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Comparison of the scintigraphic diagnosis of the myocardial infarction with two radioactive substances is presented. Pyrophosphate labelled with radioactive 99mTc and anti-myosins labelled with radioactive 111In were used for this purpose.
Electron diffraction technique was used to identify a single crystal in synovial fluid and tissue obtained from patients with pseudogout. One hundred and ten kinds of reciprocal lattice planes of the triclinic calcium pyrophosphate dihydrate (CPPD) crystal were made from its crystallographical data. Electron diffraction patterns obtained from synthesized crystal closely fitted to the reciprocal lattice planes. Synovial fluid of ten patients who had chondrocalcinosis in the knee joint were examined. Diffraction patterns of a single rhomboid-shaped crystal fitted to the reciprocal lattice planes and these kinds of crystals were identified as triclinic CPPD crystals. A single triclinic crystal in the calcified meniscus prepared for transmission electron microscopy was identified in the same way as above. On the other hand, there weren't enough crystallographical data on the monoclinic CPPD crystal to construct the reciprocal lattice planes. Instead of comparing diffraction patterns with the reciprocal lattice planes, diffraction patterns of a single rod-like crystal were compared with those of a synthesized monoclinic CPPD crystal. This comparison combined with energy dispersive elemental analysis made it possible to identify a single rod-like crystal as a monoclinic CPPD crystal.
The articular cartilage, synovial membrane, and meniscus from ten patients who had calcium pyrophosphate dihydrate (CPPD) crystal deposition disease showed strong immunoreactivity for dermatan sulfate proteoglycan, Type I collagen, and S-100 protein in hypertrophic chondrocytes around the crystals, their pericellular matrix, and deposits of the crystals. Electron microscopy revealed that small crystals were formed around the hypertrophic chondrocytes, especially in the degenerated matrix containing electron-dense granular materials and cellular debris. Chondrocytes of this kind were never observed in the articular tissue from ten patients who had osteoarthrosis. These hypertrophic chondrocytes with several unique immunohistochemical characteristics may initiate the formation of CPPD crystals.
We report a method for studying microcrystals which combines scanning electron microscopy, electron-dispersive X-ray analysis, and X-ray diffraction. Application of all three techniques to the same crystalline bodies permits correlation of their three-dimensional morphology at high magnification with unambiguous identification by means of their crystallographic properties. The method was applied to triclinic calcium pyrophosphate dihydrate.
Administration of the vitamin-coenzyme complex containing thiamin pyrophosphate:lipoate:4-phosphopantothenate:nicotinate:flavinad enine mononucleotide (0.2:3:5:8:1) led to increased utilization of alpha-ketoglutarate in nervous tissue via alpha-ketoglutarate dehydrogenase and GABA-transaminase pathways. In these systems content of glutamate and GABA was decreased, suggesting their elevated consumption as energy-providing substrates. If 4-phosphopantothenate was substituted by CoASH and nicotinate--by NAD+, increased decarboxylation of 5(-14)C-alpha-ketoglutarate, 1(-14)C-GABA and 4(-14)C-Asp was detected in brain homogenates in vitro. The neurometabolic effects were accompanied by pronounced antihypoxic effects as shown by the test "hypoxy of closed space".
For animal experimentation, the 95m and 96 technetium isotopes offer many advantages over technetium-99m. Their long physical half-lives and the emission of extranuclear electrons of low penetrating power make it possible to obtain autoradiograms of a great precision. The uptake of technetium stannous pyrophosphate by the epiphyseal plate was studied using liquid-emulsion microautoradiography, 3 hr after i.v. injection into 10-week-old rabbits. Microautoradiograms showed a well-defined and rather specific pattern of localization with intense uptake beneath the epiphyseal disk on the extremities of the vascular buds and a lack of accumulation in the cartilage, whether calcified or uncalcified. In the metaphysis, the label was located where new bone was being laid down and also over the cytoplasm of osteoclasts. We deduce from these results that in normal bone the general distribution of this tracer reflects mainly the arrangement of the blood supply, but the specific sites of accumulation are the bone-forming surfaces and the active resorbing osteoclasts.
