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Owen, LJ, S. Gillingwater, and BG Keevil. "Prednisolone measurement in human serum using liquid chromatography tandem mass spectrometry." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 42, no. 2 (March 1, 2005): 105–11. http://dx.doi.org/10.1258/0004563053492810.
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Prednisolone is a commonly prescribed corticosteroid used in the treatment of many diseases. Despite high doses of prednisolone, some patients appear to have subtherapeutic concentrations of the drug. It would be useful to measure prednisolone in this group to determine if they have poor absorption or compliance. Hence, we have developed a liquid chromatography-tandem mass spectrometry method for the determination of prednisolone in serum. Chromatography was performed using a C18 column, giving a retention time for both prednisolone and deuterated prednisolone (internal standard) of 1.6 min. Two transitions were monitored for both prednisolone and deuterated prednisolone. These were m/z 361.2>343.0 and m/z 361.2>146.9 for prednisolone, and m/z 367.2>349.0 and m/z 367.2>149.9 for the internal standard. The intra- and inter-batch imprecision was <7% in both cases over a concentration range of 62.5-750 μg/L. The imprecision at the lower limit was 8%, the lower limit of quantitation was determined to be 30 μg/L and the method was linear up to 5000 μg/L. The method allows rapid prednisolone analysis because of a simplified sample extraction step, and has a cycle time of 3.5 min.
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Ramshanker, Nilani, Maiken Aagaard, Rikke Hjortebjerg, Thomas Schmidt Voss, Niels Møller, Jens Otto Lunde Jørgensen, Niels Jessen, et al. "Effects of Prednisolone on Serum and Tissue Fluid IGF-I Receptor Activation and Post-Receptor Signaling in Humans." Journal of Clinical Endocrinology & Metabolism 102, no. 11 (September 13, 2017): 4031–40. http://dx.doi.org/10.1210/jc.2017-00696.
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Abstract Context Short-term glucocorticoid exposure increases serum insulinlike growth factor I (IGF-I) concentrations but antagonizes IGF-I tissue signaling. The underlying mechanisms remain unknown. Objective To identify at which levels glucocorticoid inhibits IGF-I signaling. Design and Methods Nineteen healthy males received prednisolone (37.5 mg/d) and placebo for 5 days in a randomized, double-blinded, placebo-controlled crossover study. Serum was collected on days 1, 3, and 5, and abdominal skin suction blister fluid (SBF; ~interstitial fluid) was taken on day 5 (n = 9) together with muscle biopsy specimens (n = 19). The ability of serum and SBF to activate the IGF-I receptor (IGF-IR) (bioactive IGF) and its downstream signaling proteins was assessed using IGF-IR–transfected cells. Results Prednisolone increased IGF-I concentrations and bioactive IGF in serum (P ≤ 0.001) but not in SBF, which, compared with serum, contained less bioactive IGF (~28%) after prednisolone (P < 0.05). This observation was unexplained by SBF concentrations of IGFs and IGF-binding proteins (IGFBPs) 1 to 4. However, following prednisolone treatment, SBF contained less IGFBP-4 fragments (P < 0.05) generated by pregnancy-associated plasma protein A (PAPP-A). Concomitantly, prednisolone increased SBF levels of stanniocalcin 2 (STC2) (P = 0.02) compared with serum. STC2 blocks PAPP-A from cleaving IGFBP-4. Finally, prednisolone suppressed post–IGF-IR signaling pathways at the level of insulin receptor substrate 1 (P < 0.05) but did not change skeletal muscle IGF-IR, IGF-I, or STC2 messenger RNA. Conclusion Prednisolone increased IGF-I concentrations and IGF bioactivity in serum but not in tissue fluid. The latter may relate to a STC2-mediated inhibition of PAPP-A in tissue fluids. Furthermore, prednisolone induced post–IGF-IR resistance. Thus, glucocorticoid may exert distinct, compartment-specific effects on IGF action.
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Gleeson, Dermot. "Standard Treatment in Adults: Which Steroid? Or without Steroids?" Digestive Diseases 33, Suppl. 2 (2015): 75–82. http://dx.doi.org/10.1159/000440751.
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Key Messages: (1) Standard treatment of autoimmune hepatitis in adults should be steroid based. In early trials, prednisolone +/- azathioprine was superior to the azathioprine mono-therapy (which was not significantly better than placebo). Prednisolone plus azathioprine has similar efficacy to, but is better tolerated than a higher-dose of prednisolone alone and therefore has become standard therapy. (2) In most treated patients, serum transaminases and globulin/IgG fall, but percentage attaining normal values within 6 months varies between 10 and 90%. Patients failing to do so have a worse longer-term outcome. (3) A higher initial prednisolone dose (1 mg/kg/day) plus azathioprine achieved 76% serum transaminase normalisation after 6 months but needs longer-term evaluation. (4) Histological remission (minimal hepatitis on re-biopsy) lags behind transaminase normalisation by 6-12 months and is achieved in 55-70% of patients after 24-36 months prednisolone. This lag and the inefficacy of azathioprine mono-therapy justifies continuing prednisolone (5-10 mg/day), even after transaminase normalisation, for a total of >2 years. (5) Repeat biopsy should be considered because 40-60% of patients still have (usually mild) persisting inflammation, despite normal serum transaminases and IgG. In such patients, fibrosis is less likely to regress and long-term mortality is higher. (6) In a large trial, non-cirrhotic treatment-naïve patients given budesonide (9 mg/day) plus azathioprine were more likely to achieve normal serum ALT after 6 months than those receiving prednisolone plus azathioprine and had less side effects. This trial was short term in nature and lacked follow-up histology. Budesonide is recommended in non-cirrhotic patients who develop prednisolone-related side effects. In an open study of mycophenolate plus prednisolone, 88% of treatment-naïve patients achieved normal serum transaminases. However, half relapsed during or after steroid withdrawal and only one of eight re-biopsied patients achieved histological remission. Mycophenolate is teratogenic, limiting its use in younger women. Conclusion: Despite its limitations, no regime has yet been shown clearly to be better than prednisolone and azathioprine-based therapy.
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Kirimi, E., O. Tuncer, M. Kösem, E. Ceylan, A. Tas, I. Tasal, R. Balahoroğlu, and H. Caksen. "The Effects of Prednisolone and Serum Malondialdehyde Levels in Puppies with Experimentally Induced Meconium Aspiration Syndrome." Journal of International Medical Research 31, no. 2 (April 2003): 113–22. http://dx.doi.org/10.1177/147323000303100207.
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The aim of this study was to investigate the effect of different doses of prednisolone in puppies experimentally induced with meconium aspiration syndrome (MAS). Meconium was collected from human babies in the first day of life and was released into the trachea of 11 newborn puppies to induce MAS. Puppies were treated with 2 mg/kg prednisolone (standard dose), 30 mg/kg prednisolone (megadose) or 0.9% saline, all administered intravenously. The study ended 20 h after meconium aspiration and the lungs were then scored for histopathology. Animals not treated with prednisolone deteriorated after 8 h while respiration rate, oxygenation, pH and partial pressure of carbon dioxide values were better in the prednisolone-treated groups. Histopathology scores were better in the treatment groups compared with the control group, with megadose giving the best result. At the end of the study, serum malondialdehyde levels were significantly higher in the megadose prednisolone group compared with the other two groups. In conclusion, we determined that prednisolone reduced physiological and histological changes in puppies with MAS and that a 30 mg/kg dose was more effective than 2 mg/kg.
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Mobisson, Samuel K., Peter C. Onyebuagu, Iheanyichukwu Wopara, Desmond Izunwanne, Emmanuel C. Madu, Augustine C. Emeruem, Justin B. Monye, and Agona O. Obembe. "Impact of Cannabidiol oil and prednisolone on liver enzymes, oxidative stress markers and liver histology in cadmium induced toxicity in male Wistar rats." Journal of African Association of Physiological Sciences 11, no. 1 (August 28, 2023): 36–44. http://dx.doi.org/10.4314/jaaps.v11i1.4.
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Background: This study aimed to ascertain the effect of cannabidiol (CBD) oil and prednisolone on serum liver enzyme markers and hepatic oxidative stress markers on cadmium-induced toxicity in male Wistar rats. Forty (40) male Wistar rats weighing between 150g to 200g were assigned into 8 groups (A-H) of five animals each. Group 1 served as control, Groups 2-8 received 1mg/kg body weight of prednisolone; 1.5mg/kg bw of cadmium; 1mg/kg bw of prednisolone + 0.2mg/kg bw of CBD-oil; 0.2mg/kg bw of CBD-oil + 2mg/kg bw of cadmium; 3mg/kg bw of prednisolone + 2mg/kg of cadmium; 0.1mg/kg bw of CBD-oil and 0.2mg/kg bw of CBD-oil respectively. The administration was done using an orogastric tube (gavage) for 14 days. Results revealed a significant decrease in the concentration of aspartate aminotransferase (AST) in all treated groups compared to control. Furthermore, serum alanine aminotransferase (ALT) showed a significant (p<0.05) decrease in all treated groups compared to control. There was a significant decrease in the concentration of alkaline phosphatase (ALP) in treated groups compared to the control. Liver catalase significantly increased in rats fed with pred +cadmium compared to control and other treated groups. Liver superoxide dismutase (SOD) significantly decreased in (p<0.05) the group treated with cadmium compared to the control and prednisolone groups. Liver malondialdehyde concentration did not reveal any significant change (p>0.05). Liver glutathione peroxidase significantly decreased in treated groups than in control. Liver-reduced glutathione significantly decreased across treated groups than the control. Histology of the liver revealed degeneration of hepatocytes and vascular congestion in groups treated with prednisolone, prednisolone+ cadmium, and CBD oil (0.2mg/kg). We conclude that CBD oil, prednisolone, and Cadmium administration at different doses decreased the concentration of serum liver enzyme and oxidative stress markers but caused local inflammation of the liver. If this study is applicable to humans, CBD-oil and prednisolone should be cautiously taken as they may likely present adverse effects, especially in people with liver disease.
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Schou, A. J., and O. D. Wolthers. "Serum Fructosamine, Total Cholesterol, and High-Density Lipoprotein in Children with Asthma during Glucocorticoid Treatment." ISRN Allergy 2011 (August 14, 2011): 1–4. http://dx.doi.org/10.5402/2011/295124.
