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Pretreatment Values (pretreatment + value)
Selected AbstractsThe effect of therapeutic glucocorticoids on the adrenal response in a randomized controlled trial in patients with rheumatoid arthritis,ARTHRITIS & RHEUMATISM, Issue 5 2006John R. Kirwan Objective To measure the effect of low-dose systemic glucocorticoid treatment on the adrenal response to adrenocorticotropic hormone (ACTH) in patients with rheumatoid arthritis (RA). Methods Patients with RA who took part in a randomized double-blind placebo-controlled trial of budesonide (3 mg/day and 9 mg/day) and prednisolone (7.5 mg/day) underwent a short (60-minute) test with injection of ACTH (tetracosactide hexaacetate) at baseline and the day after completing the 3-month treatment program. Plasma cortisol measurements at baseline and 3 months were compared within and between the treatment groups. Individual patients were classified as normal responders to ACTH or as abnormal responders if changes were >2 SD below the pretreatment value in the entire group of study patients. Results Short tests with ACTH injection were performed on 139 patients before beginning the study medication and on 134 patients after cessation of the medication. There were no changes in the placebo group. Mean plasma cortisol levels following treatment were reduced in all active treatment groups. In addition, mean values were significantly reduced for the 30-minute and 60-minute responses to ACTH. The maximum reduction (35%) occurred in the prednisolone group at 60 minutes. Following treatment, 34% of patients taking budesonide 9 mg and 46% of those taking prednisolone 7.5 mg failed to reach the normal maximum cortisol response to ACTH. Four patients failed to achieve the normal percentage increase in cortisol levels, but only 1 patient failed to meet both criteria. Conclusion Low doses of a glucocorticoid resulted in depression of baseline and ACTH-stimulated cortisol levels after 12 weeks of therapy. Although the responsiveness of the hypothalamic,pituitary,adrenal axis in individual patients generally remained within the normal range, these changes should be investigated further. [source] Zonisamide Prophylaxis in Refractory Pediatric HeadacheHEADACHE, Issue 5 2006Ann Pakalnis MD Introduction.,Currently, no medications are approved for pediatric headache prophylaxis in the United States. Zonisamide is an antiepileptic drug with preliminary studies suggesting some efficacy in the adult headache population. Methods.,A retrospective chart review was conducted on refractory headache patients in our multidisciplinary Headache Clinic who were treated with zonisamide, an antiepileptic drug, for headache prophylaxis. Records were reviewed for pertinent data including patient history, diagnosis, prior treatment regimens, and zonisamide response, along with headache frequency. Results.,Twelve patients were identified (8 girls); mean age was 13.5 years. Eight of the 12 patients had a positive response to zonisamide with greater than 50% reduction in headaches from pretreatment values. Conclusion.,Zonisamide had some efficacy in headache reduction. It was well tolerated with only minor side effects. Further prospective studies with zonisamide are warranted in refractory pediatric headache patients. [source] Effectiveness of antipsychotic polypharmacy for patients with treatment refractory schizophrenia: an open-label trial of olanzapine plus risperidone for those who failed to respond to a sequential treatment with olanzapine, quetiapine and risperidoneHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 6 2008Takefumi Suzuki Abstract Objective To evaluate the effectiveness of antipsychotic polypharmacy in a methodologically sound manner. Methods In this open-label study, 17 patients with treatment-refractory schizophrenia, who failed to respond to a sequential monotherapy with olanzapine, quetiapine and risperidone, were subsequently treated with a combination therapy with olanzapine plus risperidone for at least 8 weeks. Results Seven responded according to the primary endpoint defined as the post-treatment