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121.
Dr. Daisy Saw MD Ernest Pitman MD Maung Maung MD Panas Savasatit MD Daniel Wasserman MD C. K. Yeung MD 《Digestive diseases and sciences》1996,41(2):322-325
Summary A wide variety of diseases and injuries can cause granulomatous hepatitis, and drug-induced granulomatous hepatitis is a well-described entity. Sulfonylurea derivatives, which are commonly used oral hypoglycemic agents in the treatment of non-insulin-dependent diabetes mellitus, have been implicated in liver disease. However, glyburide, a second-generation sulfonylurea and a potent hypoglycemic drug, is considered to have less hepatic side effects than chlorpropamide. It has been reportedly associated with cholestatic jaundice and hepatitis and with hypersensitivity angiitis. A case of necrotizing granuloma has been reported. We present a second case of granulomatous hepatitis occurring in a patient who had been taking glyburide for approximately three years, and we review the literature for glyburide-associated hepatitis. 相似文献
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124.
Antonia Fuster Jaume Sauleda Ernest Sala Bernard�� Barcel�� Jaume Pons Miguel Carrera Aina Noguera Bernat Togores Alvar GN Agust�� 《INT J CHRONIC OBSTR》2008,3(1):149-153
Objective
Patients with chronic obstructive pulmonary disease (COPD) present systemic inflammation. Strenuous resistive breathing induces systemic inflammation in healthy subjects. We hypothesized that the increased respiratory load that characterizes COPD can contribute to systemic inflammation in these patients.Patients and methods
To test this hypothesis, we compared leukocyte numbers and levels of circulating cytokines (tumor necrosis factor alpha [TNFα], interleukin-1β [IL-1β], IL-6, IL-8, and IL-10), before and 1 hour after maximal incremental inspiratory loading in 13 patients with stable COPD (forced expiratory volume in one second [FEV1] 29 ± 2.5% ref) and in 8 healthy sedentary subjects (FEV1 98 ± 5% ref).Results
We found that: (1) at baseline, patients with COPD showed higher leukocyte counts and IL-8 levels than controls (p < 0.01); and, (2) one hour after maximal inspiratory loading these values were unchanged, except for IL-10, which increased in controls (p < 0.05) but not in patients with COPD.Conclusions
This study confirms the presence of systemic inflammation in COPD, shows that maximal inspiratory loading does not increase the levels of pro-inflammatory cytokines (IL-1β, IL-8) in COPD patients or controls, but suggests that the former may be unable to mount an appropriate systemic anti-inflammatory response to exercise. 相似文献125.
Ernest V Garcia 《Journal of nuclear cardiology》2007,14(1):16-24
Single photon emission computed tomography (SPECT) myocardial perfusion imaging has attained widespread clinical acceptance as a standard of care for cardiac patients. Yet, physical phenomena degrade the accuracy of how our cardiac images are visually interpreted or quantitatively analyzed. This degradation results in cardiac images in which brightness or counts are not necessarily linear with tracer uptake or myocardial perfusion. Attenuation correction (AC) is a methodology that has evolved over the last 30 years to compensate for this degradation. Numerous AC clinical trials over the last 10 years have shown increased diagnostic accuracy over non-AC SPECT for detecting and localizing coronary artery disease, particularly for significantly increasing specificity and normalcy rate. This overwhelming evidence has prompted our professional societies to issue a joint position statement in 2004 recommending the use of AC to maximize SPECT diagnostic accuracy and clinical usefulness. Phantom and animal studies have convincingly shown how SPECT AC recovers the true regional myocardial activity concentration, while non-AC SPECT does not. Thus, AC is also an essential tool for extracting quantitative parameters from all types of cardiac radionuclide distributions, and plays an important role in establishing cardiac SPECT for flow, metabolic, innervation, and molecular imaging, our manifest destiny. 相似文献
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Richter syndrome describes the development of high-grade non-Hodgkin lymphoma (NHL) or Hodgkin lymphoma in patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL). Richter transformation occurs in 3·3 to 10·6% of patients with CLL. The large cell lymphoma clone occurs by transformation of the original CLL clone in the majority of patients, and as a separate and independent neoplasm in fewer cases. Richter transformation may be triggered by viral infections, such as Epstein-Barr virus infection, which are common in immunosuppressed patients. Trisomy 12 and chromosome 11 abnormalities, as well as multiple genetic defects, have been described in patients with Richter syndrome. These abnormalities may cause CLL cells to proliferate and, by facilitating the acquisition of new genetic abnormalities, to transform into Richter syndrome cells. Presenting features typically include a rapid clinical deterioration with fever in the absence of infection, progressive lymph node enlargement, and an elevation in serum lactate dehydrogenase. Extranodal Richter syndrome has also been reported to occur in the central nervous system, eye, gastrointestinal system, nose, skin, face, bone and bronchus. The therapeutic options include cytoreductive therapy consisting of chemotherapy and immunotherapy, followed by allogeneic stem cell transplantation as postremission therapy. 相似文献
128.