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Background/Aims. Glucocorticoids may have adverse effects on carbohydrate and lipid metabolism. The present study was conducted to investigate possible effects on carbohydrate and lipid metabolism of inhaled and oral glucocorticoids in children with asthma. Methods. Two randomised controlled trials with blinded crossover designs were performed. Active treatment was 400 μg inhaled budesonide or 5 mg prednisolone orally daily during one week. The budesonide trial included 17 and the prednisolone trial 20 school children. Serum fructosamine, total cholesterol and high-density lipoprotein were assessed. Results. Serum fructosamine was increased during active treatment (prednisolone 252.3 μM versus placebo 247.3 μM; P = 0.03 and budesonide 228.1 μM versus no treatment 223.1 μM; P = 0.02). Total cholesterol and high-density lipoprotein were not statistically significantly increased. Conclusion. Short-term treatment with oral prednisolone and inhaled budesonide may adversely affect mean blood glucose concentration. Possible long-term consequences require further investigations.
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Alizadeh Dehnavi, Reza, Jouke T. Tamsma, and A. Edo Meinders. "The effect of prednisolone on serum sodium concentration." European Journal of Internal Medicine 17, no. 3 (May 2006): 201–3. http://dx.doi.org/10.1016/j.ejim.2005.11.018.
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Rebolledo, Rolando A., Bo Liu, Mohammed Z. Akhtar, Petra J. Ottens, Jian-ning Zhang, Rutger J. Ploeg, and Henri G. D. Leuvenink. "Steroid Anti-Inflammatory Effects Did Not Improve Organ Quality in Brain-Dead Rats." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/207534.
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Effect of glucocorticoid administration on improving the outcomes of kidney and liver allografts has not been clearly elucidated. This study investigated the effect of prednisolone administration after onset of brain death (BD) on kidney and liver in a controlled rat model of BD. BD was induced in rats by inflating an epidurally placed balloon catheter. Animals were treated with saline or prednisolone (5, 12.5, or 22.5 mg/kg) one hour after the onset of BD. After 4 hours of BD, experiments were terminated and serum and tissues were collected. Tissue gene and protein expression were measured for markers of inflammation, apoptosis, and cellular stress response markers. Prednisolone caused a reduction of plasma levels of IL-6, while the tissue expression ofIL-6, IL-1β,andMCP-1in both kidney and liver were also reduced. Creatinine plasma levels, complement (C3) expression,HSP-70, HO-1, Bcl2/BAXratio, and PMN influx did not significantly change in kidney nor liver. Plasma AST and LDH levels were increased in the prednisolone treated group. Our results demonstrate prednisolone can has an anti-inflammatory effect mediated through reducing serum circulating cytokines. However, this anti-inflammatory effect does not translate into improved kidney function and indeed was associated with increased liver injury markers.
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Qaisar, Imran, Abid Ali Anjum, Abdul Rehman, and Iftikhar Ahmed. "Comparison of efficacy of single dose versus split dose prednisolone therapy in achieving remission in patients with nephrotic syndrome in children." Journal of Fatima Jinnah Medical University 15, no. 4 (April 7, 2022): 181–83. http://dx.doi.org/10.37018/ewsh7228.
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Background: Nephrotic syndrome is a medical problem clinically characterized by proteinuria, generalized body edema and hypercholesterolemia. We did this study to compare the effectiveness of single dose versus split dose prednisolone in achieving remission in patients with nephrotic syndrome in children.Patients and methods: This open-ended randomized control trial was done in pediatric unit of tertiary care hospital from January to December 2019.We included one hundred Patients of nephrotic syndrome in the study who met the inclusion criteria. We divided total Patients into 2 groups (group A & B) 50 patients in each group. Group A was given single dose prednisolone, while group B was given split dose prednisolone therapy. Both groups were compared with respect of achievement of remission.Results: Out of 50 patients of group A who were given single dose prednisolone 37 (74%) were male, while in group B who were given split dose prednisolone 22 (44%) were male (p-value=0.137). Mean age of patients of study group A and B was 4.5 ±1.67 years and 4.9 ±1.49 years respectively (p-value=0.1876). Mean serum creatinine level in study group A and B was 0.744±0.189 and 0.736±0.167 (p-value=0.823). Similarly mean serum albumin level in study group A and B was 2.34±0.358 and 2.39±0.33 (p-value=0.473). When both groups were compared with regard to response to treatment, in group A mean remission duration was 16.48 ±3.69. In group B mean remission duration was 19.42 ±3.11 days (p-value<0.05).Conclusion: From our study we concluded that single dose prednisolone is more effective in achieving remission in steroid sensitive nephrotic syndrome as compared to split dose prednisolone.
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Sandhu, Milap S., Elizabeth Gray, Masha Kocherginsky, Arun Jayaraman, Gordon S. Mitchell, and William Z. Rymer. "Prednisolone Pretreatment Enhances Intermittent Hypoxia-Induced Plasticity in Persons With Chronic Incomplete Spinal Cord Injury." Neurorehabilitation and Neural Repair 33, no. 11 (September 15, 2019): 911–21. http://dx.doi.org/10.1177/1545968319872992.
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Objective. To test the hypothesis that an anti-inflammatory corticosteroid drug enhances spinal motor plasticity induced by acute intermittent hypoxia (AIH) in persons with chronic incomplete spinal cord injury (iSCI). Methods. Fourteen subjects with incomplete spinal cord injury (ASIA level C or D; mean age = 46 years) participated in a randomized, double-blinded, crossover, and placebo-controlled study. Subjects received either 60 mg oral prednisolone or a matching placebo, 1 hour before administration of AIH (15, 60-second hypoxic exposures; fraction of inspired oxygen [FiO2] = 0.09). Changes in voluntary ankle strength, lower extremity electromyograms (EMG), and serum inflammatory biomarkers were quantified. Results. Maximal ankle plantarflexion torque was significantly higher following prednisolone + AIH versus placebo + AIH (mean difference [MD] 9, 11, and 7 newton meter [N∙m] at 30, 60, and 120 minutes post-AIH, respectively; all Ps <.02). Soleus surface EMG during maximal voluntary contraction was also significantly increased following prednisolone + AIH (MD 3.5, P = .02 vs placebo + AIH), while activity of other leg muscles remained unchanged. Individuals had significantly higher levels of the anti-inflammatory serum biomarker interleukin-10 after prednisolone versus placebo ( P = .004 vs placebo + AIH). Conclusions. Pretreatment with prednisolone increased the capacity for AIH-induced functional motor plasticity, suggesting that suppression of inflammation enhances the efficacy of AIH administration in individuals with spinal cord injury. Clinical trial registration number: NCT03752749.
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Kumar, Dinesh, Harpal Singh, and T. G. Shrivastav. "Homologous ELISA for detection of prednisolone in human serum." Food and Agricultural Immunology 29, no. 1 (September 26, 2017): 369–85. http://dx.doi.org/10.1080/09540105.2017.1376184.
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Döppenschmitt, S. A., B. Scheidel, F. Harrison, and J. P. Surmann. "Simultaneous determination of prednisolone, prednisolone acetate and hydrocortisone in human serum by high-performance liquid chromatography." Journal of Chromatography B: Biomedical Sciences and Applications 674, no. 2 (December 1995): 237–46. http://dx.doi.org/10.1016/0378-4347(95)00317-7.
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Bayton, William, Penny J. Watson, and Nicholas H. Bexfield. "Prednisolone therapy for chronic hepatitis in English springer spaniels: a prospective study of 12 cases." Veterinary Record 186, no. 18 (February 12, 2020): e21-e21. http://dx.doi.org/10.1136/vr.105642.
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BackgroundEnglish springer spaniels (ESS) show an increased risk of chronic hepatitis (CH). In a previous study of 68 ESS with CH, in which only one dog received corticosteroids, a median survival time of 189 days was noted. Some ESS with CH appear to improve with prednisolone treatment; therefore, we aimed to investigate the response to prednisolone in this breed.ParticipantsESS with histologically confirmed idiopathic CH were treated with prednisolone 1–2 mg/kg/day. Nine female and three male ESS were enrolled (median age at diagnosis of five years). Patients were monitored clinically and had biochemistry samples taken to assess markers of hepatocellular damage and function.ResultsThe mean starting dose of prednisolone was 1.1 mg/kg/day. All symptomatic patients showed an initial clinical improvement. Two cases were euthanased while receiving prednisolone. The median time since diagnosis is 1715 days (range: 672–2105 days) and the remaining patients are clinically well, with seven patients still receiving a mean dose of 0.4 mg/kg prednisolone every other day. Statistical analysis demonstrated significant (P<0.05) reductions in serum alkaline phosphatase, alanine aminotransferase and bilirubin following 2–4 weeks of prednisolone treatment.ConclusionThis study demonstrates improved clinical and biochemical parameters when some ESS with CH are managed with prednisolone and standard supportive treatments.
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Yeh, Su-Peng, Chang-Fang Chiu, Yu-Min Liao, Wen-Jyi Lo, Yu-Ching Liaw, Chiao-Lin Lin, Jan-Gowth Chang, and Chung-Tsen Hsueh. "Serum Level of Interleukin-10 Correlates Well with the Activity of Chronic Graft-Versus-Host Disease and the Responsiveness to Corticosteroid Treatment." Blood 104, no. 11 (November 16, 2004): 1647. http://dx.doi.org/10.1182/blood.v104.11.1647.1647.
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Abstract Current evidence suggest the interaction between subset of T cells, the T help1 (Th1) and T help2 (Th2), plays an important role in the pathogenesis of GVHD. Cytokines, either produced by Th1/Th2 or other cells, are important regulators in the whole process and will define the polarization of Th1 or Th2 from naïve T cell. In this study, we used ELISA (R&D, Minneapolis, MN, US) to monitor the serum level of Interleukin-4 (IL-4), IL-10, IL-12, and interferon-γ (INF-γ) in patients receiving allogeneic transplant weekly from day 0 to at least day 200. From Jan. 2003, consecutive 20 patients were enrolled. The GVHD prophylaxis consisted of Cyclosporine-A and short course Methotrexate. Of the 20 patients, 2 had grade 3/4 acute GVHD (aGVHD) and 7 had extensive chronic GVHD (cGVHD). The serum levels of IL-4 and IL-12 were below the detectable level (0.13pg/ml and 0.5pg/ml respectively) in most occasions, even during the period of GVHD. Nevertheless, the serum level of IL-10 correlated well with the activity of cGVHD and we used data gathered from 5 patients to demonstrate this good correlation in figure 1 and 2. Patient 1 (open square, figure 1) had no GVHD and the IL-10 levels were below 5pg/ml during the whole period of follow-up. Patient 2 (solid triangle, figure 1) and 3 (open triangle, figure 2) had de novo cGVHD. The IL-10 level increased gradually when cGVHD developed, however, both clinical manifestations of cGVHD and serum IL-10 level decreased rapidly after the administration of Prednisolone (black bar on figure 1 and 2, with the thickness indicating the relative dosage of Prednisolone). Patient 4 (open circle, figure 2) had grade 2 aGVHD that resolved quickly after Prednisolone treatment. However, IL-10 level increased gradually after discontinuing Prednisolone and cGVHD developed subsequently. After adding Prednisolone again, cGVHD improved and IL-10 decreased to undetectable level rapidly. Patient 5 (solid square, figure 2) had steroid-refractory cGVHD. The IL-10 level kept above 5pg/ml for more than 1 month despite Prednisolone 1mg/kg/day giving at the same time and the patient eventually needed further salvage treatment (thalidomide). The serum INF-γ were undetectable in most occasions. It became detectable during period of cGVHD in patients 3, 4 and 5 but not patient 2. In conclusion, post-transplant serum IL-10 level correlates well with the clinical activity of cGVHD as well as the responsiveness to corticosteroid treatment. This novel finding will allow the functional evaluation of individuals’ immune system after allogeneic transplant and should give insight for the adjustment of immunosuppression necessary for cGVHD control. Figure Figure Figure Figure
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Heuck, C., and OD Wolthers. "A placebo-controlled study of three osteocalcin assays for assessment of prednisolone-induced suppression of bone turnover." Journal of Endocrinology 159, no. 1 (October 1, 1998): 127–31. http://dx.doi.org/10.1677/joe.0.1590127.