Brief Psychiatric Rating Scale being less than 70% of the pretreatment values, and they were classified as such an average of 10 weeks after the initiation of polypharmacy. Two of them were successful in a later conversion to monotherapy. None dropped out prematurely. Four (out of 13 inpatients) got better enough to be discharged from the hospital, while six patients did not show any response. The Global Assessment of Functioning score improved from 37.1 to 53.0 in responders (mean maximum dose: olanzapine 12.9,mg; risperidone 3.14,mg), while it showed non-significant changes among others (mean maximum dose: olanzapine 14.5,mg; risperidone 5.50,mg). Body weight, prolactin, and total cholesterol increased significantly. Conclusions Antipsychotic polypharmacy might be sometimes helpful for difficult populations but at the cost of adverse effects. More studies of antipsychotic combination therapy versus clozapine, augmentation strategies or tenacious longer- term monotherapy are warranted for refractory schizophrenia. Copyright © 2008 John Wiley & Sons, Ltd. [source] Fecal calprotectin, lactoferrin, and endoscopic disease activity in monitoring anti-TNF-alpha therapy for Crohn's diseaseINFLAMMATORY BOWEL DISEASES, Issue 10 2008Taina Sipponen MD Abstract Background: Fecal calprotectin and lactoferrin are promising noninvasive biomarkers for intestinal inflammation. In Crohn's disease (CD), during anti-TNF-alpha (TNF-,) treatment, the clinical significance of these markers has, however, been insufficiently explored. Methods: Among CD patients receiving anti-TNF-, therapy we assessed the role of fecal calprotectin and lactoferrin as surrogate markers for mucosal healing. Before and 3 months after the beginning of anti-TNF-, induction, 15 patients underwent ileocolonoscopy with scoring of the Crohn's Disease Index of Severity (CDEIS). Fecal samples for calprotectin and for lactoferrin measurements were collected and the Crohn's Disease Activity Index (CDAI) was calculated at the time of the endoscopies and 2 and 8 weeks after the first treatment. Results: The median CDEIS fell from 13.0 to 4.8 (P = 0.002) and CDAI from 158 to 68 (P = 0.005). Accordingly, the median fecal calprotectin concentration fell from 1173 ,g/g to 130 ,g/g (P = 0.001) and fecal lactoferrin from 105.0 ,g/g to 2.7 ,g/g (P = 0.001). Of the 15 patients, 11 (73%) showed an endoscopic response to treatment and 5 of these achieved endoscopic remission (CDEIS < 3). In those 5 patients the fecal calprotectin concentration declined from 1891 ,g/g (range 813,2434) to 27 ,g/g (13,130) and lactoferrin from 92.4 ,g/g (35.5,235.6) to 1.9 ,g/g (0.0,2.1). Conclusions: Compared to pretreatment values, concentrations of fecal calprotectin and lactoferrin after the anti-TNF-, treatment were significantly lower. During anti-TNF-, therapy these fecal neutrophil-derived proteins may thus be useful surrogate markers for mucosal healing. (Inflamm Bowel Dis 2008) [source] Predictive factors for platelet increase after partial splenic embolization in liver cirrhosis patientsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2007Hiromitsu Hayashi Abstract Background and Aim:, Partial splenic embolization (PSE) is often performed for improving thrombocytopenia in cirrhotic patients. We investigated the largely unclear predictive factors for platelet increase at both 1 month and 1 year after PSE. Methods:, Aimed at increasing the platelet count, PSE was performed in 42 cirrhotic patients with thrombocytopenia (platelets < 80 × 104/mL) caused by hypersplenism. The clinical data were analyzed to clarify the predictive factors for platelet increase at 1 month (n = 42) and 1 year (n = 38) after PSE. Results:, The mean splenic infarction ratio was 76.7% ± 11.2%. The platelet count increased to 259% ± 112% and 228% ± 75% of the pretreatment values at 1 month and at 1 year after PSE, respectively. Stepwise multiple linear regression analysis showed that the infarcted splenic volume had a positive independent association with the increase in platelet count at both 1 month (P = 0.00004) and 1 year (P = 0.005) after PSE (increase in platelet count (×104/mL): at 1 month = 0.752 + 0.018 × infarcted splenic volume (mL), R2 = 0.344; at 1 year = 2.19 + 0.01 × infarcted splenic volume (mL), R2 = 0.203). Receiver operating characteristic analysis yielded a cut-off value of 388 mL of infarcted splenic volume for achieving an increase of 5.0,8.0 × 104/mL in platelet count at 1 year. Conclusions:, PSE can reduce the platelet pool and induce an increase in platelet count. This increase is greatly dependent on the infarcted splenic volume. [source] Use of aminoglutethimide in the treatment of pituitary-dependent hyperadrenocorticism in the dogJOURNAL OF SMALL ANIMAL PRACTICE, Issue 3 2002M. D. Pérez Alenza The aim of this study was to evaluate the efficacy and safety of aminoglutethimide in the treatment of dogs with pituitary-dependent hyperadrenocorticism (PDH). Ten dogs were diagnosed with PDH based on clinical and laboratory data, adrenal function tests (adrenocorticotropic hormone [ACTH] stimulation test and urinary cortisol/creatinine ratio [UCCR] combined with a high dose oral dexamethasone suppression test) and ultrasonographic evaluation of the adrenal glands. Aminoglutethimide was administered daily at a dose of 15 mg/kg bodyweight for one month. Median basal cortisol concentration and post-ACTH cortisol concentration one month after treatment were significantly lower than pretreatment values. Complete response was achieved in one dog, and partial response was obtained in three dogs. Severe side effects of anorexia, vomiting and weakness occurred in one dog and medication was withdrawn. Two further dogs developed decompensations of concurrent diseases and medication was stopped in these animals as well. Mild toxicity occurred in four dogs. Moderate to severe elevations in liver enzymes occurred in all dogs. The efficacy of this drug is lower than that observed using mitotane and ketoconazole, and adverse effects limit its use. Aminoglutethimide, using the protocol described, cannot be recommended for long-term management of PDH in the dog. [source] The pharmacokinetics and effects of intravenously administered carprofen and salicylate on gastrointestinal mucosa and selected biochemical measurements in healthy catsJOURNAL OF VETERINARY PHARMACOLOGY & THERAPEUTICS, Issue 2 2000Parton The pharmacokinetics of carprofen, a propionic acid-derived nonsteroidal anti-inflammatory (NSAID), and its effect on gastrointestinal mucosa, complete blood counts (CBC) and biochemical indicators of liver and renal function were investigated in healthy cats using a randomized crossover design. A single dose of 4 mg/kg of carprofen (Zenecarp® Injection), normal saline, or 20 mg/kg of DL-lysine acetyl salicylate (Vetalgine®) was given intravenously (i.v.) to each of five cats with a washout period of 2 weeks between treatments. Endoscopy of the stomach and duodenum 8 h postinjection revealed one acetyl salicylate-(aspirin)-treated cat with minor pinpoint erosions. None of the other cats in the three treatment groups had evidence of bleeding or ulceration. Serum biochemistry measurements of blood urea nitrogen (BUN), alanine transferase (ALT) and alkaline phosphatase (ALP) and complete blood counts (CBC) were not significantly altered from pretreatment values by the single dose of salicylate or carprofen (P < 0.05). Early and extended sample time points suggest that the pharmacokinetics of carprofen in the cat fit a 2-compartment model, with a long elimination half-life (t1/2) of 20.1 ± 16.6 h, an area under the plasma concentration,time curve (AUC) of 637 (± 237) ,g.mL/h and a volume of distribution (Vdss) of 0.14 ± 0.05 L/kg. Intravenously administered aspirin fit a 2-compartment model and had a long elimination half-life (t1/2) of 22.2 ± 3.1 h, an AUC of 3824.2 ± 506.7 ,g.mL/h and a volume of distribution (Vdss) of 0.17 ± 0.01 L/kg. [source] Predicting seizure control: Cortical excitability and antiepileptic medicationANNALS OF NEUROLOGY, Issue 1 2010Radwa A. B. Badawy MBBCh Objective Approximately 30% of patients with newly diagnosed epilepsy do not respond to antiepileptic drugs (AEDs), but this is not predictable. We used transcranial magnetic