating or predisposing to glucose intolerance following even a single prednisone dose. Furthermore, it has been reported that interstitial hyperglycaemia associated with prednisolone treatment is predominantly manifested in the afternoon and evening in patients receiving prednisolone treatment while undergoing continuous glucose monitoring Accordingly, the OGTT was conducted during the mid-late afternoon.
Nonetheless, these results suggest that in susceptible individuals, modest doses of prednisone may impair glucose tolerance acutely. It remains unknown whether the acute impairment of glucose tolerance i. It is interesting to note that the glycaemic excursion during the OGTT after multiple prednisone doses appeared to diminish over time. Of the bone formation markers analysed, osteocalcin was the most sensitive to GC treatment.
Although GCs have been reported to affect primarily bone formation, a significant increase in bone resorption, as indicated by increased serum NTX, was observed for higher prednisone doses. Finally, Dkk-1 has previously been suggested to play a role in GC-induced osteoporosis by interfering with canonical Wnt signaling.
In contrast to results from in vitro studies with cultured human osteoblasts 33 , 34 , however, in this study, Dkk-1 concentrations were found to be unchanged in response to prednisone administration.
Possible explanations for these results are that longer prednisone administration may be required to affect Dkk-1 expression or that the GC-induced effects on Dkk-1 occur locally and are not detectable in serum. In summary, dose-responsive anti-inflammatory efficacy biomarkers were identified following single and multiple prednisone dose administration.
The short time-course of these dose-dependent, anti-inflammatory changes was also observed for markers of glucose tolerance and bone metabolism.
To our knowledge, this is the first time a comprehensive review of GC effects on inflammation, glucose, and bone has been conducted in the same healthy individuals. S Mesens and S Ramael have no conflict of interests to report.
The authors want to thank Gary Herman and Alice Reicin for their contributions to the study design and for several helpful discussions, as well as Belma Dogdas for her analysis of the cutaneous allergen challenge results.
Dr Brian Schapiro performed the quantitative histological analysis of skin biopsy samples. We are also very grateful to Dr Paul Atkins for his insights, suggestions and critical reviews of drafts of this manuscript. Mechanisms involved in the side effects of glucocorticoids. Vegiopoulos A , Herzig S. Glucocorticoids, metabolism and metabolic diseases. Molecular and Cellular Endocrinology 43 — Novel insights into glucocorticoid-mediated diabetogenic effects: towards expansion of therapeutic options?
European Journal of Clinical Investigation 39 81 — Posttransplantation diabetes: a systematic review of the literature. Diabetes Care 25 — Glucocorticoid-induced diabetes mellitus: prevalence and risk factors in primary renal diseases. Clinical Practice c54 — c Schneiter P , Tappy L. Kinetics of dexamethasone-induced alterations of glucose metabolism in healthy humans. American Journal of Physiology E — E Saag KG.
Glucocorticoid-induced osteoporosis. Endocrinology and Metabolism Clinics of North America 32 — , vii. Before start of the treatments, mice were allowed to adjust to the environment for at least 1 wk. Except for the fed and 24 h fasting, all experiments started at h after an overnight fast food removed at h the day before on the day after the last treatment.
Blood glucose concentrations were measured in awake mice in blood drops collected by tail tip bleeding with a Lifescan EuroFlash glucose meter Lifescan Benelux, Beerse, Belgium. Mice were killed by cardiac puncture under isoflurane anesthesia. Organs were quickly removed and snap frozen in liquid nitrogen for RNA isolation and determination of metabolite concentrations.
To determine insulin sensitivity of glucose metabolism under high insulin concentrations, mice were subjected to a hyperinsulinemic euglycemic clamp as previously described 20 with minor adjustments. Five days before the experiment, i. Treatment was continued during the recovery period.
Mice were individually housed in small plexiglas cages during the experiment, allowing frequent collection of blood samples in freely moving mice. Louis, MO at a constant rate of 0. For this, blood glucose levels were measured every 15 min in blood drops collected by tail tip bleeding with a Lifescan EuroFlash glucose meter. Every hour, blood spots for gas chromatography-mass spectrometry GC-MS analysis were taken by tail bleeding on filter paper, air-dried, and stored at room temperature until further analysis.