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Serum osteocalcin is a sensitive marker of suppressive effects of exogenous glucocorticoids on bone turnover. It has been suggested, however, that the degree of suppression detected by different assays may vary. Whether discrepancies between various assays influence conclusions from group studies of exogenous glucocorticoids has not been evaluated. The aim of the present study was to compare the CAP fluoroimmunoassay (FEIA), OSTK-PR and ELSA-OSTEO assays for assessment of prednisolone-induced effects on serum osteocalcin. Twelve men and eight premenopausal women aged 19-45 (mean 31) years were studied. All subjects were healthy. The design was a randomised double-blind, placebo-controlled parallel- group study with 2 days run-in, 3 days treatment and 4 days run-out. During run-in and run-out no medication was given. During the treatment period the subjects took either 20 mg prednisolone twice daily or placebo. Blood was collected on the last day of each period. Intra- and intergroup comparisons showed prednisolone treatment to be associated with a statistically significant suppression of osteocalcin which was detected by all assays (ANOVA;P<0.0001). In the individual subjects the response to prednisolone was the same for each assay. The CAP FEIA, OSTK-PR and ELSA-OSTEO assays seem equally sensitive for evaluation of osteocalcin in group studies of oral glucocorticoids.
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Huybers, Sylvie, Ton H. J. Naber, René J. M. Bindels, and Joost G. J. Hoenderop. "Prednisolone-induced Ca2+ malabsorption is caused by diminished expression of the epithelial Ca2+ channel TRPV6." American Journal of Physiology-Gastrointestinal and Liver Physiology 292, no. 1 (January 2007): G92—G97. http://dx.doi.org/10.1152/ajpgi.00317.2006.
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Glucocorticoids, such as prednisolone, are often used in clinic because of their anti-inflammatory and immunosuppressive properties. However, glucocorticoids reduce bone mineral density (BMD) as a side effect. Malabsorption of Ca2+ in the intestine is supposed to play an important role in the etiology of low BMD. To elucidate the mechanism of glucocorticoid-induced Ca2+ malabsorption, the present study investigated the effect of prednisolone on the expression and activity of proteins responsible for active intestinal Ca2+ absorption including the epithelial Ca2+ channel TRPV6, calbindin-D9K, and the plasma membrane ATPase PMCA1b. Therefore, C57BL/6 mice received 10 mg/kg body wt prednisolone daily by oral gavage for 7 days and were compared with control mice receiving vehicle only. An in vivo 45Ca2+ absorption assay indicated that intestinal Ca2+ absorption was diminished after prednisolone treatment. We showed decreased duodenal TRPV6 and calbindin-D9K mRNA and protein abundance in prednisolone-treated compared with control mice, whereas PMCA1b mRNA levels were not altered. Importantly, detailed expression studies demonstrated that in mice these Ca2+ transport proteins are predominantly localized in the first 2 cm of the duodenum. Furthermore, serum Ca2+ and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] concentrations remained unchanged by prednisolone treatment. In conclusion, these data suggest that prednisolone reduces the intestinal Ca2+ absorption capacity through diminished duodenal expression of the active Ca2+ transporters TRPV6 and calbindin-D9K independent of systemic 1,25(OH)2D3.
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Ludwig, Elizabeth A., Richard L. Slaughter, Mohammed Savliwala, Corstiaan Brass, and William J. Jusko. "Steroid-Specific Effects of Ketoconazole on Corticosteroid Disposition: Unaltered Prednisolone Elimination." DICP 23, no. 11 (November 1989): 858–61. http://dx.doi.org/10.1177/106002808902301104.
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Ketoconazole inhibits the clearance of methylprednisolone by 60 percent and extends cortisol suppression beyond that produced by methylprednisolone alone. This study examined prednisolone pharmacokinetics and cortisol suppression in four healthy male volunteers following administration of prednisone 20 mg. Studies were performed with and without ketoconazole 200 mg po for six days. Blood samples were obtained serially over 24 hours and serum prednisone, prednisolone, and cortisol concentrations were determined by HPLC. Prednisolone clearance before and after ketoconazole therapy was not significantly different (160 ±38 vs. 148 ±23 mL/h/kg). In addition, no significant differences were found in mean residence time (5.03 ±0.69 vs. 6.18 ±1.77 h), terminal slope (0.23 ±0.03 vs. 0.19 ±0.05 h−1), or volume of distribution (0.79±0.11 vs. 0.84±0.12 L/kg). The ratio of cortisol area under the concentration versus time curve (AUC) 0–24 hours after prednisone administration to the AUC under baseline conditions was used as a measure of adrenal suppression. This ratio was not significantly different after prednisolone with and without ketoconazole (0.40 ±0.10 vs. 0.45 ±0.03). Renal excretion of prednisone and prednisolone was not significantly changed with ketoconazole. Based on this preliminary study, ketoconazole minimally alters prednisolone clearance in contrast to the significant ketoconazole–methylprednisolone interaction previously reported.
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Lowe, Andrew D., Thomas K. Graves, Karen L. Campbell, and David J. Schaeffer. "A Pilot Study Comparing the Diabetogenic Effects of Dexamethasone and Prednisolone in Cats." Journal of the American Animal Hospital Association 45, no. 5 (September 1, 2009): 215–24. http://dx.doi.org/10.5326/0450215.
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Fourteen cats received either daily prednisolone (4.4 mg/kg per os [PO]) or dexamethasone (0.55 mg/kg PO) for 56 days. These doses were clinically equipotent. Serum fructosamine and urine glucose were measured on days 0, 28, and 56. Insulin sensitivity, glucose tolerance, and peak insulin secretion were measured in each group prior to and at the end of the courses of glucocorticoid administration. On day 56, the prevalence of glucosuria was significantly greater (P=0.027), and a trend was seen toward greater fructosamine concentrations (P=0.083) in dexamethasone-treated cats compared to prednisolone-treated cats. The results of this pilot study also showed a trend toward a greater decrease in insulin sensitivity (P=0.061) and a significantly lower compensatory increase in insulin secretion (P=0.081) in the dexamethasone-treated cats than in cats administered prednisolone. These preliminary data suggest that dexamethasone exhibits greater diabetogenic effects in cats than equipotent doses of prednisolone. Further study is justified to support this hypothesis.
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Iida, Keisuke, Yuki Honda, and Yoichiro Homma. "Granulocyte colony-stimulating factor-induced aortitis with temporal arteritis and monoarthritis." BMJ Case Reports 16, no. 2 (February 2023): e251216. http://dx.doi.org/10.1136/bcr-2022-251216.
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We present the case of a patient in his 80s receiving gemcitabine-cisplatin therapy for bladder cancer who developed neutropenia and was treated with filgrastim. In 10 days, the patient developed a mild fever with left jaw claudication and right knee arthritis. Contrast-enhanced CT findings indicated aortitis. Prednisolone was started for granulocyte colony-stimulating factor (G-CSF)-induced aortitis, and symptoms and elevated serum inflammatory markers resolved rapidly, allowing early discontinuation of prednisolone. Right knee arthritis relapsed at the initial follow-up. Contrast-enhanced CT revealed aortitis had disappeared. Therefore, recurrence of G-CSF-induced arthritis was suspected; prednisolone was resumed for 29 days without relapse. Most previous reports of G-CSF-induced aortitis have described inflammation of the aorta, carotid arteries and subclavian arteries; however, G-CSF-induced aortitis may present with more peripheral symptoms, such as temporal arteritis and knee arthritis. Furthermore, G-CSF-induced aortitis reportedly responds well and rapidly to prednisolone, although early discontinuation may lead to relapse.
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Mobisson, Samuel Kelechi, Peter Chukwuma Onyebuagu, Iheanyichukwu Wopara, James Boobondah Woha, Harris Opusunju Boma, Sunday Otoabasi Abaka, Justin Bonaparte Monye, Fidelis Udochukwu Ibe, and Agona Odeh Obembe. "Cannabidiol Oil and Prednisolone Treatment Altered Hematologic Indices, Serum Urea, Creatinine and Cellular Architecture of Kidney on Cadmium Induced Toxicity in Male Wistar Rats." Journal of Pharmaceutical Research International 35, no. 21 (August 3, 2023): 14–27. http://dx.doi.org/10.9734/jpri/2023/v35i217408.
