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Biomedical subjects

L S Simon

Publications and source records attributed to L S Simon.

At least 55 records · Page 3Linked to original sources
PubMed1995

Quantification of inflammation in the wrist with gadolinium-enhanced MR imaging and PET with 2-[F-18]-fluoro-2-deoxy-D-glucose.

PURPOSE: To quantify the activity of joint inflammation with magnetic resonance (MR) imaging and positron emission tomography (PET). MATERIALS AND METHODS: Gadolinium-enhanced MR imaging and 2-[fluorine-18]fluoro-2-deoxy-D-glucose (FDG) PET of the wrist were performed prospectively in 12 patients receiving antiinflammatory therapy. Patients were studied three times: off medications for 2 weeks, after 2 weeks of treatment with prednisone or nonsteroid antiinflammatory drugs, and after 12 weeks of treatment with methotrexate. Volume of enhancing pannus (VEP) was determined from fat-suppressed MR images (12 patients). FDG uptake was calculated from PET images (11 patients). RESULTS: VEP and FDG uptake were closely correlated (r > .86, P < .0001), as were changes in VEP and standardized uptake volume (r > .91, P < .0002). VEP and FDG uptake were strongly associated with clinical findings in wrists (P < .002) but not with treatment outcomes (P > .05). CONCLUSION: Contrast material-enhanced MR imaging and PET allow quantification of volumetric and metabolic changes in joint inflammation and comparison of efficacies of antiinflammatory drugs.

Acetaminophen↗
PubMed1995

NSAID-induced gastrointestinal toxicity.

Recommendations that can be made to decrease the incidence of untoward NSAID-induced GI events include identification of the high-risk patient (Table 3). If it is important to treat these high-risk patients with NSAIDs, either the lowest possible dose of the NSAID, an alternative non-NSAID analgesic, or the nonacetylated salicylates should be used. If that is impossible and a nonsalicylate NSAID is required in the high-risk patient, one should treat concomitantly with tolerable doses of misoprostol and prescribe that the NSAID be taken with food. If the patient is intolerant of misoprostol, H2 antagonists or omeprazole should be considered to decrease the risk of developing an NSAID-induced duodenal ulcer. If patients are not in the defined high-risk groups, given the present costs of H2 antagonists, omeprazole, and misoprostol, there seems to be little justification in treating the patient prophylactically. However, if the patient develops progressive iron-deficiency anemia or occult fecal blood loss not due to an obvious malignancy, endoscopy can be recommended to determine the cause. If there is evidence of a significant NSAID-induced gastric or duodenal ulcer, the NSAID should be stopped and the ulcer treated. If that is impossible, the NSAID dosage should be as low as possible, and the ulcer treated. If an ulcer is found, either a biopsy for H. pylori or a serum assay for the organism should be obtained. Once the ulcer is healed through appropriate therapy, and if NSAIDs are still to be used, prophylaxis with misoprostol should be considered.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1994

Actions and toxic effects of the nonsteroidal anti-inflammatory drugs.

The nonsteroidal anti-inflammatory drugs (NSAIDs) continue to be important for palliation of pain and decreasing inflammation and fever throughout the world. The literature over the past year has continued to broaden our understanding of the potential toxic events associated with the use of these agents. In addition, there have been interesting observations concerning their modes of action. In this article, studies describing the identification of two different isoforms of the prostaglandin synthase enzyme (cyclooxygenase) are reviewed, which might explain some of the observed differences in effects noted for the various available NSAIDs. Problems related to NSAID-induced renal dysfunction and hepatic events and gastroduodenal as well as large- and small-bowel effects of the NSAIDs are also considered.

Aged↗
PubMed1993

A quantitative assessment of limited joint mobility in patients with diabetes. Goniometric analysis of upper extremity passive range of motion.