The determination of blood glucose kinetics without inducing hyperinsulinemia was done as recently described van Dijk, T. Laskewitz, T. Boer, V. Bloks, A. Grefhorst, F. Kuipers, A. Groen, and D. Reijngoud, submitted for publication. Before and at the indicated time points after injection, blood glucose concentrations were measured in blood collected by tail tip bleeding. At the same time points, a small blood spot was taken on filter paper, in which the fractional contribution of d -[6,6- 2 H 2 ]-glucose to the whole blood glucose pool was measured by GC-MS.
Whole body glucose turnover and clearance were calculated by kinetic analysis of the wash-out of injected d -[6,6- 2 H 2 ]-glucose from the circulation. A blood sample was taken by orbital puncture after the test for insulin measurements. Food was removed 1 h after the last treatment, and mice were fasted for 24 h. Blood glucose levels were measured every 6 h by tail tip bleeding.
At the same time points, a small amount of blood was obtained by orbital puncture under light anesthesia. In the dark period, a red light was used to facilitate the procedure. After 24 h of fasting, mice were killed by cardiac puncture under isoflurane anesthesia. Organs were quickly removed and snap frozen in liquid nitrogen for RNA isolation and metabolite concentrations. The homeostasis model assessment HOMA -score was calculated adjusted for basal mouse values taken from vehicle-treated group.
Liver homogenates for lipid and protein measurements were made in ice-cold PBS. Hepatic lipids were extracted from the liver homogenates according to Bligh and Dyer Commercially available kits were used for determination of hepatic and plasma triglycerides Roche Diagnostics, Mannheim, Germany and free and total cholesterol Wako Chemicals, Neuss, Germany.
Hepatic glycogen concentrations were determined as described before previously Expression levels were normalized for RPLP0 levels. The sequences of the used primers and probes for Gr NR3C1; accession no. Extraction of glucose from blood spots on filter paper from the hyperinsulinemic-euglycemic clamp and blood glucose kinetics test, derivatization of the extracted compounds, and GC-MS measurements of derivatives was done according to the analytical procedure described by van Dijk et al.
Samples were analyzed by GC-MS with positive ion chemical ionization with methane. The fractional isotopomer distribution measured by GC-MS m 0 -m 6 was corrected for the fractional distribution due to natural abundance of 13 C by multiple linear regression as described by Lee et al. Formulas for calculating the endogenous glucose production and metabolic clearance rate MCR under hyperinsulinemic euglycemic clamped conditions were previously described The calculations for the blood glucose kinetics were described recently van Dijk, T.
In short, a single-pool, first-order kinetic model was assumed for this test. The excess fractional distribution of mass isotopomers was used to calculate the first order absorption process in an one-compartment model using SAAM-II software version 1. The formulas used to calculate the concentration vs. Formulas used to calculate the concentration vs.
C 0 ab , Initial concentration by extrapolation of the absorption period; C 0 el , initial concentration by extrapolation of the elimination period; C lag , concentration at lag time calculated from elimination or absorption curve; D, dose d -[6,6- 2 H 2 ]-glucose administrated; [glc], total blood glucose concentration; k ab , absorption rate constant; k el , elimination rate constant; M 2 , mole percent enrichment of blood glucose; t lag , time between administration and appearance in sampled compartment; EGP, endogenous glucose production.
The first set of experiments were performed to test the consequences of a chronic, 7-d prednisolone treatment protocol in mice. Activation of the hypothalamic-pituitary-adrenal axis by prednisolone results in a reduction of plasma corticosterone levels 28 and glucocorticoid-induced apoptosis of thymocytes results in a severely reduced thymus weight The values for plasma FGF21 are from pooled plasma samples.
Blood glucose levels in 9-h fasted mice tended to be higher upon prednisolone treatment Table 2. In addition, prednisolone treatment resulted in elevated plasma insulin levels.
Consequently, the HOMA-score was increased upon chronic prednisolone treatment, suggesting insulin resistance. Surprisingly, the hepatic expression of the classic GR-target genes Tat encoding for tyrosine aminotransferase 30 and Per1 encoding for the clock-gene Period-1 31 was reduced upon prednisolone treatment in the 9-h fasted mice Fig.
