Aldolase in the diagnosis of myositis.
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Creatine Kinase↗
Biomedical subjects
B F Mandell
Publications and source records attributed to B F Mandell.
Avascular necrosis of the femoral head presenting as trochanteric bursitis.
Five patients are described with avascular necrosis of the femoral head who presented with ipsilateral trochanteric bursitis, in the absence of clearcut hip joint disease. Avascular necrosis was indicated by magnetic resonance imaging. It is suggested that clinical trochanteric bursitis, especially when refractory to local corticosteroid treatment, may be the initial sign of hip disease. In the patient with risk factor(s) for avascular necrosis that diagnosis should be considered and evaluated with appropriate studies, such as magnetic resonance imaging, to prevent weight bearing at an early stage and permit possible surgical decompression in the hope of postponing or obviating the need for total hip replacement.
Adult↗
Suppression of acute and chronic inflammation by dietary gamma linolenic acid.
We examined the effect of diets enriched in gamma linolenic acid (GLA) on acute inflammation induced by monosodium urate crystals, and on subacute and chronic inflammation induced by complete Freund's adjuvant in the rat subcutaneous air pouch and in rats with adjuvant induced arthritis. Diets were enriched (15% fat) with borage seed oil (23% GLA) or safflower oil (less than 1% GLA). Diets enriched with GLA suppressed inflammation markedly in all models, whereas the safflower oil diet did not influence the inflammatory response. The degree of inflammation was quantified by measuring pouch exudate cell concentration, lysosomal enzyme activity, volume, protein concentration and prostaglandin E2 and leukotriene B4 concentrations. In the chronic air pouch model, the pouch lining was thickened, invaded by mononuclear cells and exhibited proliferation of lining cells 14 days after adjuvant injection. The lesion was far less severe and usual pouch lining architecture was maintained in animals given dietary GLA. Livers of rats fed borage seed oil were enriched in GLA and dihomo gamma linolenic acid (DGLA), and the DGLA/arachidonate ratio was increased 5-fold compared with animals fed safflower oil. Enrichment of diet with plant seed oils rich in GLA may provide a way to alter generation of prostaglandins and leukotrienes and to influence acute and chronic inflammatory responses.
Acute-Phase Reaction↗
Thrombotic disorder associated with a protein C inhibitor.
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Humans↗
Suppression of monosodium urate crystal-induced acute inflammation by diets enriched with gamma-linolenic acid and eicosapentaenoic acid.
A subcutaneous air pouch formed in Sprague-Dawley rats was used to study the effect of diets enriched in gamma-linolenic acid (GLA) (in plant seed oil) and eicosapentaenoic acid (EPA) (in fish oil) on acute inflammation induced by monosodium urate crystals. The GLA-enriched diet suppressed significantly the cellular phase of inflammation (polymorphonuclear leukocyte accumulation, crystal phagocytosis, and lysosomal enzyme activity), but it had little effect on the fluid phase (exudate volume and protein concentration). In contrast, the EPA-enriched diet suppressed the fluid phase but not the cellular phase of inflammation. The findings indicate that the fluid and cellular phases of acute inflammation can be controlled independently. A combined diet of fish oil and plant seed oil (EPA-enriched and GLA-enriched) reduced both the cellular and fluid phases of inflammation. Thus, dietary provision of alternative substrates for oxidative metabolism (other than arachidonic acid) modifies monosodium urate crystal-induced acute inflammation.
Animals↗
Suppression of acute inflammation by 15 methyl prostaglandin E1.