OBJECTIVE: The syndrome of limited joint mobility is a common but not widely recognized musculoskeletal complication of diabetes. The purpose of this study was to further characterize this syndrome using quantitative goniometric measures. METHODS: Cross-sectional analysis of a sample population was performed to establish the prevalence, location, and severity of limited joint mobility and to determine its relationship to extraarticular manifestations and complications of diabetes. Passive range of motion of both upper extremities was measured by goniometry in 70 adult patients with insulin-dependent diabetes mellitus and 70 nondiabetic controls who were group-matched for age, sex, and general activity level. Joint mobility was assessed by both individual joint motions and a composite scoring technique. RESULTS: Analysis of individual joints and composite scores revealed significant differences between dominant and nondominant extremities in both the control and the diabetic groups. Diabetic patients were generally less flexible than nondiabetic subjects throughout the arm, especially in shoulder and finger joints. In the full study population, multivariate analysis revealed that advanced age, male sex, and the presence of diabetes were associated with decreased passive range of motion for a majority of joints (P < 0.05). In the diabetes group, passive range of motion was significantly correlated (P < 0.05) with age, sex, duration of diabetes, and to a variable extent, glucose control, but was not correlated with the presence of clinically significant neuropathy, retinopathy, nephropathy, or peripheral vascular disease, with activity level, or with hand dominance. Stepwise regression analysis failed to identify single key joint motion(s) to serve as possible screening tests in predicting generalized limited joint mobility of the upper extremity. Finally, the effect of limb usage on range of motion in flexion may differ in diabetic and nondiabetic subjects. CONCLUSION: Limited joint mobility is a generalized phenomenon occurring throughout the upper extremities of many diabetic patients. It is significantly related to age, sex, and to a variable extent duration of diabetes and glucose control. It is not related to the standard complications of diabetes as defined in this study.

Adult↗
PubMed1993

Nonsteroidal anti-inflammatory drug toxicity.

The nonsteroidal anti-inflammatory drugs continue to be a mainstay of therapy for patients with chronic pain and inflammation. Because large numbers of these drugs are prescribed, even the most unusual adverse reactions are not uncommon. During the past year several reviews have appeared on the problems of nonsteroidal anti-inflammatory drug-induced gastroduodenal erosive disease. Several authors have also grappled with the possible uses of concomitant prophylactic therapy to decrease the possibility of an adverse event. Although several of these reviews are well-done meta-analyses of the available literature, others are more personal reflections on this difficult problem. Colitis and other small- and large-bowel adverse reactions to the nonsteroidal anti-inflammatory drugs have also been addressed this year. Unfortunately, there is not much new information on the interesting problem of small- and large-bowel diaphragm formation, which has been thought to be due to nonsteroidal anti-inflammatory drug therapy in certain patients. There are, however, intriguing data on the effects of indomethacin on rat intestine. There has also been useful work on further defining the renal effects of the nonsteroidal anti-inflammatory drugs. In addition, a syndrome of acute renal failure following binge drinking and therapy with nonsteroidal anti-inflammatory drugs is discussed. There have been significant articles that have improved our understanding of the various and at times confusing clinical problems of nonsteroidal anti-inflammatory drug-induced adverse reactions.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1992

Effects of naproxen on renal function in older patients with mild to moderate renal dysfunction.

We have evaluated 45 elderly patients with both musculoskeletal problems and mild to moderate renal dysfunction. We treated these patients with a non-steroidal anti-inflammatory drug (NSAID) for 2 weeks. The serum creatinine, urinary creatinine clearance and blood pressure were monitored before and after therapy. In some patients serum levels of thromboxane B2 (TxB2) and the urinary prostaglandins E2 (PGE2) and I2 (prostacyclin) measured as 6-keto-PGF1 alpha were also monitored before and after therapy and correlated with the clinical measurements. This study has demonstrated that in the entire patient group, the trial drug was tolerated extremely well. There were no changes in the serum creatinine or in the urinary creatinine clearance after 2 weeks of therapy. There was also no change in the early morning diastolic blood pressure. In the 11 patients in whom the serum and urinary prostaglandins were measured, the serum thromboxane levels fell with therapy to a level of 1.5% of the initial value. The urinary levels of PGE2 also fell but not to the same degree. The urinary PGE2 levels fell to 28% of the baseline values. There was no significant change in the levels of urinary 6-keto-PGF1 alpha (prostacyclin). These observations suggest that prostacyclin may be the important prostaglandin in maintaining normal renal haemodynamics when patients are treated with NSAIDs.

Aged↗
PubMed1992

Toxicities of the nonsteroidal anti-inflammatory drugs.