The expression of genes encoding proteins involved in GNG, e. Pck1 , G6pc , and Pdk4 , was also significantly reduced in the livers of 9-h fasted prednisolone-treated mice. Hepatic gene expression of 9-h fasted mice treated with vehicle white bars or prednisolone black bars. To evaluate the characteristics of the reduced insulin sensitivity upon prednisolone treatment in more detail, a hyperinsulinemic euglycemic clamp was performed.
Again, mice treated with prednisolone and fasted for 9 h had increased blood glucose concentrations Fig. Surprisingly, the glucose infusion rate needed to maintain euglycemic conditions during the clamping period did not differ between treated and nontreated mice Fig. Altogether, these data indicate that the hyperinsulinemic euglycemic clamp is not the preferred method to study prednisolone-induced insulin resistance, probably related to the artificially high plasma insulin concentrations.
Parameters of the hyperinsulinemic euglycemic clamp experiment performed in mice treated with vehicle white bars or prednisolone black bars.
A, Fasting blood glucose concentration. B, Average blood glucose concentration during the steady-state period of the experiment 3—6 h. C, Average glucose infusion rate GIR needed to maintain euglycemic conditions during the steady-state period of the experiment 3—6 h ; D, HGP during the steady-state period of the experiment. E, MCR of glucose during the steady-state period of the experiment.
To determine hepatic and peripheral insulin sensitivity of glucose kinetics without inducing high plasma insulin concentrations, 9-h fasted mice were ip injected with a tracer amount of d -[6,6- 2 H 2 ]-glucose. This injection did not affect the blood glucose levels Fig.
From the decay of the blood d -[6,6- 2 H 2 ]-glucose vs. The increased HGP at higher plasma insulin concentrations indicates hepatic insulin resistance. Parameters of the blood glucose kinetics test performed in mice treated with vehicle white circles and bars or prednisolone black circles and bars. A, Blood glucose concentrations during the test. D, Plasma insulin concentrations after the test. The hyperinsulinemic euglycemic clamp induced a state with supraphysiological insulin concentrations and therefore mimics a fed situation.
Yet, the HOMA index and blood glucose kinetics were determined in fasted conditions with low plasma insulin concentrations. We therefore investigated the combined effects of prednisolone and fasting on glucose metabolism. Mice were fasted for 24 h after the seventh day of treatment.
At the start of the fasting period, 1 h after the last treatment, prednisolone-treated mice had significantly reduced blood glucose levels Fig. In vehicle-treated mice, plasma insulin concentrations gradually declined upon fasting, but this effect was less clear in prednisolone-treated mice Fig.
Metabolic parameters from a different 24 h fasting experiment are shown in Table 3. In the fed state, the prednisolone-treated mice had higher plasma NEFA concentrations than the vehicle-treated mice. During fasting, these concentrations remained unchanged in the prednisolone-treated mice, but rose in the mice that received the vehicle. In both vehicle-treated and prednisolone-treated mice, prolonged fasting increased hepatic TG and reduced hepatic glycogen concentrations.
Parameters of the 24 h fasting experiment from mice treated with vehicle white circles and bars or prednisolone black circles and bars. A, Blood glucose during the h fasting period shaded area represents the dark period. B, Plasma insulin concentrations in fed and and h fasted mice. D, Hepatic gene expression of mice treated with vehicle white circles or prednisolone black circles terminated after a h fast or at the same time point without fasting mice. Metabolic parameters of fed and 24 h fasted vehicle- and prednisolone-treated mice.
ND, Not determined. Fasting resulted in an increased Pck1 expression Fig. Expression of Srebp-1c was reduced in fed prednisolone-treated mice compared with fed control mice. Methods: A randomized double-blind crossover clinical trial conducted in the department of Endocrinology of the University Hospital la Rabta in Tunis, during Ramadan , on 53 patients with known corticotrope deficiency treated with hydrocortisone 20 mg per day and who were willing to fast during Ramadan.
Patients were randomized into two groups; AB that received hydrocortisone twice daily for 14 days then prednisolone once daily with a placebo for 14 days and group BA that received the two treatments in the reverse order.
Patients had to complete a daily follow-up sheet about their eating and sleeping habits, the occurrence of complications and blood glucose monitoring and also to respond to the AddiQoL questionnaire at the end of each treatment period.