Prostaglandins are important regulators of inflammatory responses. The rat subcutaneous air pouch, a model for synovial inflammation, was used to study the effect of systemic injections of prostaglandin E1 (PGE1) and its stable analog 15S,15 methyl prostaglandin E1 (15M PGE1) on nonimmunologically induced acute inflammation. The 15M PGE1 analog was a more effective longer-lasting antiinflammatory agent. Acute inflammatory responses were induced with three diverse stimuli including monosodium urate crystals, leukotriene B4 and formylmethionylleucyl-phenylalanine. Animals were treated with 15 M PGE1 for 2 days before induction of inflammation. Analysis of pouch fluid 6 hours after injection of the inflammatory stimulus indicates that 15M PGE1 treatment suppressed exudate volume and protein concentration, polymorphonuclear leucocyte accumulation and activity of the lysosomal enzyme beta-galactosidase. Treatment with 15M PGE1 was least effective in preventing the fluid phase of inflammation (exudate volume and protein concentration) when leukotriene B4 was used to induce inflammation. Direct observation (dissecting microscope) of pouch lining vessels indicated that 15M PGE1 reduced markedly the intense vascular reactivity (increased number of dilated vessels and filamentous, corkscrew-shaped vessels) usually seen in an acute inflammatory response. The antiinflammatory effect of 15M PGE1 was also documented by histopathology of pouch lining tissue. Treatment with 15M PGE1 reduced substantially the invasion of pouch tissue by polymorphonuclear leucocytes which was induced by all three stimuli of inflammation. Results of these experiments show that systemic administration of 15M PGE1 is capable of suppressing acute inflammation induced by monosodium urate crystals, by the potent soluble naturally occurring mediator of inflammation leukotriene B4, and by the synthetic chemotactic peptide, formylmethionylleucylphenylalanine.
Acute Disease↗
Angiography and polyarteritis nodosa.
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Aneurysm↗
Rapid simultaneous assessment of neutrophil superoxide generation and lysosomal enzyme release.
A rapid method for the simultaneous measurement of neutrophil superoxide generation and beta-glucuronidase release is described. Assay of beta-glucuronidase using a fluorescent substrate is shown to be valid in the presence of reduced or unreduced ferricytochrome C, a prerequisite for the simultaneous assessment of this enzyme activity and O-2 generation.
Cytochrome c Group↗
Independent regulation of leukotriene B4-elicited polymorphonuclear leukocyte exocytosis and superoxide generation by a serum factor.
Serum from a patient with inactive systemic lupus erythematosus (SLE) and ibuprofen-induced transient neutropenia was used as a probe to define further the control of human polymorphonuclear leukocyte (PMN) exocytosis and superoxide (O2-) generation. Thirty-minute preincubation of normal PMNs with 10-50% v/v of this serum, followed by washing, produced a specific dose-related suppression of leukotriene B4 (LTB4)-elicited beta-glucuronidase and lysozyme release of up to 45% and 30% respectively. If cells were not washed, the inhibition increased to 60% and 40%. Superoxide production stimulated by LTB4 was unaffected. The serum had no effect on formyl-met-leu-phe (FMLP) or phorbol myristate acetate-stimulated O2- or exocytosis. O2- and beta-glucuronidase release elicited by zymosan-treated serum (ZTS) were both decreased by 15%, but there was no increased inhibition seen if cells were not washed, or if the time of preincubation was increased from 7 to 30 min. In contradistinction, the serum inhibition of LTB4 exocytosis did show time dependence. Serum obtained when the patient was not leukopenic and sera from 6 normal controls, 2 patients with inactive SLE, 1 patient with SLE and chronic leukopenia, and 2 controls taking ibuprofen did not influence any PMN function. The serum inhibition of ZTS-induced functions was qualitatively similar to that observed when PMNs were preincubated and desensitized with ZTS in vitro. Selective inhibition of LTB4 exocytosis was not seen when PMNs were desensitized with LTB4 in vitro. These observations indicate that LTB4-elicited O2- and exocytosis can be independently and specifically regulated. The cellular site at which this serum factor acts is not clear, but the current studies strongly suggest that this inhibition is not due to in vitro deactivation by LTB4 activity.
Exocytosis↗
Severe systemic hypersensitivity reaction to ibuprofen occurring after prolonged therapy.
A 23-year-old woman with systemic lupus erythematosus had a severe hypersensitivity reaction to the drug ibuprofen. The reaction, documented by rechallenge during hospitalization, was characterized by marked hypotension, fever, rigors, conjunctivitis, meningitis, nausea, arthralgias, and leukopenia. In addition to illustrating the potential diagnostic confusion with infection or lupus flare, this case is of interest in that the reaction developed suddenly despite the patient's uneventful use of the drug for over two years. Collected cases are reviewed from the literature, and the common features are summarized.
Adult↗
Cardiovascular involvement in systemic lupus erythematosus.