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This study investigated the impact of CBD oil and prednisolone on hematologic indices, urea, and creatinine among cadmium-induced toxicity in male rats. Forty male rats weighing 150g to 200g were assigned into 8 groups (1-8) with five rats each. Group 1 served as control, Group 2-8 received 1mg/kg body weight of prednisolone; 1.5mg/kg bw of cadmium; 1mg/kg bw of prednisolone + 0.2mg/kg bw of CBD-oil; 0.2mg/kg bw of CBD-oil + 2mg/kg bw of cadmium; 3mg/kg bw of Pred + 2mg/kg of cadmium; 0.1mg/kg bw of CBD-oil and 0.2mg/kg bw of CBD-oil respectively. The administration was done using gavage for 14 days. The present results revealed that PCV, haemoglobin, and RBC count of the treated groups were decreased significantly (p<0.05) comparedto the control. TWBC count significantly increased in treated groups than in control. Platelet count significantly increased in groups treated with pred+ cd, CBD-oil (0.1ml), and CBD-oil (0.2ml) than control. Neutrophil count was significantly reduced in groups treated with CBD oil (0.1ml) than in control and other groups. Lymphocyte count significantly increased in groups treated with cadmium+ CBD oil and CBD oil (0.1ml) than in other groups. Eosinophil count significantly decreased in groups treated with prednisolone and pred +CBD oil than control. Monocyte count significantly increased in groups treated with cadmium, pred +cadmium, and CBD oil (0.1ml) than in control. There was a significant decrease in groups treated with pred +CBD-oil, cadmium + CBD-oil, and CBD-oil (0.2ml) than control. Serum urea significantly decreased in the group treated with pred + CBD oil than control. Serum creatinine significantly increased in groups treated with cadmium + CBD oil and CBD oil (0.2ml) compared to the control and prednisolone groups. Histology of the kidney revealed mesangial expansion, hypertrophy of renal corpuscle, hemorrhage, and lymphocyte infiltration in groups treated with pred+ CBD oil and CBD oil (0.1ml) compared to the control. We conclude that CBD oil, prednisolone, and cadmium administration at different doses induced biochemical alterations, altered hematologic indices, and cytoarchitecture of the kidney. Therefore, if these results apply to humans, combined use of CBD oil and prednisolone should be supplemented with blood tonics, especially in chronic kidney disease.
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Liang, Ma, Zhang Liwen, Chen Bingfang, Ding Yanbo, and Chen Jianping. "Eosinophilic gastroenteritis with multiple serous membrane effusion as the first sign: a case report and literature review." Journal of International Medical Research 48, no. 4 (April 2020): 030006052091727. http://dx.doi.org/10.1177/0300060520917274.
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Multiple serous membrane effusion (MSSE) as the first sign of eosinophilic gastroenteritis is extremely rare, and its clinical features and treatment methods have not been well described. The clinical characteristics, diagnosis, and treatment methods of MSSE in a 44-year-old woman were retrospectively reviewed. Laboratory testing revealed an elevated eosinophil count and serum immunoglobulin E level. The levels of all tumor markers were normal, but the CA125 level in serum and ascitic fluid was significantly increased. Ultrasonography showed a large amount of ascites and a moderate amount of pleural effusion. Echocardiography showed a small amount of pericardial effusion. Chest and abdominal computed tomography showed gastrointestinal wall thickening. Moreover, eosinophilic infiltration was detected in duodenal and rectal biopsy samples that had been collected during endoscopic examination of the upper gastrointestinal system. The patient was treated with 30 mg of prednisolone, and seafood was excluded from her diet for 4 weeks. The prednisolone was tapered over 8 weeks and continued at 5 mg prednisolone daily thereafter. The MSSE and peripheral eosinophilia showed a dramatic response to the steroid treatment. This case indicates that we should be highly aware of MSSE as the first clinical manifestation of eosinophilic gastroenteritis.
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Ziemba, Michael, Molly Barkhouse, Kitipong Uaesoontrachoon, Mamta Giri, Yetrib Hathout, Utkarsh J. Dang, Heather Gordish-Dressman, Kanneboyina Nagaraju, and Eric P. Hoffman. "Biomarker-focused multi-drug combination therapy and repurposing trial in mdx mice." PLOS ONE 16, no. 2 (February 22, 2021): e0246507. http://dx.doi.org/10.1371/journal.pone.0246507.
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Duchenne muscular dystrophy is initiated by dystrophin deficiency, but downstream pathophysiological pathways such as membrane instability, NFĸB activation, mitochondrial dysfunction, and induction of TGFβ fibrosis pathways are thought to drive the disability. Dystrophin replacement strategies are hopeful for addressing upstream dystrophin deficiency; however, all methods to date use semi-functional dystrophin proteins that are likely to trigger downstream pathways. Thus, combination therapies that can target multiple downstream pathways are important in treating DMD, even for dystrophin-replacement strategies. We sought to define blood pharmacodynamic biomarkers of drug response in the mdx mouse model of Duchenne muscular dystrophy using a series of repurposed drugs. Four-week-old mdx mice were treated for four weeks with four different drugs singly and in combination: vehicle, prednisolone, vamorolone, rituximab, β-aminoisobutyric acid (BAIBA) (11 treatment groups; n = 6/group). Blood was collected via cardiac puncture at study termination, and proteomic profiling was carried out using SOMAscan aptamer panels (1,310 proteins assayed). Prednisolone was tested alone and in combination with other drugs. It was found to have a good concordance of prednisolone-responsive biomarkers (56 increased by prednisolone, 39 decreased) focused on NFκB and TGFβ cascades. Vamorolone shared 45 (80%) of increased biomarkers and 13 (33%) of decreased biomarkers with prednisolone. Comparison of published human corticosteroid-responsive biomarkers to our mdx data showed 14% (3/22) concordance between mouse and human. Rituximab showed fewer drug-associated biomarkers, with the most significant being human IgG. On the other hand, BAIBA treatment (high and low dose) showed a drug-associated increase in 40 serum proteins and decreased 5 serum proteins. Our results suggest that a biomarker approach could be employed for assessing drug combinations in both mouse and human studies.
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Varalakshmi, T. Naga, and V. Chitra. "Evaluation of Nephroprotective Activity of Hydroalcoholic Extract of Trachyspermum ammi Leaves and Citrus paradisi Fruits against Prednisolone Induced ADPKD in Experimental Rats." INTERNATIONAL JOURNAL OF DRUG DELIVERY TECHNOLOGY 13, no. 02 (June 25, 2022): 627–43. http://dx.doi.org/10.25258/ijddt.13.2.25.
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The study evaluated the nephroprotective activity of hydroalcoholic extracts of Trachyspermum ammi leaves and Citrus paradisi fruits against prednisolone-induced ADPKD in experimental rats. The hydroalcoholic extracts were given orally at 100 and 200 mg/kg for a period of 28 days. Kidney function was evaluated by measuring serum and urine creatinine, urea, uric acid, and proteinuria. Histopathological studies were also conducted. Materials and methods: Animal model was used to evaluate the nephroprotective effect of hydroalcoholic extract from T. ammi leaves & C. paradisi fruits against prednisolone induced ADPKD in Wistar rats.
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Ma, M. K. M., D. Y. H. Yap, C. L. Li, M. M. Y. Mok, G. C. W. Chan, L. P. Y. Kwan, K. N. Lai, and S. C. W. Tang. "Low-dose corticosteroid and mycophenolate for primary treatment of minimal change disease." QJM: An International Journal of Medicine 113, no. 6 (November 26, 2019): 399–403. http://dx.doi.org/10.1093/qjmed/hcz297.
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Abstract Background Mycophenolate has been shown to be effective in glomerular disease. However, the role of mycophenolate in the first-line treatment of adult-onset idiopathic minimal change disease (MCD) has not been systematically studied in a randomized fashion. Aim To evaluate the therapeutic efficacy of enteric-coated mycophenolate sodium combined with low-dose corticosteroid as first-line treatment for MCNS. Design A prospective, open-label, randomized clinical trial. Methods Twenty adult patients with biopsy proven MCD were recruited and randomly assigned to receive either enteric-coated Mycophenolate Sodium (EC-MPS) plus low-dose prednisolone (Group 1: Prednisolone 0.25 mg/kg/day, n = 10) or standard-dose prednisolone (Group 2: Prednisolone 1 mg/kg/day, n = 10). Results After 24 weeks of therapy, eight patients in Group 1 vs. seven of patients in Group 2 achieved complete remission (P = 0.606). Both groups showed a significant reduction of urine protein excretion (P < 0.05) and increased serum albumin (P < 0.001) vs. baseline levels. However, no significant between-group differences were demonstrated. The relapse rate was also similar in both groups. Both treatment regimens were well tolerated but there were more patient reported adverse effects in the standard-dose prednisolone group. Conclusion EC-MPS plus low-dose prednisolone is non-inferior to standard-dose prednisolone therapy in inducing clinical remission and preventing relapse in adult-onset idiopathic MCD and is associated with better tolerability and less adverse effects. This trial is registered with the ClinicalTrials.gov number NCT01185197.
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Frystyk, Jan, Anders J. Schou, Carsten Heuck, Henrik Vorum, Mikkel Lyngholm, Allan Flyvbjerg, and Ole D. Wolthers. "Prednisolone reduces the ability of serum to activate the IGF1 receptor in vitro without affecting circulating total or free IGF1." European Journal of Endocrinology 168, no. 1 (January 2013): 1–8. http://dx.doi.org/10.1530/eje-12-0518.
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ObjectiveEnd-point bioassays based on thymidine or sulfate incorporation have demonstrated that glucocorticoid (GC) treatment inhibits serum IGF1 action, but the mechanism is unknown as serum IGF1 concentrations have been reported to either increase or remain unchanged.AimTo investigate whether GC treatment affects the ability of serum to activate the IGF1 receptor (IGF1R) in vitro (i.e. bioactive IGF1), using a specific cell-based IGF1 kinase receptor activation assay.Subjects and methodsTwenty children with stable asthma (age 7.7–13.8 years) treated for 1 week with 5 mg prednisolone in a randomized, double-blind, placebo-controlled crossover study. Non-fasting serum samples were collected in the afternoon after each 7-day period and assayed for bioactive IGF1, free IGF1, total IGFs, IGF-binding proteins (IGFBPs), and insulin.ResultsPrednisolone treatment reduced IGF1 bioactivity by 12.6% from 2.22±0.18 to 1.94±0.15 μg/l (P=0.01) compared with placebo. In contrast, no changes were observed for (μg/l; placebo vs prednisolone) total IGF1 (215±27 vs 212±24), free IGF1 (1.50±0.16 vs 1.43±0.17), total IGF2 (815±26 vs 800±31), IGFBP3 (3140±101 vs 3107±95), IGFBP2 (238±21 vs 220±19), IGFBP1 (32±6 vs 42±10), or IGFBP1-bound IGF1 (24±5 vs 26±7). Insulin remained unchanged as did IGFBP levels as estimated by western ligand blotting. Prednisolone had no direct effects on IGF1R phosphorylation.ConclusionsOur study gives evidence that GC treatment induces a circulating substance that is able to inhibit IGF1R activation in vitro without affecting circulating free or total IGF1. This may be one of the mechanisms by which GC inhibits IGF1 action in vivo. However, the nature of this circulating substance remains to be identified.
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Oka, K., T. Hirano, H. Shimodaira, M. Homma, E. Sakurai, T. Tamaki, and M. Kozaki. "Suppression of endogenous cortisol for evaluating pharmacodynamics of prednisolone in early allograft rejection in renal transplantation." Clinical Chemistry 36, no. 3 (March 1, 1990): 481–86. http://dx.doi.org/10.1093/clinchem/36.3.481.