Ferric pyrophosphate (Fe-PyP) was investigated in an animal model of acute myocardial infarction for its potential to provide contrast enhancement of the peri-infarct zone using magnetic resonance (MR) imaging. Radiotracer studies compared the biodistribution of soluble 59Fe-PyP with 99mTc-PyP in excised tissue samples. Preferential localization of 59Fe-PyP in the peri-infarct zone was found to be similar to 99mTc-PyP. The ratio (percent dose/gram of tissue) at the edge of the infarct to normal tissue was 1.30 +/- 0.16 and 1.44 +/- 0.33 for 99mTc-PyP and 59Fe-PyP, respectively. In initial studies with high doses of the contrast agent, gated T1-weighted MR images of animals with 48-hour-old infarcts were obtained at 15-minute intervals after injection of Fe-PyP at a dose of 350 mg/kg. Contrast enhancement of the infarct zone was observed in all studies and was maximal 15-30 minutes after injection. Signal intensity ratios (infarct/normal) increased from a baseline 1.31 +/- 0.22 to a peak 1.90 +/- 0.57. Studies were then performed with smaller amounts of Fe-PyP. Images obtained with 50 mg/kg Fe-PyP showed contrast enhancement beginning at 60 minutes. Toxicology studies showed primarily respiratory effects, which became significant at doses of 190 mg/kg. These preliminary studies suggest that Fe-PyP potentially could serve as an MR contrast agent to localize and size acute myocardial infarcts; however, its clinical use may be limited by potential toxicity and dose limitations.
The diagnostic value of 111In-antimyosin (AM) imaging for identifying myocardial infarction was evaluated in comparison with 99mTc-pyrophosphate (PPi) imaging. Twenty-four patients with various stages of myocardial infarction, ranging from three days to nine months after the onset of infarction, underwent both AM and PPi scans. Of 26 infarct lesions AM scan identified 22 (85%), while PPi scans detected 10 (38%) (p less than 0.01). When less than a week had passed since the onset both scans demonstrated all infarct lesions. For seven subacute lesions studied within one to two weeks of onset, AM scans detected (100%), while PPi scans identified only 2 (29%). Furthermore, AM scans showed discrete myocardial uptake in 7 (64%) of those studied more than two weeks after onset. The intensity of AM uptake in the infarcts studied more than seven days after onset was less than that in acute infarcts studied within seven days of onset (p less than 0.05). These preliminary data indicate that the abnormal myocardial uptake of AM persists beyond the first two weeks when PPi no longer accumulates. Thus, AM scans can be considered to provide a sensitive diagnosis of subacute as well as acute myocardial necrosis.
The proposed method of sequential scintigraphy of the kidneys and joints in a single administration of 99mTc-pyrophosphate permits obtaining objective information on function and topography of the kidneys and pyodestructive processes in the joints. Dynamic scintigraphy helps to assess visually renal hemodynamics and the antomotopographic position of the kidney and to obtain exhaustive information on accumulative-evacuatory function of each kidney individually. Scintigraphy also helps to investigate all the joints and to detect pyoinflammatory changes in them. The proposed method considerably reduces the time of investigation and lessens radiation exposure of patients, permitting repeated investigations to assess and correct the treatment of patients with rheumatic arthritis.
