ISSN:1076-1608    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:1076-1608    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Treatment of gout and hyperuricemia can be difficult in patients with chronic renal failure. At present, there is no study available comparing the efficacy of the most widely used agent, allopurinol, and the uricosuric benzbromarone for the control of hyperuricemia in patients with renal insufficiency. We describe an open, randomized, actively controlled, comparative trial in patients with clearance of creatinine from 20 to 80 mL/ min/1.73m2. Patients were randomized to take benzbromarone (100–200 mg/day) or allopurinol (100–300 mg/day). Outcome variables were the following: reduction of serum urate (Sur), Sur & tl; 6 mg/dL (357 μmol/L), reduction of gouty bouts and reduction of tophi. During 9–24 months of follow-up 36 patients were studied.The reduction of Sur was higher with benzbromarone, and only 1 of 17 patients taking benzbromarone did not achieve Sur < 6 mg/dL versus 7 of 19 taking allopurinol. Patients who did not reach optimal Sur levels with allopurinol were more frequently taking diuretics and showed lower fractional excretion of urate and higher initial Sur levels than patients with proper control of Sur. Seven patients with suboptimal control of serum urate were changed to benzbromarone 100 mg/day, which showed efficacy similar in those who were initially randomized to benzbromarone. A reduction of gouty bouts and size of tophi was observed after proper control of Sur. Allopurinol is effective in controlling hyperuricemia, but patients with higher initial Sur levels or taking concomitant diuretic therapy are less prone to reach therapeutic goals.Benzbromarone is useful for the control of hyperuricemia in patients with renal insufficiency even with concomitant diuretic administration; patients benefited include those who previously had no improvement by taking allopurinol.

ISSN:1076-1608    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Patients with chronic fatigue syndrome (CFS) frequently associate the disease onset with a period of high physical and/or emotional stress. Alterations in hypothalamic-pituitary adrenal axis (HPA) function have been demonstrated. Although Cortisol production in patients with CFS has proven to be low, Dehydroepiandrosterone (DHEA) production has not been measured. DHEA output may be altered in this population. The purpose of this uncontrolled, prospective, 6 month study of 23 white women, ages 35–55 was to identify CFS patients with suboptimal serum levels of DHEA-sulphate (DHEA-S), defined as DHEA-S <2.0μg/mL, and to treat those patients with oral DHEA. DHEA-S levels were re-measured after 4–6 weeks of oral DHEA therapy (25 mg). If DHEA-S remained <2.0μg/ mL, or if no clinical response was achieved after 4–6 weeks of therapy, then an increased dose of DHEA was given. Physical and psychological impairment and disability status were measured by the MHAQII before DHEA intervention and at 3-month intervals. Of initially screened patients with CFS, 76% (116 of 153) were ages 35–55, and 89% (103 of 116) had suboptimal (<2.0μg/mL) production of DHEA-S.Supplementation with DHEA to CFS patients lead to a significant reduction in the symptoms of CFS: pain (improved by 18%,p= 0.035), fatigue (decreased by 21%,p= 0.009)), activities of daily living (improved by 8.5%,p= 0.058), helplessness (decreased by 11%,p= 0.015), anxiety (decreased by 35%,p< 0.01), thinking (improved by 26%,p< 0.01), memory (improved by 17%,p< 0.05), and sexual problems (improved by 22%,p= 0.06) over the period of the trial. Further study is necessary to determine the safety and efficacy of supplementation of DHEA to this population in a controlled setting.

ISSN:1076-1608    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

At present, there is no consensus regarding the utility of liver enzyme monitoring in rheumatology patients undergoing treatment with azathioprine (AZA). To further investigate this issue, we retrospectively reviewed for current or past use of AZA all patient records in our Disease Modifying Antirheumatic Drug (DMARD) clinic from May 1986 through September 1996. Information available from individual DMARD charts included AZA data (dates initiated, dose, indication for changing dose or stopping AZA), co-administered DMARDs, and aspartate aminotransferase (AST) serum values. In patients followed in the clinic through February 1994, serum alkaline phosphatase (AP) values additionally were available. Published reports of AZA hepatotoxicity in rheumatoid arthritis (RA) patients were found by a MEDLINE search, supplemented by a manual search of reference lists.We screened 429 patient records, and all patients who had received AZA at any time during the study period (n = 56) were identified for further review. The mean daily AZA dose was 96 mg (median = 100 mg/ day, range = 25–200 mg/day). All of the 56 patients had undergone routine periodic monitoring of serum AST while taking AZA (mean interval = 26 days); 30 of these patients additionally underwent monitoring of serum AP (mean interval = 24 days). Twenty-three (41%) of the patients had at least one episode of an abnormally elevated serum AST and/or AP while taking AZA. Only 1 of these 2 laboratory values was abnormal in 12 patients. The average time from AZA initiation to first appearance of an abnormal AST and/or AP value was 27 days (range = 7–62 days). During observation alone, all abnormal laboratory test results became normalized in 20 of 23 patients (87%) during the study period. There were no interventions in response to an abnormal laboratory value, and no patient experienced an adverse clinical outcome attributable to AZA hepatotoxicity during the 10-year study period.AZA use for rheumatic conditions may be associated with elevations in both the serum AST and/or AP values. Most of these elevations were transient, and none were clinically significant in our patient population. This study supports current American College of Rheumatology guidelines, which do not recommend routine periodic monitoring with liver enzyme tests in RA patients taking AZA. Furthermore, this study suggests that the utility of the baseline liver enzyme test in these patients is not well established.