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Abstract Concentrations of endogenous cortisol were examined in 34 kidney-transplant recipients by improved "high-performance" liquid chromatography. Ten recipients were treated with prednisolone and azathioprine, the others with prednisolone and cyclosporine. Peripheral serum samples were collected just before transplantation, daily for two weeks after the transplant, weekly until discharge for about two months, and then monthly or occasionally. Mean (+/- SD) cortisol concentrations, initially 145 +/- 87 micrograms/L, decreased immediately to 5.93 +/- 5.11 micrograms/L after transplant, remained at almost these same values for two months, and then swiftly increased to 51 +/- 59 micrograms/L by 1000 days. Cortisol concentrations within the period characterized by a cumulative dose of prednisolone at 300-700 mg were correlated significantly with the presence or absence of acute allograft rejection; patients with cortisol greater than 4 micrograms/L had a higher risk of rejection. The majority of stable patients showed cortisol concentrations between 1 and 4 micrograms/L throughout the cumulative prednisolone period characterized above. Concentrations less than 1 microgram/L after high-dose administration of methylprednisolone were accompanied by severe lung infection. We conclude that suppressed concentrations of endogenous cortisol, as assessed by highly specific HPLC, might provide a basis for predicting the therapeutic efficacy and adverse effects of prednisolone.
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Holla, A., S. Vidyasagar, B. Nandakrishna, L. Bairy, B. A. Shastry, A. Kamath, and S. Adiga. "EFFECT OF GLUCOCORTICOIDS EXPOSURE ON SERUM OSTEOCALCIN LEVELS." INDIAN DRUGS 56, no. 11 (November 28, 2019): 54–58. http://dx.doi.org/10.53879/id.56.11.11848.
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Glucocorticoids (GCs) treatment has a profound effect on bone turnover and the mechanism is complex and not elucidated completely. One of the actions on bone explained by many studies is its effect on serum osteocalcin levels. To investigate changes in the osteocalcin levels among patients who are on GCs and to correlate these levels with various doses of different GCs, a prospective observational study on 88 subjects who were on GC therapy was undertaken. Mean age of subjects was 42.29 ±13.86 years, with a marginal female preponderance (58%). Median dose of glucocorticoids was 1mg/kg (0.89, 2.60). Median baseline serum osteocalcin concentration was 4.4ng/ml (2.2, 9.0), which reduced significantly after starting GC therapy to 2.2ng/ml (1.01, 4.74) (p value=0.009). The median dose of prednisolone was 0.9 (0.72, 0.90) and of methylprednisolone 2.6 (2.1, 3.4) mg/kg. The serum osteocalcin level was reduced significantly (p<0.01), irrespective of GCs. We found that osteocalcin levels were negatively correlated with the dose of prednisolone (r= -0.06, p=0.6) and methylprednisolone(r=-0.11 p=0.53). Further, a weak negative correlation was seen in patients taking less than 1mg/kg and more than 1 mg/kg (r=-0.21 p value=0.32 and r=-0.352 p value-0.005), showing greater reduction in patients on higher doses. Osteocalcin reduction is solely dependent on dose of glucocorticoids, not on type of glucocorticoids. This may have important clinical implications and may help to reduce bone related side effects.
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HODSMAN, ANTHONY B., JOHN H. TOOGOOD, BARBARA JENNINGS, LAWRENCE J. FRAHER, and JON C. BASKERVILLE. "Differential Effects of Inhaled Budesonide and Oral Prednisolone on Serum Osteocalcin*." Journal of Clinical Endocrinology & Metabolism 72, no. 3 (March 1991): 530–40. http://dx.doi.org/10.1210/jcem-72-3-530.
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H�fle, G�nter, Hannes Holzm�ller, Ghazaleh Gouya, Klaus Hergan, Michael Hubmann, Peter Langer, and Heinz Drexel. "Lower serum ?-CrossLaps in male cardiac transplant recipients treated without prednisolone." Transplant International 16, no. 7 (July 1, 2003): 523–28. http://dx.doi.org/10.1007/s00147-003-0577-3.
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Lisakovska, Olha, Ihor Shymanskyy, Anna Mazanova, Anna Khomenko, and Mykola Veliky. "Vitamin D3 protects against prednisolone-induced liver injury associated with the impairment of the hepatic NF-κB/iNOS/NO pathway." Biochemistry and Cell Biology 95, no. 2 (April 2017): 213–22. http://dx.doi.org/10.1139/bcb-2016-0070.
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The study was carried out to define whether prednisolone-induced damage to hepatic cells is accompanied by excessive nitric oxide (NO) levels associated with nuclear factor kappa B (NF-κB)/inducible NO synthase (iNOS) activation and evaluate the efficacy of the treatment with vitamin D3. Histopathological examination, activities of liver transaminases (alanine aminotransferase and aspartate aminotransferase), and cell death assays consistently showed that prednisolone (5 mg/kg body weight, 30 days) induces chronic liver injury in female Wistar rats. Specifically, increased hepatocellular necrosis and caspase-3-dependent apoptosis were observed. Prednisolone enhanced iNOS protein expression, NO generation, and tyrosine nitration in liver cells. Despite unchanged hepatic level of the NF-κB/p65 protein, prednisolone increased inhibitory κB-α (IκB-α) degradation, nuclear translocation, and phosphorylation of NF-κB/p65 at Ser311, indicating that NF-κB activation can be involved in the induction of iNOS/NO. All changes were associated with a 2.9-fold decrease in the serum content of 25-hydroxyvitamin D3 and significant reduction of hepatic vitamin D3 receptor (VDR) expression that points reliably to vitamin D3 deficiency and failures in VDR signaling. Vitamin D3 co-administration (100 IU/rat, 30 days) prevented glucocorticoid-evoked abnormalities in hepatic tissue. In conclusion, prednisolone-induced liver disturbances were associated with the impairment of NF-κB/iNOS/NO responses that can be ameliorated by vitamin D3 treatment through VDR-mediated mechanisms.
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Breitschwerdt, E. B., M. G. Davidson, B. C. Hegarty, M. G. Papich, and C. B. Grindem. "Prednisolone at anti-inflammatory or immunosuppressive dosages in conjunction with doxycycline does not potentiate the severity of Rickettsia rickettsii infection in dogs." Antimicrobial Agents and Chemotherapy 41, no. 1 (January 1997): 141–47. http://dx.doi.org/10.1128/aac.41.1.141.
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Dogs were experimentally inoculated with Rickettsia rickettsii to determine if anti-inflammatory or immunosuppressive dosages of prednisolone, when administered in conjunction with an antirickettsial antibiotic (doxycycline), induced therapeutically relevant pathophysiological consequences that ultimately influence disease outcome. Although the duration of rickettsemia was prolonged in dogs receiving immunosuppressive, but not anti-inflammatory, corticosteroids, concurrent administration of doxycycline and corticosteroids conferred no other detected detrimental effects. Treatment with doxycycline or doxycycline in conjunction with prednisolone resulted in decreased R. rickettsii-specific antibody titers; however, examination of appropriately timed acute- and convalescent-phase serum samples would have facilitated an accurate diagnosis of Rocky Mountain spotted fever (RMSF) in all 16 dogs. We conclude that the concurrent use of anti-inflammatory or immunosuppressive doses of prednisolone in conjunction with doxycycline, early in the course of experimental RMSF, confers no clinically relevant detrimental effects and that additional studies might be indicated to detect possible beneficial effects in cases of severe or potentially fulminant RMSF. However, because the illness induced in these dogs was of mild to moderate severity, the results of this study should definitely not be construed as supporting the safety or efficacy of prednisolone for treatment of severe canine or human RMSF.
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Jeries, Helana, Nina Volkova, Claudia Grajeda-Iglesias, Mahmoud Najjar, Mira Rosenblat, Michael Aviram, and Tony Hayek. "Prednisone and Its Active Metabolite Prednisolone Attenuate Lipid Accumulation in Macrophages." Journal of Cardiovascular Pharmacology and Therapeutics 25, no. 2 (October 24, 2019): 174–86. http://dx.doi.org/10.1177/1074248419883591.
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Background: Synthetic forms of glucocorticoids (GCs; eg, prednisone, prednisolone) are anti-inflammatory drugs that are widely used in clinical practice. The role of GCs in cardiovascular diseases, including atherosclerosis, is highly controversial, and their impact on macrophage foam cell formation is still unknown. We investigated the effects of prednisone and prednisolone on macrophage oxidative stress and lipid metabolism. Methods and Results: C57BL/6 mice were intraperitoneally injected with prednisone or prednisolone (5 mg/kg) for 4 weeks, followed by lipid metabolism analyses in the aorta and peritoneal macrophages. We also analyzed the effect of serum samples obtained from 9 healthy human volunteers before and after oral administration of prednisone (20 mg for 5 days) on J774A.1 macrophage atherogenicity. Finally, J774A.1 macrophages, human monocyte-derived macrophages, and fibroblasts were incubated with increasing concentrations (0-200 ng/mL) of prednisone or prednisolone, followed by determination of cellular oxidative status, and triglyceride and cholesterol metabolism. Prednisone and prednisolone treatment resulted in a significant reduction in triglyceride and cholesterol accumulation in macrophages, as observed in vivo, ex vivo, and in vitro. These effects were associated with GCs’ inhibitory effect on triglyceride- and cholesterol-biosynthesis rates, through downregulation of diacylglycerol acyltransferase 1 and HMG-CoA reductase expression. Glucocorticoid-induced reduction of cellular lipid accumulation was mediated by the GC receptors on the macrophages, because the GC-receptor antagonist (RU486) abolished these effects. In fibroblasts, unlike macrophages, GCs showed no effects. Conclusion: Prednisone and prednisolone exhibit antiatherogenic activity by protecting macrophages from lipid accumulation and foam cell formation.
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Mortier, F., S. Daminet, S. Vandenabeele, and I. Van de Maele. "Canine lymphoma: a retrospective study (2009 – 2010)." Vlaams Diergeneeskundig Tijdschrift 81, no. 6 (December 28, 2012): 341–51. http://dx.doi.org/10.21825/vdt.v81i6.18317.
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This study reviews the medical records of 56 dogs diagnosed with lymphoma based on the cytological and/or histological results between January 1, 2009 and December 31, 2010. Most of the dogs were middle-aged to old, and were diagnosed with multicentric lymphoma (ML) (n=36). The majority of the dogs were presented in stages III to V (n=55) and substage b (n=43). A complete blood count and serum biochemistry, urinalysis, serum protein electrophoresis, thoracic radiographs and/or abdominal ultrasound were performed. The results correlated with previously described results in the literature. Therapy was initiated in 80% of the dogs (n=45). After diagnosis, the median survival time of 62% of these dogs (n=28) treated with only prednisolone was 32 days (range 3 – 224 days). For 24% of the dogs (n=11) treated with chemotherapy, the median survival time was 119 days (range 11 - 273 days). Surgical resection of the macroscopic tumor was performed in the remaining six dogs (13%). Three of these dogs received subsequent prednisolone therapy. The median survival time of these six dogs was 47 days (range 0 – 669 days). The dogs that received chemotherapy had significantly longer survival times than those treated with only prednisolone, although negative prognostic factors were present in all of the cases treated with chemotherapy.