We studied the effects of joint movement and immobilization on acute and chronic calcium pyrophosphate dihydrate (CPPD) crystal induced arthritis in lapine knee joints. Exercised CPPD injected joints, in both acute (single 10 mg CPPD intraarticular (IA), duration: 5 h) and chronic (repeated 10 mg CPPD IA, duration: 20 and 42 days) experiments, demonstrated a more intense histologic synovitis compared to cast immobilized knees (p = 0.0001). In chronic experiments, both CPPD injected and noninjected immobilized knees showed greater cartilage histopathologic-histochemical abnormalities (p less than 0.004) and significant reduction in cartilage hexosamine content (p less than 0.005), compared to exercised joints. CPPD injected knees, both exercised and immobilized, demonstrated an initial phase of increased cartilage biosynthetic activity (35S incorporation) at 20 days, compared to noninjected knees (p = 0.02), followed by a decline at 42 days (p less than 0.005). Our data indicate that joint movement enhances acute and chronic experimental CPPD crystal induced synovitis. Articular cartilage is more adversely affected by joint immobilization than by chronic crystalline inflammation. An optimum balance between exercise and rest seems necessary for patients with arthritis so that cartilage can be preserved but pain from active inflammation also controlled.
A prospective, controlled study of patients with primary hyperparathyroidism has been carried out to establish the relation of this endocrinopathy to calcium pyrophosphate dihydrate crystal deposition disease. Eight of 26 patients with documented hyperparathyroidism were found to have chondrocalcinosis compared to four of 104 individuals in the control group (p less than 0.01). Two of these eight patients had confirmed pseudogout attacks shortly after parathyroidectomy. Four other patients, including two without chondrocalcinosis, gave a history of typical pseudogout. Patients with hyperparathyroidism and chondrocalcinosis were significantly older than those without the articular lesion (p = 0.006). We could not delineate specific metabolic abnormalities of hyperparathyroidism which contributed to the development of chondrocalcinosis.
The deposition and ultrastructure of calcium pyrophosphate (CPPD) crystals in joint tissues of pseudogout patients and cadavers were studied. Nine calcified menisci, 2 articular cartilages and 6 samples of synovial fluid were examined by scanning electron microscopy (SEM). Some of them were examined by analytical electron microscopy (EMMA). In the samples of menisci and cartilages, the findings were compared with those in the soft X-ray examinations and polarized light microscopy. The results are summarized as follows: 1) SEM observation of the cut surfaces of calcified menisci and cartilages showed a three-dimensional ultrastructure for the CPPD crystals. The crystals in the synovial fluid taken from pseudogout knees were also clearly demonstrated by this method. The EMMA analysis provided the possibility to examine the structure and content of the crystals simultaneously. 2) Crystal deposition in the meniscus varied with the depth of the tissues; it was diffuse in the collagen framework of the superficial layer, but showed accumulation in the deep layer where a clear line of demarcation between the collagen framework and crystals was seen. 3) The crystals in the meniscus were rod, granular or rectangular in shape, and 0.2-6.5 micro by 0.2-3.5 micro in size. Crystals from the articular cartilage were granular or rod-like in shape, and 0.2-3.5 micro by 0.2-1.0 micro in size. Most of the crystals found in the synovial fluid were rod-shaped. 4) X-ray microanalysis of the meniscus crystals by EMMA showed the same pattern of PK alpha, CaK alpha, and CaK beta content as that of CPPD crystals commercially available. The P/Ca ratio was about 0.7. 5) SEM and EMMA examination can be very useful for accurate identification of the form and content of the tiny crystals in joint tissues and synovial fluid. This can also be useful in proving a diagnosis of crystal-induced synovitis.
An 82-year-old man developed periarticular roentgenographic calcifications of the knee joint. Fragments of meniscus and peritendinous tissue were collected during total knee arthroplasty. Crystals were released from tissues by collagenase digestion. Calcium pyrophosphate dihydrate crystals were identified in the meniscus, and basic calcium phosphate crystals were identified in the peritendinous tissue. Methods of crystal identification included compensated polarized light microscopy, scanning electron microscopy with X-ray energy dispersive analysis, and X-ray diffraction.
Preparations of a highly purified pyruvate dehydrogenase complex (PDC) from human heart contain endogenous thiamine pyrophosphate (TPP) in an amount accounting for about 10% of the maximum activity. At pH values of 7.5 and 8.0, the effective Michaelis constants with respect to exogenous TPP for the PDC apoenzyme form were 0.22 microM and 1.8 microM, respectively.
