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V Patients (v + patient)
Selected AbstractsLaser Hair Removal with Alexandrite versus Diode Laser Using Four Treatment Sessions: 1-Year ResultsDERMATOLOGIC SURGERY, Issue 11 2001Sorin Eremia MD Background. Laser hair removal is the treatment of choice for hypertrichosis. The two most commonly used hair removal lasers are compared. Objective. To present the results of a comparative study examining the role of wavelength, fluence, spot size, pulse width, and cooling systems on long-term results after a series of four laser hair removal treatments using the 755 nm alexandrite and 800,810 nm diode lasers. Methods. The axillae of 15 untanned, type I,V patients were treated side by side four times at 4- to 6-week intervals with a 755 nm, 3-msec pulse width, cryogen spray-equipped alexandrite laser and an 800 nm, variable pulse width, cooled sapphire window-equipped diode laser. Each patient was pretested and treated with the maximum fluence tolerated at the largest spot size available for each laser (12 mm round/113 mm2 for the alexandrite and 9 mm for the diode). Results. Evaluations were done at 3, 6, 9, and 12 months after the last treatment. Twelve-month results with the alexandrite and diode lasers achieved 85% versus 84% hair reduction. The fact that tan avoidance was strictly followed permitted the use of relatively high fluences (25,30+ J/cm2) even in type IV patients. For most patients, four treatment sessions using high fluences (30,40 J/cm2) with relatively large spot sizes (12 mm round for the 755 nm alexandrite and 9 mm for the 800 nm diode) resulted in 12-month hair reductions in the 90% range. Conclusion. Both the alexandrite and diode lasers in this 12-month study produced excellent long-term hair reductions. [source] Type V Osteogenesis Imperfecta: A New Form of Brittle Bone Disease,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 9 2000Francis H. Glorieux Abstract Osteogenesis imperfecta (OI) is commonly subdivided into four clinical types. Among these, OI type IV clearly represents a heterogeneous group of disorders. Here we describe 7 OI patients (3 girls), who would typically be classified as having OI type IV but who can be distinguished from other type IV patients. We propose to call this disease entity OI type V. These children had a history of moderate to severe increased fragility of long bones and vertebral bodies. Four patients had experienced at least one episode of hyperplastic callus formation. The family history was positive for OI in 3 patients, with an autosomal dominant pattern of inheritance. All type V patients had limitations in the range of pronation/supination in one or both forearms, associated with a radiologically apparent calcification of the interosseous membrane. Three patients had anterior dislocation of the radial head. A radiodense metaphyseal band immediately adjacent to the growth plate was a constant feature in growing patients. Lumbar spine bone mineral density was low and similar to age-matched patients with OI type IV. None of the type V patients presented blue sclerae or dentinogenesis imperfecta, but ligamentous laxity was similar to that in patients with OI type IV. Levels of biochemical markers of bone metabolism generally were within the reference range, but serum alkaline phosphatase and urinary collagen type I N-telopeptide excretion increased markedly during periods of active hyperplastic callus formation. Qualitative histology of iliac biopsy specimens showed that lamellae were arranged in an irregular fashion or had a meshlike appearance. Quantitative histomorphometry revealed decreased amounts of cortical and cancellous bone, like in OI type IV. However, in contrast to OI type IV, parameters that reflect remodeling activation on cancellous bone were mostly normal in OI type V, while parameters reflecting bone formation processes in individual remodeling sites were clearly decreased. Mutation screening of the coding regions and exon/intron boundaries of both collagen type I genes did not reveal any mutations affecting glycine codons or splice sites. In conclusion, OI type V is a new form of autosomal dominant OI, which does not appear to be associated with collagen type I mutations. The genetic defect underlying this disease remains to be elucidated. [source] Partial percutaneous discectomy for treatment of thoracolumbar disc protrusion: retrospective study of 331 dogsJOURNAL OF SMALL ANIMAL PRACTICE, Issue 10 2005S. Kinzel Objectives: To determine retrospectively the prognosis and outcome for dogs diagnosed with thoracolumbar intervertebral disc disease treated with partial percutaneous discectomy (PPD). Methods: Three hundred and thirty-one dogs presenting with symptoms of thoracolumbar intervertebral disc disease from 1998 to 2003 were treated with PPD. Diagnosis and location of intervertebral disc disease was confirmed by clinical examination, radiography, myelography and magnetic resonance imaging. PPD was performed via fluoroscopy-guided removal of a 5 mm bore cylinder out of the central intervertebral space. Results: Clinical success after surgery was achieved in 159 (88·8 per cent) grade II to IV patients and 58 (38·2 per cent) grade V patients. The mean (sd) time from percutaneous discectomy to first improvement was 8·3 (13·2) days. Clinical Significance: The PPD approach to the thoracolumbar spine involves minor trauma (yielding rapid recovery) and less pain, and produces results comparable with open fenestration. Consequently, this simple minimal invasive technique can be recommended as an alternative to the technique of fenestration and can be easily performed in addition to open surgical decompression techniques or prophylactically. However, it is not a replacement for surgical treatment