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Shimada, T., M. Higashida-Konishi, K. Izumi, S. Hama, T. Oshige, H. Oshima, and Y. Okano. "POS1423 CHARACTERISTICS OF CYTOMEGALOVIRUS-POSITIVE VERSUS NEGATIVE, AND CYTOMEGALOVIRUS-TREATED VERSUS UNTREATED PATIENTS DURING IMMUNOSUPPRESSIVE THERAPY FOR RHEUMATIC DISEASES." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 1054.3–1055. http://dx.doi.org/10.1136/annrheumdis-2022-eular.2193.
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BackgroundImmunosuppressive treatment is a common cause of cytomegalovirus (CMV) reactivation.ObjectivesTo elucidate the characteristics of CMV-positive and negative patients during the treatment for rheumatic diseases.MethodsWe retrospectively evaluated consecutive patients admitted to our department from January 2006 to October 2021 whose C7-HRP antigen were measured. We collected their age, sex, primary problem and its lesion, and test results within 3 months before C7-HRP measurement. We also investigated the use of immunosuppressants, and maximum and cumulative dose of administered prednisolone within 6 months before C7-HRP measurement. Maximum and cumulative dose of prednisolone contained methylprednisolone pulse, which was converted into prednisolone equivalent. We investigated the characteristics of CMV-positive and negative patients, and those of CMV-positive patients with or without anti-CMV drug use.ResultsOf a total of 472 patients, 85 were positive and 387 were negative for C7-HRP. The average age was 71.2 vs. 64.4 (p=0.0021). Their male-to-female ratio was 20/65 vs. 120/267 (p=0.0290). The following diseases were significantly common among CMV-positive patients: microscopic polyangiitis (21.2% vs. 3.9%, p<0.0001), adult-onset Still’s disease (7.1% vs. 1.3%, p=0.0002), and systemic sclerosis (4.7% vs. 2.1%, p=0.0273). Significantly common comorbidities of CMV-positive patients were interstitial lung disease (35.3% vs. 16.0%, p<0.0001), nephritis (23.5% vs. 11.6%, p=0.0005), peripheral nervous system disorders (11.8% vs. 5.7%, p=0.0070), alveolar hemorrhage (5.9% vs. 0.8%, p=0.0001), and peripheral circulatory disorders (4.7% vs. 1.6%, p=0.0111). Average neutrophil counts (7720 /μL vs. 6440 /μL, p=0.0001), serum creatinine (1.0 mg/dL vs. 0.9 mg/dL, p=0.0104), and hemoglobin A1c (6.3% vs. 5.7%, p=0.0030) were significantly higher among CMV-positive patients, whereas hemoglobin (10.1 g/dL vs. 11.1 g/dL, p<0.0001), lymphocyte counts (820 /μL vs. 1190 /μL, p<0.0001), platelet counts (233000 /μL vs. 259000 /μL, p<0.0001), and serum albumin (2.9 g/dL vs. 3.4 g/dL, p<0.0001) were lower. Higher maximum dose of prednisolone (534.9 mg/day vs. 135.5 mg/day, p<0.0001), intravenous cyclophosphamide (27.1% vs. 11.4%, p<0.0001), rituximab (9.4% vs. 2.1%, p<0.0001), azathioprine (23.5% vs. 14.2%, p=0.0053), cyclosporin (8.2% vs. 3.6%, p=0.0101) were significantly more often used among CMV-positive patients. Average cumulative dose of prednisolone was 3022.6 mg vs. 1408.7 mg (p<0.0001). We also performed multivariate analysis, including the patients’ age, sex, maximum and cumulative dose of prednisolone, and the use of intravenous cyclophosphamide, rituximab, azathioprine, and cyclosporin. Elderly (p=0.0006), female (p=0.0293), high cumulative dose of prednisolone (p=0.0155), and the use of cyclosporin (p=0.0479) were significantly associated with CMV-positivity. Anti-CMV drug was administered to 63.5% of CMV-positive patients. The average age was significantly higher in anti-CMV-drug-treated patients than untreated patients (73.7 vs. 67.1, p=0.0492). The CMV-treated patients had significantly higher neutrophil counts (8540 /μL vs. 6280 /μL, p<0.0001), erythrocyte sedimentation rate (57.6 mm/h vs. 40.5 mm/h, p<0.0001), and C-reactive protein (5.3 mg/dL vs. 2.6 mg/dL, p<0.0001) than the untreated patients while the other data such as complete blood counts and serum chemistry revealed no significant difference. Average maximum dose of prednisolone was significantly higher in CMV-treated patients (617.1 mg/day vs. 391.1 mg/day, p=0.0261) while average cumulative dose of prednisolone and the use of any other immunosuppressants revealed no significant difference.ConclusionIntense immunosuppression, especially with higher dose of glucocorticoids, seemed to be the major risk factor of CMV reactivation. These medications may often require anti-CMV therapy.Disclosure of InterestsNone declared
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Van Laar, J. M., A. Lei, M. Safy-Khan, J. Almquist, C. Astbury, M. Belvisi, A. Platt, et al. "POS0089 AZD9567 VERSUS PREDNISOLONE IN PATIENTS WITH ACTIVE RHEUMATOID ARTHRITIS: A PHASE 2A, RANDOMISED, DOUBLE-BLIND, PARALLEL-GROUP EFFICACY AND SAFETY STUDY." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 253–54. http://dx.doi.org/10.1136/annrheumdis-2021-eular.632.
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Background:Oral corticosteroids such as prednisolone are potent anti-inflammatory drugs but their use is limited by side effects caused by unwanted actions on the glucocorticoid receptor (GR), such as increased insulin resistance, and off-target actions on the mineralocorticoid receptor (MR) that disrupt electrolyte balance and increase water retention. AZD9567 is an oral, selective, non-steroidal glucocorticoid receptor modulator being developed to treat inflammatory diseases. Pre-clinical and phase 1 clinical data indicate that AZD9567 is the first GR modulator with an improved efficacy–dysglycaemic side effect profile versus prednisolone.Objectives:To compare the efficacy, safety and tolerability of AZD9567 with prednisolone in patients with active rheumatoid arthritis (RA), at doses with predicted equivalent anti-inflammatory activity.Methods:In this phase 2a, randomised, double-blind, parallel-group, multicentre study in RA patients with DAS28-CRP ≥ 3.2 despite stable treatment with conventional disease-modifying anti-rheumatic therapies (NCT03368235), patients were randomised 1:1 to AZD9567 40 mg or prednisolone 20 mg orally once daily for 14 days. The primary endpoint was change from baseline in DAS28-CRP at day 15. Secondary outcomes included components of DAS28-CRP, TJC68, SJC66, ACR response (ACR20, ACR50, ACR70) and safety outcomes, including serum electrolytes.Results:All 21 randomised patients (AZD9567, n = 11; prednisolone, n = 10) completed the study. There was a slight imbalance between the treatment groups at baseline, with higher age (mean ± SD: 64.5 ± 8.4 vs 55.5 ± 13.6 years), more women (8 vs 5) and greater disease severity (DAS28-CRP, mean ± SD: 5.26 ± 0.98 vs 4.90 ± 0.74) in the AZD9567 group versus the prednisolone group. There was no statistically significant or clinically meaningful (i.e. > 1.2) difference in change from baseline to day 15 in DAS28-CRP between AZD9567 and prednisolone, although this was numerically lower with AZD9567 (Table 1). Similar results were observed for TJC68, SJC66, CRP and GH (Table 1). The proportions of patients achieving ACR20, 50 and 70 response criteria were similar in both groups, albeit numerically lower with AZD9567. Similar numbers of patients in each group reported treatment-emergent adverse events (AZD9567, n = 10, prednisolone, n = 9); most were mild in severity. One serious adverse event, suicidal depression, was reported after completing AZD9567 treatment. Morning fasting serum sodium/potassium ratio at day 15 was not altered with AZD9567 but was increased from baseline with prednisolone (Figure 1).Conclusion:AZD9567 40 mg had a similar efficacy profile to prednisolone 20 mg in patients with active RA. Both drugs were well tolerated, with no new safety signals. Unlike prednisolone, AZD9567 had no effect on serum sodium/potassium ratio, suggesting selectivity of AZD9567 for the GR over the MR. These results support further trials of AZD9567 in patients with inflammatory disease.Table 1.Change from baseline to day 15 in clinical disease activity measures.AZD9567 (n = 11)Prednisolone (n = 10)Comparison(AZD9567 – prednisolone)LSM CFB (SE)95% CILSM CFB (SE)95% CILSMD (SE)95% CIp valueDAS28−CRP score−1.93 (0.35)−2.66, −1.21−2.40 (0.34)−3.11, −1.700.47 (0.46)−0.49, 1.430.315TJC28 score−6.12 (1.25)−8.76, −3.49−6.07 (1.21)−8.61, −3.52−0.05 (1.60)−3.43, 3.320.973SJC28 score−5.14 (0.65)−6.51, −3.76−5.40 (0.63)−6.73, −4.080.26 (0.84)−1.50, 2.030.757GH score−27.7 (7.3)−42.8, −12.5−37.4 (7.1)−52.3, −22.69.8 (9.7)−10.5, 30.10.325CRP, mg/L−10.8 (2.4)−15.9, −5.8−15.6 (2.5)−20.9, −10.34.8 (3.5)−2.5, 12.00.187TJC68 score−9.02 (2.46)−14.21, −3.82−7.90 (2.36)−12.88, −2.91−1.12 (3.12)−7.69, 5.460.724SJC66 score−6.24 (0.89)−8.13, −4.36−6.66 (0.86)−8.48, −4.850.42 (1.14)−1.98, 2.810.717CFB, change from baseline; CRP, C-reactive protein; DAS28, 28-joint disease activity score; GH, global health; LSM(D), least-squares mean (difference); SJC, swollen joint count; TJC, tender joint count.Acknowledgements:Medical writing support was provided by Richard Claes PhD of PharmaGenesis London, London, UK, funded by AstraZeneca, Gothenburg, Sweden in accordance with Good Publication Practice 3 (GPP3) guidelines (http://www.ismpp.org/gpp3).This study was funded by AstraZeneca. AZD9567 is an investigational medical product with no approved indication.Disclosure of Interests:Jacob M. van Laar Consultant of: Honoraria from - Abbvie, Arxx Tx, Galapagos, Gesyntha, Leadiant, Magenta, Roche, Sanofi Genzyme, Grant/research support from: AstraZeneca, Pfizer, Roche, Alejhandra Lei Shareholder of: AstraZeneca., Grant/research support from: Boehringer Ingelheim in 1998, Bristol-Myers Squibb in 1999, Employee of: AstraZeneca. Past employee of Almirall, Grünenthal, Boehringer Ingelheim, CESIF Pharma, Mary Safy-Khan Grant/research support from: Student grant from AstraZeneca 2015-2018., Joachim Almquist Shareholder of: AstraZeneca, Consultant of: AstraZeneca., Employee of: AstraZeneca., Carol Astbury Shareholder of: AstraZeneca., Employee of: AstraZeneca., Maria Belvisi Shareholder of: AstraZeneca., Grant/research support from: AstraZeneca and Chiesi, Employee of: AstraZeneca., Adam Platt Shareholder of: AstraZeneca., Employee of: AstraZeneca., Susanne Prothon Shareholder of: AstraZeneca., Employee of: AstaZeneca., Sara Samuelsson Shareholder of: AstraZeneca, Employee of: AstraZeneca, Petter Svanberg Employee of: AstraZeneca, Christina Keen Shareholder of: AstraZeneca., Employee of: AstraZeneca.