❿Prednisone fasting
Prednisone fasting
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Use of glucocorticoids for anti-inflammatory efficacy is limited by their side effects. This study examined, in the same individuals, prednisone's acute, dose-dependent effects on inflammation as well as biomarkers of glucose regulation and bone homeostasis.
Differential peripheral WBC counts changed significantly within hours of prednisone administration. Oral glucose tolerance tests revealed significant increases in glycaemic excursion on days 1 and 7, whereas increases in insulin and C-peptide excursions were more notable on day 7 with all doses of prednisone. The bone formation markers osteocalcin, and procollagen I N- and C-terminal peptides decreased significantly on days 1 and 7 vs placebo.
The anti-inflammatory effects of glucocorticoids GCs have proven extremely valuable in the treatment of diseases such as asthma, arthritis and transplant organ rejection. However, the side effects following prolonged use of GCs at pharmacologic concentrations limit both their full dose-range potential and long-term use 1. Two of the most common and debilitating adverse effects of GC therapy are glucose intolerance that can lead to or exacerbate pre-existing diabetes and effects on bone that over time can develop into GC-induced osteoporosis.
GC treatment results in numerous effects influencing glucose metabolism 123. It is well known that GCs inhibit insulin secretion, induce triglyceride breakdown in adipose tissue, decrease insulin-mediated glucose uptake in skeletal muscle and increase hepatic glucose production by increasing gluconeogenesis.
Changes in glucose tolerance have been detected by oral glucose tolerance test OGTT within hours of treatment 6. However, studies examining the dose-dependent effects of GCs and, in particular, dose-dependent single dose effects have not been performed.
GC therapy is also associated with accelerated decline in bone density and an increase in fractures reviewed in 78. GCs reduce osteoblast function and replication as well as increase osteoblast apoptosis 189 Although the specific mechanism by which GCs interfere with osteoblast function remains unclear, reductions in bone formation markers have been reported to occur within days of treatment with prednisone 1112131415and increases of about two- or three-fold in the relative risk of hip and vertebral fractures in patients receiving GCs have been reported 16 Although the most severe adverse effects associated with GC treatment generally occur in patients undergoing chronic treatment with high doses, the onset of changes in glucose tolerance and bone turnover occurs soon after treatment initiation, as described above.
Given the significant therapeutic value of GCs, there has been intense effort to identify dissociated GC receptor agonists that possess the anti-inflammatory properties of classic GC receptor agonists, such as prednisolone and dexamethasone, without inducing the undesirable side effects reviewed in A better understanding of the time course relationship between GC dose and biomarkers of both efficacy and adverse effects in the same population should facilitate this search.
The current investigation, in which healthy young individuals were treated with the commonly prescribed oral GC prednisone, was conducted to identify biological markers of inflammation, glucose tolerance or bone turnover which demonstrate acute, dose-dependent relationships. To our knowledge, this is the first published study comparing the time- and dose-dependent anti-inflammatory effects of prednisone with adverse effects in the same individuals.
Principal exclusion criteria included a history of glucose intolerance, adrenal impairment and significant illnesses or abnormal laboratory evaluations. The study was conducted in accordance with principles of Good Clinical Practice and was approved by the appropriate institutional review boards and regulatory agencies.
All subjects provided written informed consent. During the course of the study, patients were required to refrain from excessive sun exposure, strenuous physical activity, use of lotion on the arms or back and use of any prescription or non-prescription medicine. This was a randomized, double-blind, placebo-controlled, parallel group, 7-day study Study Protocol with varying doses of prednisone.
The LPR to the antigen was assessed at baseline and on days 1 and 7. Allergen 0. The primary endpoint in the examination of bone turnover was serum concentration of the bone formation marker osteocalcin Bioanalytical Research Corporation, Ghent, Belgium. All subjects treated were included in the data analyses. All analyses were performed on data collected on days 1 and 7 of dosing using the change from baseline as the outcome measure.
Treatment group comparisons were evaluated using a pre-specified analysis of covariance ANCOVA model with terms for allergen stratum as well as baseline and treatment. For each outcome measure, the treatment effect each dose of prednisone compared with placebo was evaluated in a stepwise fashion, starting with the highest dose, until lack of significance was observed. No adjustment for multiplicity was performed for multiple testing on days 1 and 7.