in dogs with thoracolumbar disc disease that require removal of disc fragments causing spinal cord or nerve root compression. [source] Development of a drug,disease simulation model for rituximab in follicular non-Hodgkin's lymphomaBRITISH JOURNAL OF CLINICAL PHARMACOLOGY, Issue 4 2009David Ternant WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT , Serum concentrations of rituximab influence its clinical efficacy in follicular lymphoma (FL), but its concentration,effect relationship has not been described by pharmacokinetic,pharmacodynamic (PK,PD) modelling. , The genetic polymorphism of FCGR3A influences rituximab efficacy and its in vitro concentration,effect relationship. , Increasing rituximab dose and/or number of infusions may lead to a better clinical response in FL. WHAT THIS PAPER ADDS , This study is the first to describe the concentration,effect relationship of rituximab in populations of FL patients. , This PK,PD model relates progression-free survival with rituximab concentrations and takes into account the influence of FCGR3A polymorphism. , Clinical trials testing new dosing regimens of rituximab can be designed using this PK,PD model. AIM Rituximab has dramatically improved the survival of patients with non-Hodgkin's lymphomas (NHL), but the dosing regimen currently used should be optimized. However, the concentration,effect relationship of rituximab has never been described by pharmacokinetic,pharmacodynamic (PK,PD) modelling, precluding the simulation of new dosing regimens. The aim of this study was to develop a PK,PD model of rituximab in relapsed/resistant follicular NHL (FL). METHODS A model describing the relationship between rituximab concentrations and progression-free survival (PFS) was developed using data extracted from the pivotal study, which evaluated 151 relapsed/resistant FL patients. The influence of FCGR3A genetic polymorphism on the efficacy of rituximab was quantified using data from 87 relapsed/resistant FL patients. The predictive performance of the model was analysed using two independent datasets: a study that evaluated rituximab combined with chemotherapy [rituximab, cyclophosphamide, vincristine, adriamycin and prednisone (R-CHOP)] in 334 relapsed/resistant FL patients and a study that evaluated rituximab monotherapy in 47 asymptomatic FL patients with known FCGR3A genotype. RESULTS For R-CHOP, observed and model-predicted PFS (90% confidence interval) at 24 months were 0.50 and 0.48 (0.40, 0.56), respectively, for the observation arm, and 0.62 and 0.59 (0.50, 0.65), respectively, for the rituximab maintenance arm. For rituximab monotherapy, observed and predicted PFS at 24 months were 0.67 and 0.63, respectively, for FCGR3A -V/V patients, and 0.41 and 0.36 (0.25, 0.49), respectively, for FCGR3A -F carriers. CONCLUSIONS Our model provides a satisfactory prediction of PFS at 24 months. It can be used to simulate new dosing regimens of rituximab in populations of FL patients and should improve the design of future clinical trials. [source] Mutation of keratin 8 in patients with liver diseaseJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 9 2006Maximilian Schöniger-Hekele Abstract Background:, Epithelial tissues of the gastrointestinal tract and the liver express predominantly cytokeratin 8 and cytokeratin 18. In vitro experiments and animal studies have demonstrated a protective influence of keratin 8 and keratin 18 against toxic damage of hepatocytes. A specific mutation of keratin 8 (G61C) was found to be a genetic risk factor for the development of cryptogenic liver cirrhosis. The purpose of the present paper was therefore to determine the prevalence of cytokeratin 8 (G61C) and cytokeratin 18 mutations (Y53H) in patients with liver disease. Methods:, Overall 152 patients (male, n = 93, 61%; female, n = 59, 39%) were included in the present study. The 152 patients consisted of 107 patients with liver disease (70.4%; male, n = 71, 66.4%; female, n = 36, 33.6%) and 45 control patients (29.6%; male, n = 22, 48,9%; female, n = 23, 51,1%) without liver disease. Of the patients with liver disease 46 had alcoholic liver disease; 25, chronic hepatitis C; 15, cryptogenic liver disease; and 21, other liver diseases of various etiologies. Cytokeratin 8 and 18 genotypes were specified by polymerase chain reaction (PCR) amplification and direct sequence analysis was used to detect the previously described mutations in cytokeratin 8 (G61C) and in cytokeratin 18 (Y53H). Results:, Four out of 152 patients (male n = 2, female n = 2) with a mutation (G61C) in cytokeratin 8 were found. The etiology was alcoholic liver disease (n = 1), cryptogenic liver disease (n = 1) and idiopathic liver disease with minimal changes in liver biopsy (n = 1). Also, one out 45 disease control patients with an adenoma of the colon but without liver disease was found to carry the mutation G61C of cytokeratin 8. Therefore, the mutation G61C in cytokeratin 8 was found in 2.8% of patients with liver disease and in 2.2% of control patients without liver disease. Two of 15 patients (13.3%) with cryptogenic liver disease had the mutation G61C in cytokeratin 8 (P = 0.069 vs patients with non-cryptogenic liver disease). In the 152 patients studied, no mutation in cytokeratin 18 was found. Discussion:, The mutation G61C in the cytokeratin 8 gene was found in one patient with alcoholic liver disease and in two patients with liver disease of unknown etiology. Also, one patient without liver disease had the cytokeratin 8 G61C mutation. In summary, the cytokeratin 8 mutation G61C, which has been found to be associated with cryptogenic liver cirrhosis, was also found in the present patient population. However, the clinical relevance is yet to be determined in further investigations. [source] | ||||||||||