There has been significant progress in defining the risks associated with the use of nonsteroidal anti-inflammatory drugs. There is now clear consensus that certain patient subsets are at an increased risk for gastroduodenal mucosal damage when those patients are treated with these drugs. The therapy for treating mucosal damage or preventing it has also been better defined. The studies published this year have provided a better understanding of those patients who should be considered as candidates for possible therapy for prophylaxis against mucosal damage and which drugs might be useful. The patients who are at risk to develop renal dysfunction remain less well defined. This paper reviews the current relevant literature.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

Toxicity of the nonsteroidal anti-inflammatory drugs.

The nonsteroidal anti-inflammatory drugs continue to be prescribed frequently around the world to palliate the pain and inflammation associated with various medical conditions. These are a heterogenous group of drugs with similar mechanisms of action, yet they are very different chemically and at times possess different potential risks for toxicity. The risk factors for renal dysfunction after therapy with various nonsteroidal anti-inflammatory drugs are reviewed. In addition glomerulopathy and tubular dysfunction are discussed. Further information about nonsteroidal anti-inflammatory drug-induced gastroduodenal erosive disease and who is at risk is presented. Potential methods for preventing mucosal ulcers or treating them once established are discussed. Other recently described nonsteroidal inflammatory drug-induced toxicities, including hepatotoxicity, esophagitis, and the formation of small and large bowel mucosal diaphragms precipitating obstruction are reviewed.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1988

Changes in serum levels of type I and III procollagen extension peptides during infusion of human parathyroid hormone fragment (1-34).

Parathyroid hormone (PTH) inhibits collagen synthesis in vitro, in organ or cell culture and cell-free translation systems. We have designed studies to measure the effects of PTH on collagen synthesis in vivo in humans, utilizing measurements of the serum levels of procollagen extension peptides during and after infusion of synthetic human PTH (hPTH) fragment (1-34). Radioimmunoassays for the carboxy-terminal peptide of type I procollagen (pColl-C) and the amino-terminal peptide of type III procollagen (pColl-III-N) were used to measure acute changes in serum during and after hPTH(1-34). In all six osteoporotic subjects and two normal individuals, serum levels of pColl-I-C were decreased by 16 hr of infusion and returned towards normal 14 hr after the infusion was discontinued; serum levels of pColl-III-N did not change significantly during the infusion, but were increased at 14 hr after the infusion was discontinued. The PTH-induced decrease in levels of pColl-I-C correlated with an increase in blood levels of ionized calcium. In all but two subjects the serum levels of 1,25-dihydroxy vitamin D [1,25(OH)2D] were also increased during the period when serum levels of pColl-I-C were decreased. These results are compatible with the conclusion that infusion of PTH acutely inhibits type I (bone) collagen synthesis, but not type III collagen synthesis. These effects could be direct or indirect, related in part to PTH-induced increased 1-alpha-hydroxylation of 25-(OH) vitamin D and the resultant increased serum levels of 1,25(OH)2D.

Adult↗
PubMed1987

Procollagen type I carboxy-terminal extension peptide in serum as a marker of collagen biosynthesis in bone. Correlation with Iliac bone formation rates and comparison with total alkaline phosphatase.

We measured iliac bone formation rates on all surfaces after double tetracycline labeling, serum levels of type 1 procollagen carboxy-terminal extension peptide (pColl-I-C), and serum levels of total alkaline phosphatase activity (TAP) in four normal subjects and in 44 patients with various forms of metabolic bone disease. In three patients with enzymatic evidence of liver disease both biochemical serum markers were disproportionately raised. In a patient with idiopathic axial osteosclerosis serum pColl-I-C was selectively increased by more than ten-fold. In the remaining 44 subjects pColl-I-C and TAP levels correlated significantly with each other (r = 0.70) and both showed the same directional changes and broadly similar correlations with iliac bone formation rate expressed in different ways. In general, pColl-I-C levels correlated better with cancellous bone formation rates and TAP levels cortical bone formation rates. There was a modest improvement in prediction of bone formation rate with multiple regression using both markers. In 15 patients with typical uncomplicated postmenopausal osteoporosis, neither biochemical marker, singly or jointly, correlated significantly with any expression of bone formation rate. Disadvantages to the use of pColl-I-C as a marker include a significant contribution to the serum level from type 1 collagen biosynthesis in tissues other than bone, and (probably) variable metabolic clearance. For both biochemical markers the most consistently high correlations (r = 0.77-0.79) were found with total bone formation rate for the entire biopsy core volume, which is the best estimate available from a biopsy of formation rate at the bone organ level of organization in vivo. The core volume as a referent also allows the amount of bone formed on cortical, endocortical, and cancellous surfaces to be compared. Measurement of serum pColl-I-C levels merits further study as a noninvasive index of bone metabolism. Differences between normal and abnormal subjects in the relationships between a variety of biochemical markers and a variety of histologic indices have the potential for providing insight into the pathogenesis of osteoporosis.