Baseline characteristics were not significantly different among treatment groups, and are shown in Table 1. Baseline characteristics. Data is presented as mean s. Citation: European Journal of Endocrinology3; Neutrophil counts increased, whereas lymphocyte and monocyte counts all decreased significantly in a dose-dependent manner. Eosinophil counts also decreased significantly, but a dose-dependent effect was not seen at the doses of prednisone administered Supplementary Table 1Ssee section on supplementary data given at the end of this article.
However, this correction did not qualitatively change the results. The values are presented as geometric mean percent change from baseline s. The increases in fasting glucose were comparable for both days 1 and 7, although the increases in fasting insulin were at least twofold higher on day 7 compared with day 1.
Fasting C-peptide was also higher on day 7 compared with day 1. All prednisone doses resulted in significantly increased insulin resistance compared with placebo, using the homeostatic model assessment of insulin resistance HOMA-IR 23Table 3.
Furthermore, this impairment appeared to be exacerbated with longer treatment. These effects appeared to be transient since the differences compared with placebo were not seen on day 7.
Prednisone treatment decreased glucose tolerance in a dose-dependent manner as indicated by the glycaemic excursion observed during an OGTT, with corresponding increases in serum insulin Fig.
Of note, the increases were numerically greater on day 7 than day 1. Serum concentrations of the bone formation marker osteocalcin were rapidly and significantly reduced by all prednisone doses Fig. Significant increases in a marker of bone resorption, serum NTX, also occurred for the higher prednisone doses.
There was no discernible effect of prednisone on either day 1 or 7 data not shown. The aim of the present study was to evaluate several dose-responsive, anti-inflammatory efficacy biomarkers and to compare the time-course of these dose-dependent, anti-inflammatory changes with those observed for indicators of glucose tolerance and bone metabolism following short-term administration of the widely used GC, prednisone.
Prednisone doses were selected to be representative of the therapeutic dose range typically used in clinical practice. Supraphysiologic GC activity has long been established to suppress the hypothalamic—pituitary—adrenal HPA axis.
As anticipated, all prednisone doses suppressed serum ACTH compared with placebo acutely. To our knowledge, these acute dose-dependent differences between supraphysiologic prednisone doses on the HPA axis suppression have not been previously described. In addition, acute, dose-dependent changes in peripheral WBC count were observed following single and multiple doses of all prednisone doses studied, as shown previously 2425 However, it was unknown whether attenuation of the LPR was either dose-responsive or a sensitive biomarker of GC anti-inflammatory effects.
The inability to demonstrate any significant effects on LPR size with lower prednisone doses suggests that the LPR may not be adequately sensitive to assess less potent anti-inflammatory effects. A notable complication was the significant inter-subject variability observed in LPR response, which may have served to obscure detection of the effect, particularly for the lower prednisone doses.
A post hoc analysis of the LPR data revealed several parameters which could be optimized to reduce the observed variability. Supraphysiologic GC activity leads to impaired glucose tolerance 123.
It was recently demonstrated that low doses of prednisolone 7. GC-induced insulin resistance certainly contributed to the glucose intolerance and was evident in the elevated fasting insulin and C-peptide concentrations noted on day 7 compared with day 1, and consistent with the HOMA-IR findings.
It should be noted that although all enrolled subjects demonstrated normal glucose tolerance at baseline, they were required to demonstrate hypersensitivity to allergen and had received a cutaneous allergen challenge prior to glucose administration for the OGTT. It is unknown what contribution this hypersensitive state may have had in exacerbating or predisposing to glucose intolerance following even a single prednisone dose.
Furthermore, it has been reported that interstitial hyperglycaemia associated with prednisolone treatment is predominantly manifested in the afternoon and evening in patients receiving prednisolone treatment while undergoing continuous glucose monitoring Accordingly, the OGTT was conducted during the mid-late afternoon.
Nonetheless, these results suggest that in susceptible individuals, modest doses of prednisone may impair glucose tolerance acutely. It remains unknown whether the acute impairment of glucose tolerance i. It is interesting to note that the glycaemic excursion during the OGTT after multiple prednisone doses appeared to diminish over time. Of the bone formation markers analysed, osteocalcin was the most sensitive to GC treatment.
Although GCs have been reported to affect primarily bone formation, a significant increase in bone resorption, as indicated by increased serum NTX, was observed for higher prednisone doses.