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Hofle, Gunter, Hannes Holzmuller, Ghazaleh Gouya, Klaus Hergan, Michael Hubmann, Peter Langer, and Heinz Drexel. "Lower serum beta-CrossLaps in male cardiac transplant recipients treated without prednisolone." Transplant International 16, no. 7 (July 2003): 523–28. http://dx.doi.org/10.1111/j.1432-2277.2003.tb00342.x.
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NORDAL, KNUT P., EILIF DAHL, JOHAN HALSE, LAGE AKSNES, and DAGFINN AARSKOG. "Rapid Effect of Prednisolone on Serum 1,25-Dihydroxycholecalciferol Levels in Hypercalcemic Sarcoidosis." Acta Medica Scandinavica 218, no. 5 (April 24, 2009): 519–23. http://dx.doi.org/10.1111/j.0954-6820.1985.tb08883.x.
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Wolthers, O. D., and C. Heuck. "Short-term treatment with prednisolone has no lasting effect on serum leptin." Scandinavian Journal of Clinical and Laboratory Investigation 62, no. 4 (January 2002): 321–24. http://dx.doi.org/10.1080/003655102760145898.
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Fukusima, Naoki, Nobuhisa Kakehi, Kentarou Tahara, Tsuyuko Watanabe, and Eiichi Hirano. "Successful treatment of ascites accumulation and diarrhea associated with protein-losing enteropathy with oral equine placenta extract supplementation in a dog: A case report." Open Veterinary Journal 12, no. 5 (2022): 774. http://dx.doi.org/10.5455/ovj.2022.v12.i5.24.
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Background: Protein-losing enteropathy (PLE) is characterized by leakage of serum proteins into the intestinal lumen, indicating hypoproteinemia. Immunosuppressive agents are the mainstay of treatment, but in many cases, patients are forced to taper off early owing to the induction of liver damage. Case Description: An 8-year-old, unneutered female Chihuahua presented with diarrhea and ascites effusion lasting 2 weeks. Based on the results of radiography and blood tests, a diagnosis of PLE was made. Prednisolone (3 mg/kg semel in die [SID]) and MitoMax (200 mg/day) were administered, but ascites accumulation and diarrhea did not improve. Thus, azathioprine (2 mg/kg/day) was added, but there was no improvement and liver damage developed. The liver injury did not improve immediately, but the diarrhea and ascites effusion improved after serum total protein and serum albumin levels increased after they had decreased. Subsequent tapering of prednisolone from 3 mg/kg SID to 1 mg/kg SID, combined with MitoMax (200 mg/day) and equine placenta extract (eqPE) (2 mL/day), resulted in no recurrence of ascites or diarrhea. Conclusion: In canine PLE with prolonged diarrhea and ascites effusion, supplementation with eqPE may be considered as a reasonable additional therapeutic strategy.
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Honne, Kyoko, Takao Nagashima, Masahiro Iwamoto, Toyomi Kamesaki, and Seiji Minota. "Glucocorticoid-Responsive Cold Agglutinin Disease in a Patient with Rheumatoid Arthritis." Case Reports in Rheumatology 2015 (2015): 1–4. http://dx.doi.org/10.1155/2015/823563.
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A 57-year-old man with rheumatoid arthritis developed severe anemia during treatment with adalimumab plus methotrexate. Cold agglutinin disease was diagnosed because haptoglobin was undetectable, cold agglutinin was positive (1 : 2048), and the direct Coombs test was positive (only to complement). Although the cold agglutinin titer was normalized (1 : 64) after treatment with prednisolone (0.7 mg/kg/day for two weeks), the patient’s hemoglobin did not increase above 8 g/dL. When cold agglutinins were reexamined using red blood cells suspended in bovine serum albumin, the titer was still positive at 1 : 1024. Furthermore, the cold agglutinin had a wide thermal amplitude, since the titer was 1 : 16 at 30°C and 1 : 1 at 37°C. This suggested that the cold agglutinin would show pathogenicity even at body temperature. After the dose of prednisolone was increased to 1 mg/kg/day, the patient’s hemoglobin rapidly returned to the normal range. The thermal amplitude test using red blood cells suspended in bovine serum albumin is more sensitive than the standard test for detecting pathogenic cold agglutinins.
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Seto, M., S. Kim, H. Yoshifusa, Y. Nakamura, T. Masuda, A. Hamaguchi, S. Yamanaka, and H. Iwao. "Effects of prednisolone on glomerular signal transduction cascades in experimental glomerulonephritis." Journal of the American Society of Nephrology 9, no. 8 (August 1998): 1367–76. http://dx.doi.org/10.1681/asn.v981367.
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In vitro data support that activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) regulate the gene expression of numerous growth factors and cytokines involved in the development of glomerulonephritis (GN). However, the in vivo activation and role of these transcription factors are poorly understood. This study examines whether these transcription factors are activated in antithymocyte serum (ATS)-induced GN in vivo and whether prednisolone suppresses activation of them. As assessed by gel mobility shift assay, glomerular DNA binding activity of AP-1 containing both c-Jun and c-Fos and NF-kappaB composed of P-50 and P-65 subunits was significantly increased after ATS injection. Furthermore, as estimated by in-gel kinase assay, glomerular activity of extracellular signal-regulated kinases (ERK) and c-jun NH2-terminal kinases (JNK), which are mitogen-activated protein kinases (MAPK) known to activate AP-1 and NF-kappaB in vitro, was significantly increased after ATS injection, preceding the increase in AP-1 activity. Prednisolone treatment significantly prevented the increase in urinary protein and albumin excretion and glomerular cell proliferation in ATS-induced GN, indicating the beneficial effects of prednisolone on this GN. Prednisolone significantly suppressed the increased glomerular ERK and JNK activities and AP-1 binding activity, but not glomerular NF-kappa binding activity. This study provides the first evidence of the marked increase in glomerular MAPK activities, and AP-1 and NF-kappa binding activities in ATS-induced GN. The beneficial effect of prednisolone on this GN may be partially mediated by the suppression of MAPK, followed by the suppression of AP-1.
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Kimura, Yasuyuki, Hiroko Miwa, Mitsuru Furukawa, and Yuji Mizukami. "Relapsing polychondritis presented as inner ear involvement." Journal of Laryngology & Otology 110, no. 2 (February 1996): 154–57. http://dx.doi.org/10.1017/s002221510013302x.
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AbstractWe report a rare case of relapsing polychondritis with an initial symptom of inner ear involvement. This 53-year-old Japanese man experienced a hearing difficulty, tinnitus in both ears, and dizziness of sudden onset, but lacked auricular chondritis at that time, which is the most frequent finding in relapsing polychondritis. Thus it was difficult to reach a correct diagnosis. Steroid therapy, with oral prednisolone 15 mg daily, was effective. Almost two months after we began the steroid therapy, the patient complained of losing interest in his work and reported a hallucination vision on the TV screen, so the dose of prednisolone was decreased to 10 mg. The hallucinations then disappeared, but the serum level of C-reactive protein increased highly. To reduce the dose of prednisolone, we tried low-dose oral methotrexate. However, we had to discontinue it when the patient experienced severe vomiting and diarrhoea. As adjuvant therapy, we then administered Sho-saiko-to, Chinese herbal medicines with few side effects. Symptoms and laboratory abnormalities then improved markedly.
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Hawley, James M., Laura J. Owen, Stephen J. Lockhart, Phillip J. Monaghan, Annie Armston, Carrie A. Chadwick, Heather Wilshaw, Maisa Freire, Leslie Perry, and Brian G. Keevil. "Serum Cortisol: An Up-To-Date Assessment of Routine Assay Performance." Clinical Chemistry 62, no. 9 (September 1, 2016): 1220–29. http://dx.doi.org/10.1373/clinchem.2016.255034.
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Abstract BACKGROUND Accurate serum cortisol quantification is required for the correct diagnosis and management of adrenal pathologies. Presently, most laboratories use immunoassay to measure serum cortisol with proficiency schemes demonstrating a wide dispersion of results. Here, we investigate the effects of sex, matrix, and antibody specificity on serum cortisol quantification in 6 routine assays. METHODS Surplus serum was obtained before disposal and the following cohorts were created: males, nonpregnant females, pregnant patients, and patients prescribed either metyrapone or prednisolone. Samples were anonymized and distributed to collaborating laboratories for cortisol analysis by 6 routine assays. Cortisol was also measured in all samples using an LC-MS/MS candidate reference measurement procedure (cRMP); cortisol-binding globulin (CBG) was measured in the nonpregnant and pregnant female cohorts. RESULTS Considerable inter- and intraassay variation was observed across the male and nonpregnant female cohorts relative to the cRMP. Four immunoassays underrecovered cortisol in the pregnancy cohort, and CBG was found to be significantly higher in this cohort than in the nonpregnant females. In the metyrapone and prednisolone cohorts, all immunoassays overestimated cortisol. The first generation Roche E170 and Siemens Centaur XP were particularly prone to overestimation. In all cohorts the routine LC-MS/MS assay aligned extremely well with the cRMP. CONCLUSIONS Despite the clinical importance of serum cortisol, the performance of routine immunoassays remains highly variable. Accurate quantification is compromised by both matrix effects and antibody specificity. Underpinning this study with a cRMP has highlighted the deficiencies in standardization across routine cortisol immunoassays.