stimulation to determine the effect of AEDs on cortical excitability in patients with epilepsy and correlated this with a successful response to treatment. Methods Ninety-nine drug-naďve patients with newly diagnosed epilepsy (55 idiopathic generalized epilepsy, 44 focal epilepsy) were evaluated. Motor threshold and cortical excitability on recovery curve analysis were measured before and 4 to 16 weeks after starting medication. After 1 year of treatment, 43 of 55 idiopathic generalized epilepsy and 26 of 44 focal epilepsy patients were seizure free. Results A decrease in cortical excitability occurred in the seizure-free group as indicated by an increase in motor threshold (p < 0.05) and intracortical inhibition on recovery curve analysis, maximum at the 250-millisecond interstimulus interval (p < 0.01) compared with pretreatment values. These changes were not present in the group with ongoing seizures. Interpretation Seizure freedom is marked by a reduction in transcranial magnetic stimulation measures of cortical excitability, evident shortly after beginning therapy. This virtual normalization of cortical excitability occurred regardless of the seizure characteristics or AED used. Failure to show this response to AED treatment may be valuable as an early predictor of pharmacoresistance in individual patients. ANN NEUROL 2010;67:64,73 [source] Serum homocysteine concentrations in children with growth hormone (GH) deficiency before and after 12 months GH replacementCLINICAL ENDOCRINOLOGY, Issue 5 2004Valentina Esposito Summary objective, This open, prospective study was designed to evaluate the effect of growth hormone deficiency (GHD) and GH replacement therapy on serum homocysteine (Hcy) concentration in children with GHD. subjects, Seventeen prepubertal children with GHD (11 boys and six girls) aged 8·6 ± 1·9 years were studied before and after 12 months of GH replacement therapy at a dose of GH of 30 µg/kg/day. Seventeen healthy children acted as controls and were matched for age, sex and body mass index (BMI). methods, At study entry, height, weight, blood pressure, serum Hcy, serum IGF-I, total-low density lipoprotein (LDL)- and high density lipoprotein (HDL) cholesterol, triglycerides, free T4, free T3, vitamin B12, folate, glucose and creatinine were measured in all subjects. The atherogenic index (AI) was also calculated as the ratio of total cholesterol/HDL cholesterol (T/HDL). In GHD children these parameters were also revaluated after 12 months of GH therapy. results, At study entry height and serum IGF-I were significantly lower, as expected, in GHD patients than in controls (P < 0·0001 and P < 0·007, respectively). Serum Hcy levels were significantly higher in GHD patients than in healthy children (8·4 ± 2·9 vs. 6·0 ± 2·9 µmol/l; P < 0·03), although the absolute values were within the normal values for age and sex. There were no significant differences at baseline with respect to blood pressure, serum vitamin B12, folate, fT3, fT4, lipid profile, creatinine and glucose levels. After 12 months of GH replacement therapy height and serum IGF-I increased significantly compared to pretreatment values (P < 0·0001); serum Hcy levels decreased significantly (6·0 ± 3·3 µmol/l; P < 0·002) compared to baseline values, becoming similar to control values. Total cholesterol (3·5 ± 0·6 mmol/l) and the AI (2·5 ± 0·8) decreased significantly with respect to both pretreatment (4·2 ± 1·0 mmol/l; P < 0·0002 and 3·4 ± 0·8; < 0·002, respectively) and control values (4·2 ± 0·4 mmol/l; P < 0·0005 and 3·3 ± 1·1; P = 0·02, respectively). conclusions GHD in children is associated with higher serum levels of Hcy compared to controls, without significantly affecting the lipid profile. GH replacement for 12 months significantly decreased the Hcy levels and improved the lipid profile with a decrease of total cholesterol and the total/HDL cholesterol ratio, compared to pretreatment values. Given the small number of patients, further larger studies are needed to clarify whether these results may have significant effects in the prevention of cardiovascular disease in adulthood. [source] | ||||||||||