ISSN:1076-1608    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

To assess the efficacy of nonsurgical treatment of cervical radiculopathy, 50 patients with objective signs and symptoms of cervical discogenic radiculopathy (CDR) without myelopathy, treated conservatively on an outpatient basis with a mean follow-up of 9.4 months were retrospectively reviewed. Then an additional 33 patients were entered sequentially onto a prospective study to assess conservative treatment; they were followed for 100 days or longer with a mean follow-up of 24.7 months. All 83 patients (50 + 33) had objective neurologic deficits (sensory, motor, or both).Of the initial 50 patients, 27 achieved full remission (no neurologic deficits and pain free), 17 were markedly improved (minimal residual sensory or motor deficit and mild to minimal pain), and 6 were unchanged at the time of their last examination. Of the 33 patients followed prospectively, 13 were in full remission and 16 were markedly improved requiring no treatment at the 100-day follow-up evaluation (< 0.05 by one tailed t-test). Of the 33 patients with complicating depression or fibromyalgia, 4 demonstrated minimal or no pain improvement, although 3 of the 4 had full remission of sensory/motor findings. Motor vehicle accidents precipitated symptoms of CDR in 14 patients in the retrospective and 5 in the prospective study. CDR of 15 patients was in full remission by 90 days, and 4 had ongoing chronic and/or mild sensory or motor deficits at 300 days. At the final follow-up, all 33 prospectively studied patients had maintained at least the level of improvement achieved at 100 days(p< 0.05 by one tailed f-test). No one in the total group of 83 patients required surgical intervention or hospitalization.Our results suggest that outpatient nonsurgical conservative management with careful patient education and monitoring of a coordinated conservative regimen can be successful for the majority of patients with CDR.

ISSN:1076-1608    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

The mechanism for calcinosis in connective tissue disease remains unclear. Various therapies such as warfarin, colchicine, steroids, and bisphosphon-ates have been tried. However, despite some benefit in early cases, improvement generally is not seen in advanced cases of calcinosis. Several recent studies strongly suggest a favorable response of calcinosis to diltiazem, a calcium channel antagonist. This report concerns two Filipino women, one with dermatomyositis, the other with undifferentiated connective tissue disease, who showed significant reduction of widespread calcinosis after treatment with diltiazem. (J Clin Rheumatol 1999;5:74–78)

ISSN:1076-1608    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Churg-Strauss syndrome (CSS) is a rare vasculitis characterized by the clinical triad of asthma, peripheral eosinophilia, and systemic vasculitis. Pulmonary symptoms occur commonly, but gastrointestinal, renal, cardiac, and musculoskeletal manifestations may also occur. Disease activity and expression can be variable, and progressive organ failure may occur in the absence of other clinical or biochemical evidence of disease activity. We report the case of a 73-year-old man who presented with signs and symptoms of an acute myocardial infarction, eosinophilia, a pulmonary infiltrate, and recent onset asthma. The cardiac catheterization was normal, but an endomyocardial biopsy specimen revealed eosinophilic myositis, granuloma formation, and small vessel vasculitis. A repeat endomyocardial biopsy 1 month after the initiation of high dose prednisone therapy showed no evidence of inflammation and no significant fibrosis. We suggest that a endomyocardial biopsy is a safe and useful tool in the diagnosis and monitoring of therapy in patients with CSS cardiac disease.

ISSN:1076-1608    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

A 48-year-old Caucasian woman presented a tender effusion of small volume, with a mild increase in skin temperature in her right knee and wide spread chondrocalcinosis found radiologically. She had normal renal function, had undergone a gastrectomy, and was receiving therapeutic doses of aluminum hydroxide antacids. Synovial fluid analysis showed small, irregular, nonbirefringent particles that stained intensely positive with the alizarin red stain. Scanning electron microscopy, energy disper sive X-ray analysis, and microprobe analysis showed aluminum and variable concentrations of chlorine and/or oxygen in isolated small spherical particles (average diameter about 15μ). Neither phosphorus nor calcium was ever detected in the aluminum containing particles. These findings strongly suggest the presence of a mixture of aluminum hydroxide and some form of aluminum hydroxide chloride; neither was previously reported in synovial fluid of patients with normal renal function. Aluminum-containing particles should be considered an explanation for unexplained particles in joint fluid and may be a factor in some arthritis.

ISSN:1076-1608    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

Patellar disorders are common and painful. Although in many cases no precise cause for the pain is identified, poor patellar tracking, leading to imperfect distribution of forces in the patello-femoral joint, is a frequent finding. Tightness of the lateral retinaculum or anatomic predisposition for lateral tracking (e.g., femoral anteversion or an elevated Q angle) also places patients at increased risk for patellar pain. Most patients with patellar disorders will improve with simple programs of activity modification, therapy, and other nonsurgical modalities. Nonoperative therapy can include short arc quadriceps strengthening and stretching regimens, the application of ice, and the use of knee sleeves. Surgical treatment spans a wide range of choices, each tailored to specific diagnoses. These operations are reserved only for patients for whom conservative measures fail.

ISSN:1076-1608    

出版商:OVID    

年代:1999

数据来源: OVID