Adolescent↗
PubMed1987

Metabolic consequences of bone turnover in Paget's disease of bone.

High rates of bone resorption, bone formation, and marrow fibrosis are characteristic of Paget's disease of bone. This excessive bone turnover is reflected by increased fluxes of calcium ions out of and into the skeleton. The rates of these fluxes are highly geared to each other such that calcium balances are close to zero in the absence of fracture or significant immobilization. An increased turnover of bone matrix is also evident by increased urinary excretion of collagen breakdown products (oligopeptides of hydroxyproline, hydroxylysine, and hydroxylysine glycosides) as well as products (peptides of higher molecular weight) related to collagen synthesis. Increased circulatory levels of procollagen extension fragments reflect increased synthesis of Type I collagen (bone matrix) and Type III collagen (marrow fibrosis). Increased levels of bone gamma-carboxyglutamic acid-protein presumably reflect primarily bone matrix synthesis but bone resorption as well. When bone resorption is suppressed pharmacologically, the abnormal levels of these markers of matrix turnover and osteoblastic activity (alkaline phosphatase) also decrease, presumably as a result of coupling of resorption and formation.

Bone Development↗
PubMed1986

Rheumatoid arthritis: clinical features and pathogenetic mechanisms.

Rheumatoid arthritis is a disorder characterized by chronic inflammation affecting predominantly articular tissues, leading in some instances to disruption of the normal structure and function of the joint. In some patients extra-articular manifestations are also present. In the joints, the pathologic lesion consists of synovial cell proliferation with infiltration by inflammatory cells. The complex interaction among these cells is likely responsible for the connective tissue abnormalities that characterize the rheumatoid lesion. The factors responsible for inducing the inflammatory process are unknown.

Arm↗
PubMed1986

Role of the hospital pharmacy director in experiential education.

Pharmacy departments in community hospitals frequently function as teaching sites for the externship component of the pharmacy curriculum. With the entry-level doctor of pharmacy degree replacing the bachelor of science degree at several colleges of pharmacy, the use of community hospitals as sites for experiential education will undoubtedly increase. This article explores the role of the director of pharmacy in providing an optimal environment for experiential education to take place. The following topics are emphasized: maximizing the usefulness of the hospital pharmacy department as a teaching site; fulfilling the needs and requirements of the college, the hospital pharmacy, and the student; and using educational methods that promote student learning without placing unacceptable demands upon the director's time.

Chicago↗
PubMed1985

Mononuclear cell-conditioned medium containing mononuclear cell factor (MCF), homologous with interleukin 1, stimulates collagen and fibronectin synthesis by adherent rheumatoid synovial cells: effects of prostaglandin E2 and indomethacin.

Adherent rheumatoid synovial cells produce and release into supernatant culture medium latent collagenase and PGE2. The levels of collagenase and PGE2 can be increased by a soluble factor present in mononuclear cell-conditioned medium, partially purified by gel-filtration, which has homologies with interleukin 1, and is produced by monocyte/macrophages. The synovial cell cultures produce collagens (procollagens) and fibronectin as well. The factor(s) present in the mononuclear cell conditioned medium which increases medium levels of collagenase PGE2 also stimulates synthesis of total protein as well as types I and III procollagen by the synovial cells. This stimulation by the monocyte factor is augmented in the presence of indomethacin, which blocks endogenous PGE2 production. Medium levels of fibronectin parallel those of procollagen. The addition of exogenous PGE2 abolishes the effect of indomethacin on collagen and fibronectin synthesis. These observations of mononuclear cell-mediated increases in fibronectin synthesis may account for the high levels of fibronectin found by others in rheumatoid synovium and synovial fluids as the increases in collagen synthesis might also explain the fibrosis observed in some rheumatoid joints.

Arthritis, Rheumatoid↗