Finally, Dkk-1 has previously been suggested to play a role in GC-induced osteoporosis by interfering with canonical Wnt signaling. In contrast to results from in vitro studies with cultured human osteoblasts 3334however, in this study, Dkk-1 concentrations were found to be unchanged in response to prednisone administration.
Possible explanations for these results are that longer prednisone administration may be required to affect Dkk-1 expression or that the GC-induced effects on Dkk-1 occur locally and are not detectable in serum. In summary, dose-responsive anti-inflammatory efficacy biomarkers were identified following single and multiple prednisone dose administration. The short time-course of these dose-dependent, anti-inflammatory changes was also observed for markers of glucose tolerance and bone metabolism.
To our knowledge, this is the first time a comprehensive review of GC effects on inflammation, glucose, and bone has been conducted in the same healthy individuals. S Mesens and S Ramael have no conflict of interests to report. The authors want to thank Gary Herman and Alice Reicin for their contributions to the study design and for several helpful discussions, as well as Belma Dogdas for her analysis of the cutaneous allergen challenge results.
Dr Brian Schapiro performed the quantitative histological analysis of skin biopsy samples. We are also very grateful to Dr Paul Atkins for his insights, suggestions and critical reviews of drafts of this manuscript. Mechanisms involved in the side effects of glucocorticoids. Vegiopoulos AHerzig S. Glucocorticoids, metabolism and metabolic diseases.
Molecular and Cellular Endocrinology 43 — Novel insights into glucocorticoid-mediated diabetogenic effects: towards expansion of therapeutic options? European Journal of Clinical Investigation 39 81 — Posttransplantation diabetes: a systematic review of the literature. Diabetes Care 25 — Glucocorticoid-induced diabetes mellitus: prevalence and risk factors in primary renal diseases.
Clinical Practice c54 — c Schneiter PTappy L. Kinetics of dexamethasone-induced alterations of glucose metabolism in healthy humans. American Journal of Physiology E — E Saag KG. Glucocorticoid-induced osteoporosis. Endocrinology and Metabolism Clinics of North America 32 —vii.
I think the best fast I could do would be from 8 at night until 8 in the morning and doesn't the fasting time exceed 12 hours? I think my son is. Prednisolone treatment induced a fasting-like phenotype in fed mice and hampered the effects of fasting on energy metabolism. The hyperinsulinemic euglycemic. yes intermittent fasting gives our organs a localhoster it will help you in controlling blood localhostds in high dose can make you localhost go ahead. One small study in patients with asthma reported higher prevalence of abnormal prednisone absorption and fast prednisolone clearance when. For overnight fasted subjects, prednisone treatment increased fasting glucose and insulin concentrations after 5 h following administration (Table 3). In fasted subjects, the absolute bioavailability fraction, as normalised for intravenous doses, of prednisolone from plain tablets was 1.Purpose: The aims of the study were to compare the risk of complications and the quality of life in patients with corticotrope deficiency, who fasted during Ramadan. Both hydrocortisone and prednisolone were compared as treatments. Methods: A randomized double-blind crossover clinical trial conducted in the department of Endocrinology of the University Hospital la Rabta in Tunis, during Ramadan , on 53 patients with known corticotrope deficiency treated with hydrocortisone 20 mg per day and who were willing to fast during Ramadan.
Patients were randomized into two groups; AB that received hydrocortisone twice daily for 14 days then prednisolone once daily with a placebo for 14 days and group BA that received the two treatments in the reverse order. Patients had to complete a daily follow-up sheet about their eating and sleeping habits, the occurrence of complications and blood glucose monitoring and also to respond to the AddiQoL questionnaire at the end of each treatment period. Results: Fifty patients' data were analyzed; 29 men, mean age: The frequency of complications, mean blood glucose levels and the quality of life did not differ on hydrocortisone compared to prednisolone after adjustment for the sequence of the treatment.
Conclusions: the risks of Ramadan fasting in patients with corticotrope deficiency were the same on hydrocortisone or prednisolone. Abstract Purpose: The aims of the study were to compare the risk of complications and the quality of life in patients with corticotrope deficiency, who fasted during Ramadan. Publication types Randomized Controlled Trial. Substances Blood Glucose Prednisolone Hydrocortisone.
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