SLE is an inflammatory disease of unknown etiology with the potential of affecting virtually all organ systems. Cardiovascular involvement occurs frequently, although it is often mild enough not to cause clinical concern. Pericarditis is most commonly subclinical, noted only on echocardiogram. Pericardial fluid, which can accumulate rapidly enough to cause tamponade, is inflammatory in nature and can totally mimic infection. The occurrence of Libman-Sacks endocarditis, usually a pathological diagnosis of little clinical significance, has little if any correlation with the presence of audible murmurs. However, valve replacement is occasionally necessary secondary to sterile destruction. These valvular lesions can also embolize or become infected. The incidence of ischemic coronary disease is increased, both secondary to premature atherosclerosis and, rarely, coronary arteritis. Conduction disease and arrhythmias are infrequently reported in adult patients, but congenital CHB has been noted in children born to mothers who have circulating anti-Ro antibody. Evidence is accumulating that suggests there is a mild cardiomyopathy associated with SLE that may be due to thrombotic or inflammatory microvascular coronary disease. Acute clinical myocarditis also rarely occurs. Therapeutically, at present, a reasonable course would seem to be to limit all known possible contributing factors to premature coronary artery and myocardial disease (hypertension, hypercholesterolemia, smoking, steroid therapy, etc), to be vigilant about recognizing the rarer complications associated with SLE (infectious pericarditis and endocarditis, coronary arteritis, pericardial tamponade, clinical myocarditis), and to remember that these uncommon complications are indeed uncommon. The importance of vigorously treating systemic hypertension cannot be overstressed.
Cardiovascular Diseases↗
Plasma clearance of glycoproteins with terminal mannose and N-acetylglucosamine by liver non-parenchymal cells. Studies with beta-glucuronidase, N-acetyl-beta-D-glucosaminidase, ribonuclease B and agalacto-orosomucoid.
Glycoproteins having mannose and/or N-acetylglucosamine in the terminal non-reducing position [Stockert, Morell & Scheinberg (1976) Biochem. Biophys. Res. Commun. 68, 988--993], and various lysosomal enzymes [Stahl, Schlesinger, Rodman & Doebber (1976) Nature (London) 264, 86--8] are rapidly cleared from plasma by the liver after intravenous administration. A liver cell-separation technique was used to determine the cellular localization of 125I-labelled beta-glucuronidase, ribonuclease B, agalacto-orosomucoid and asialo-orosomucoid. On a specific readioactivity basis, all ligands except 125I-labelled asialo-orosomucoid were enriched in the non-parenchymal cell fraction. Isolated cells, fixed and stained for beta-glucuronidase or N-acetyl-beta-D-glucosaminidase activity after intravenous injection of the enzymes, showed enrichment in the non-parenchymal cell fraction (probably Kupffer cells). After uptake by the non-parenchymal cells, liver lysosomal beta-glucuronidase and N-acetyl-beta-D-glucosaminidase showed degradation half-times of 2.2 and 0.4 days respectively.
Acetylglucosamine↗
Demonstration of microtubule independent protein secretion from rat liver.
The induced secretion of rat liver microsomal-beta-glucuronidase into serum is, unlike other proteins secreted from liver, not dependent upon an intact microtubule apparatus.
Animals↗
Inhibition of polymorphonuclear leukocyte capping by a chemotactic factor.
Incubation of human polymorphonuclear leukocytes with colchicine and fluorescein-concanavalin A leads to the formation of a polarized cap of fluorescence not seen if cells are incubated with fluorescein-Con A along. When cells are preincubated with a chemotactic factor before colchicine treatment, the capping is inhibited in a dose-related manner. Studies with alpha-methylmannoside indicate that the caps represent extracellular fluorescein-Con A and are not areas of Con A internalization. Experiments utilizing an irreversible inhibitor of serine esterases suggest that a chemotactic factor-activated enzyme is involved in the inhibition of cap formation in the human neutrophil.
Cell Membrane↗
A 47-year-old woman with a swollen leg.
This case illustrates the importance of expanding the differential diagnosis beyond ruling out a DVT in a patient presenting with calf swelling. A good history and examination and a compulsive search for an etiology are necessary in the pursuit of the correct diagnosis. In this patient, only after identifying the popliteal cyst and recognizing that it represented an inflammatory synovitis could the cause be determined and the proper treatment instituted.
Anti-Bacterial Agents↗
Individualizing the treatment of gout.
Treatment for gouty arthritis should be individualized to address the patient's other medical problems and the likelihood that gout will become chronic. We present a typical case and review the options, explaining their utility for this and other patients.
Adrenal Cortex Hormones↗