Carmona L González-Alvaro I Balsa A Angel Belmonte M Tena X Sanmartí R 《Annals of the rheumatic diseases》2003,62(9):897-900
Methods: Cross sectional analysis of a cohort of patients with RA randomly selected from the clinical databases of 34 centres. Standard definitions and measurements were used, and radiographs read centrally. Estimates and confidence intervals were adjusted to sampling. Results: Data were available for 788 patients. Extra-articular RA was present in 285 (36.2%) patients. Cumulative prevalence and 95% confidence intervals of extra-articular manifestations were estimated: nodules 24.5% (21.5 to 27.5), Sjögren''s syndrome 17.0% (14.4 to 19.6), atlantoaxial subluxation 12.1% (9.8 to 14.4), carpal tunnel syndrome 10.7% (7.8 to 13.6), interstitial lung disease 3.7% (2.4 to 5.0), serositis 2.5% (1.4 to 3.5), eye disease 2.5% (1.1 to 3.9), vasculitis 1.3% (0.5 to 2.1), amyloidosis 0.6% (0.1 to 1.2), and Felty''s syndrome 0.3% (<0.6). Mean (SD) activity/progression indexes were: DAS28-3 3.4 (1.2), HAQ 1.6 (0.4), Larsen score 54.7 (26.4). Less than 5% of the patients were in remission. 205 (72%) patients were receiving disease modifying antirheumatic drugs (DMARDs). Conclusion: Spanish patients with RA ever seen by a rheumatologist have, on average, a moderate degree of activity, despite widespread use of DMARDs. Measures of the degree of progression do not show a benign disease. The proportion of extra-articular manifestations in Spanish patients with RA is similar to that found in other Mediterranean populations, and lower than that reported in Anglo Saxon countries. 相似文献
129.
Dora Koller Carmen Belmonte Miriam Saiz‐Rodríguez Pablo Zubiaur Manuel Romn Dolores Ochoa Francisco Abad‐Santos 《Basic & clinical pharmacology & toxicology》2020,126(3):236-246
Aripiprazole treatment in schizophrenic patients was previously associated with lower or normalized prolactin levels. Genetic variants in cytochrome P450 (CYP) (CYP2D6), dopamine receptor (DRD2, DRD3) and serotonin receptor (HTR2A, HTR2C) genes were previously associated with antipsychotic‐induced hyperprolactinaemia. Our aim was to evaluate whether aripiprazole affects prolactin secretion and its relationship with pharmacogenetics. Thirty‐one healthy volunteers receiving a 10‐mg single oral dose of aripiprazole were genotyped for 12 polymorphisms in CYP2D6, DRD2, DRD3, HTR2A and HTR2C genes by qPCR. Aripiprazole and dehydro‐aripiprazole plasma concentrations were measured by HPLC‐MS/MS. Prolactin concentrations of the 31 volunteers taking aripiprazole and 12 volunteers receiving ibuprofen were determined by ELISA. Prolactin concentrations after ibuprofen intake were considered as control, since it is known to cause no effect. Prolactin concentrations were slightly higher in the aripiprazole group compared to the ibuprofen group. All prolactin pharmacokinetic parameters were higher in females than in males. CYP2D6 poor and intermediate metabolizers had notably higher prolactin Cmax and AUC0‐12 than normal and ultrarapid metabolizers. The DRD3 rs6280 polymorphism affected prolactin levels: volunteers carrying Ser/Ser genotype had significantly lower prolactin levels than volunteers carrying the Gly allele. Furthermore, HTR2C rs3813929 C/C homozygotes had significantly lower prolactin levels than T allele carriers. Nevertheless, aripiprazole did increase prolactin levels compared to ibuprofen. 相似文献
130.
Gary Mierau E.J. Wills Josephine Wyatt–Ashmead Edward Hoffenberg Ernest Cutz 《Ultrastructural pathology》2013,37(6):517-521
Microvillous inclusion disease is a rare lethal disorder characterized by intractable, severe, watery diarrhea beginning in early infancy. The underlying defect is thought to be an autosomal recessive genetic abnormality resulting in defective brush-border assembly and differentiation. Normally, this diagnosis is easily established through the electron microscopic demonstration of characteristic microvilli-lined inclusions lying within the apical cytoplasm of surface enterocytes. In a small number of patients appearing to have microvillous inclusion disease it has not proven possible to demonstrate the typical inclusions. The existence of another entity, termed intestinal microvillous dystrophy, has been proposed to account for such occurrences. This assertion was founded in large part upon the observation that the few subjects studied all displayed a slightly atypical clinical presentation. The case now being presented exhibited the morphologic features ascribed to intestinal microvillous dystrophy but had a clinical presentation that was entirely typical of microvillous inclusion disease. It serves thus to conceptually unite intestinal microvillous dystrophy with microvillous inclusion disease. 相似文献