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Miyawaki, Y., K. Sada, Y. Asano, K. Hayashi, Y. Yamamura, S. Hiramatsu, K. Ohashi, et al. "Progressive reduction of serum complement levels: a risk factor for relapse in patients with hypocomplementemia in systemic lupus erythematosus." Lupus 27, no. 13 (October 11, 2018): 2093–100. http://dx.doi.org/10.1177/0961203318804892.
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Objective Serologically active clinically quiescent (SACQ)-SLE is a subtype of systemic lupus erythematosus (SLE); most SACQ-SLE patients relapse. Although complement and/or anti-dsDNA level fluctuations during SACQ status are reportedly not useful for predicting relapse, they might be useful in specific clinical settings. We aimed to assess the correlation between future relapse and progressive reductions in serum complement levels following remission in patients with hypocomplementemia . Methods We retrospectively reviewed patients aged ≥15 years who were treated with ≥20 mg/day of prednisolone for remission induction. After achieving remission, the patients treated with prednisolone tapered to ≤15 mg/day without relapse and followed by hypocomplementemia (first hypocomplementemia point) were analyzed. The primary outcome was the relapse during the first 24 months. Results Seventy-six patients were enrolled; 31 (40.8%) relapsed. A ≥10% reduction after the first hypocomplementemia point in serum C3, C4, and CH50 levels was found in 10, 21, and 16 patients, respectively. Hazard ratios (95% confidence intervals) for relapse were 2.32 (0.92–5.12) for serum C3 levels and 2.46 (1.18–5.01) for serum C4 levels. Progressive reductions in serum C3 and C4 levels had relatively high specificity (93.3% and 82.2%) but limited sensitivity (22.6% and 41.9%) for predicting relapse. However, simultaneous progressive reduction in C3 levels and increase in anti-dsDNA antibody levels had the highest specificity (97.8%), and simultaneous progressive reduction in C4 levels or increase in anti-dsDNA antibody levels had the highest sensitivity (71.0%). Conclusion Simultaneous progressive reductions in complement levels and increases in anti-dsDNA antibody levels may indicate future relapse SACQ-SLE patients.
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Tawanwongsri, Weeratian, and Penpun Wattanakrai. "Serum Sickness after Equine Rabies Immunoglobulin in Identical Male Twins: Two Case Reports." Case Reports in Dermatology 11, no. 1 (February 14, 2019): 40–47. http://dx.doi.org/10.1159/000497053.
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We, hereby, report two cases of serum sickness in adult male identical twins who had received equine rabies immunoglobulin as a postexposure rabies treatment after cat scratches. The younger brother developed low-grade fever, polyarthritis, and multiple erythematous maculopapular eruptions, whereas low-grade fever and urticaria-like eruptions were detected in the elder brother. Both patients received a 7-day course of low-dose prednisolone and achieved good responses without recurrent attacks.
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Ghafar, Muhammad Hazim Abdul, Amy Oon, Nik Mohd Yunus Mohammad, and Irfan Mohamad. "Kimura Disease of Parotid Gland." International Journal of Human and Health Sciences (IJHHS) 4, no. 1 (October 31, 2019): 63. http://dx.doi.org/10.31344/ijhhs.v4i1.122.
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Kimura disease is a rare, benign, chronic inflammatory disorder. Characteristic features of the disease include painless subcutaneous mass in the head and neck region, elevated serum eosinophilia and markedly raised serum immunoglobulin E. Herein, we report a case of Kimura disease in a patient who presented with a parotid mass and received both medical and surgical management. A course of high dose oral prednisolone and subsequently parotidectomy were the important elements of the management.International Journal of Human and Health Sciences Vol. 04 No. 01 January’20 Page : 63-66
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Notghi, A., J. Dick, G. Smith, J. L. Anderton, and G. D. Chisholm. "A Comparison of Cyclosporin versus Azathioprine Treatment in Renal Transplants in Edinburgh." Scottish Medical Journal 34, no. 3 (June 1989): 459–62. http://dx.doi.org/10.1177/003693308903400305.
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Three year graft survival rates were calculated for 66 patients on cyclosporin and prednisolone immunosuppression and compared to survival rates for 73 patients on azathioprine and prednisolone. There was a temporary early advantage for the cyclosporin treatment group up to four months post transplant. There was no further significant difference between the two treatment groups with graft survival rate of 81.4% in cyclosporin and 76.7% in azathioprine group at three years post transplant. Fewer of the patients on cyclosporin had acute episodes of rejection. There was no significant difference in serum creatinine or urea at one year, but the haemoglobin level was higher in cyclosporin treated patients. Cyclosporin does not appear to have increased the survival rate significantly in our centre where there is already a high graft survival with azathioprine.
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Miyata, Kana N., Hiromi Kihira, Manabu Haneda, and Yasuhide Nishio. "IgG4-Related Tubulointerstitial Nephritis Associated with Membranous Nephropathy in Two Patients: Remission after Administering a Combination of Steroid and Mizoribine." Case Reports in Nephrology 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/678538.
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We report two cases of Japanese men who presented with proteinuria, eosinophilia, hypocomplementemia, and high serum immunoglobulin G4 (IgG4) concentration and were diagnosed with membranous nephropathy associated with IgG4-related tubulointerstitial nephritis on renal biopsy. The typical renal lesions of IgG4-related disease are tubulointerstitial nephritis, which improves remarkably with steroid therapy, and occasional glomerular changes. In our two cases, renal biopsy revealed IgG4-positive immune complex deposits in glomeruli in a pattern of membranous nephropathy and concurrent tubulointerstitial nephritis with IgG4 plasma cells. In both cases, proteinuria persisted with initial prednisolone treatment and was resolved only after the addition of mizoribine. We report the first two cases in which the combination of prednisolone and mizoribine was effective for treating membranous nephropathy associated with IgG4-related tubulointerstitial nephritis.
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Tatsuzawa, Masaomi, Ryuichi Ogawa, Naoki Kinjo, Soan Kim, Fumitaka Shimizu, Yoshiro Sakamoto, Kazuyo Shimojima, Hirotoshi Echizen, and Akihisa Miyazaki. "Consequences of Different Corticosteroids on Serum Potassium and Prostate-Specific Antigen in Patients Receiving Abiraterone for Castration-Resistant Prostate Cancer: A Retrospective Observational Study." Clinical Medicine Insights: Oncology 11 (January 1, 2017): 117955491773773. http://dx.doi.org/10.1177/1179554917737736.
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Background: Abiraterone acetate is an androgen synthesis inhibitor approved for the treatment of castration-resistant prostate cancer (CRPC). Although co-administration of either prednisone or prednisolone at 10 mg/d has been recommended to reduce the risk of abiraterone-induced hyperaldosteronism (notably hypokalemia) and to give adjunctive pain relief effects, whether these glucocorticoids can be substituted by dexamethasone remains unknown. Methods: We performed a retrospective review of medical records of patients who were given abiraterone for the treatment of CRPC with either prednisolone (ABI/PSL) 10 mg/d or dexamethasone (ABI/DEX) 0.5 or 1 mg/d between 2014 and 2017 in Juntendo University Nerima Hospital. Demographic and biochemical data including prostate-specific antigen (PSA) level were retrieved from the electronic medical records. Results: Fifty-three eligible patients (27 in ABI/PSL group and 26 in ABI/DEX group) were extracted from the records. Both groups showed no significant changes in serum potassium level before and after starting treatment. In the ABI/PSL group, 12 patients (46%) showed elevations of PSA and 7 patients (27%) discontinued treatment within 3 months. In contrast, in the ABI/DEX group, only 6 patients (25%) showed elevations of PSA and 3 patients (13%, all were given dexamethasone 1 mg/d) discontinued treatment. Conclusions: Dexamethasone and prednisolone may be equally effective in preventing abiraterone-induced hypokalemia.
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Yilmaz, Mert, Serdar Ener, Halis Akalin, Kadir Sagdic, O. Akin Serdar, and Mete Cengiz. "Effect of low-dose methyl prednisolone on serum cytokine levels following extracorporeal circulation." Perfusion 14, no. 3 (May 1999): 201–6. http://dx.doi.org/10.1177/026765919901400308.
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The systemic inflammatory response to cardiopulmonary bypass (CPB) is associated with increased production of cytokines. This systemic inflammatory response characterized by the activation of interleukin-6 (IL-6) and interleukin-8 (IL-8) during and after CPB is well documented. A prospective, randomized, double-blind study was performed so as to understand the effects of low-dose methyl prednisolone sodium succinate (MPSS) on the circulating levels of serum cytokines and clinical outcome. Twenty patients were randomly divided into two groups on the basis of the administration of low-dose (1 mg/kg) MPSS ( n = 10) and placebo ( n = 10) into the pump prime solution. All patients were scheduled to undergo a primary elective coronary artery bypass grafting operation. Patients receiving concurrent corticosteroids, salicylates, dipyridamol or anticoagulants were excluded from the study. Other exclusion criteria were concurrent chronic obstructive pulmonary disease, chronic renal failure, insulin-dependent diabetes, congestive cardiac failure, peptic ulcer history, prior cardiac operations, recent (in a one-month period) myocardial infarction and steroid dependency. Mild systemic hypothermia (30-32°C, rectal) was assured during the CPB. Four blood samples were drawn from the radial artery catheter immediately before starting CPB (T1), following protamine administration (T2) and at 24 (T3) and 48 h (T4) after completion of CPB. In each sample, creatine kinase-myocardial band (CK-MB), white blood cell (WBC), IL-6 and IL-8 levels were measured. IL-6 and IL-8 concentrations were measured by enzyme immunoassay and enzyme-linked immunoabsorbant assay methods. Serum IL-6 T2 and serum IL-6 T3 levels were significantly higher than IL-6 T1 levels in both groups ( p < 0.001) and ( p < 0.01), and there was no significant elevation in serum IL-8 levels in either group. Serum IL-6 levels were significantly higher in the placebo group than in the MPSS group at T3 ( p < 0.009). There was no significant difference in CK-MB T1 levels between the groups. Although there was no significant difference between CK-MB T1 and T2 levels in the MPSS group, the CK-MB T2 and CK-MB T3 levels were significantly higher than T1 levels in the placebo group ( p < 0.001) and ( p < 0.05). There was significant elevation of WBC levels at T2 and T3 in both groups without notable difference between the groups ( p < 0.05). This study has shown that low-dose MPSS suppresses CPB-induced inflammatory response. Further clinical studies (on larger and higher risk groups) may reveal more information on relations between morbidity and cytokine levels which may have some predictive value on clinical outcome following CPB.