Recent studies have shown that pyrroline 5-carboxylate, the intermediate in the interconversions of proline, ornithine, and glutamate, can regulate the metabolism of erythrocytes. We now report that the formation of 5-phosphoribosyl 1-pyrophosphate (PP-Rib-P) was markedly stimulated by pyrroline 5-carboxylate in intact red cells. The production of PP-Rib-P is an important point of regulation in nucleotide metabolism. We found that pyrroline 5-carboxylate increased glucose metabolism through the oxidative arm of the pentose shunt, ribose 5-phosphate formation, and PP-Rib-P production and subsequently augmented purine nucleotide production through the salvage pathway in erythrocytes. We now report that pyrroline 5-carboxylate markedly stimulated the net synthesis of inosine monophosphate from hypoxanthine in intact human red cells so that the pool of inosine monophosphate became 20-30% of the total pool of purine nucleotides. Inosine monophosphate has been considered to be a "mobile pool" of purines, i.e. a reservoir from which peripheral tissues can be supplied; the effect of pyrroline 5-carboxylate on the inosine monophosphate pool may be a mechanism for regulating the function of erythrocytes in purine delivery.
Phosphoribosyl pyrophosphate (PPRibP), required in nucleotide synthesis, increases 2-fold in rat kidney from 1 day post partum to adult stage; there is no accompanying increase in PPRibP synthetase activity measured in vitro. Ribose 5-phosphate is a key factor in the regulation of PPRibP synthesis. The activity and regulation of 3 routes of ribose 5-phosphate formation have been measured in renal growth: (i) the flux through the oxidative pentose phosphate pathway was high in the neonatal period but increased only +50% thereafter; (ii) the non-oxidative pentose phosphate pathway, including transketolase, increased by +145%; (iii) the rate-limiting enzymes of the glucuronate-xylulose route increased +200% from 1 day to the adult stage. The importance of systems reoxidizing NADPH was shown by: (i) the stimulation of renal PPRibP formation from glucose by phenazine methosulphate; (ii) the early involvement of the oxidative pentose phosphate pathway at the stage where NADPH is used for biosynthetic routes; (iii) the increasing involvement of the glucuronate-xylulose route, which acts as a transhydrogenase producing NADP+ in addition to pentose phosphate formation and (iv) the correlation between renal PPRibP content and the activity of aldose reductase, which, by utilization of NADPH, stimulates ribose 5-phosphate formation via the oxidative pentose phosphate pathway. Evidence is adduced that the contribution of the 3 routes of ribose 5-phosphate formation in the kidney varies at different stages of development.
The diagnosis of amyloid cardiomyopathy was only based, until the last few years, on the results of invasive techniques. It seems presently that the combined contribution of cardiac sonography and scintigraphy using technetium 99m pyrophosphate, makes, most of the time, this diagnosis possible without need for additional examinations. This notion is illustrated by a typical case-report and data from the literature. Demonstration on the cardiac sonogram of a thickening of the walls-while the context and especially the electrocardiogram are not in favor of a left ventricular hypertrophy--associated with a very particular "hyperechoing" aspect and an abnormal fixation on the scintigram, may be considered specific of this disease.
The aim of the study was to compare the effectiveness of planar and single photon emission computed tomography (SPECT) imaging with 99mTc-pyrophosphate in the verification of acute myocardial infarction. The study was performed on 39 patients (26 males, 13 females) aged between 41-76 years (mean 61 +/- 9) admitted to CCU for acute myocardial infarction. Patients underwent planar and SPECT imaging using a double-head-camera with a 360 degrees rotation arc within 6 days of admission. Planar images were obtained in three standard projections (anterior, LAO 45 degrees, LAO 75 degrees) with acquisitions of 500000 counts each. To obtain SPECT images ninety projections, each lasting 20 seconds, were taken; subsequently images reconstruction was performed using an iterative algorithm. Positive planar images were found in 21 out of 39 patients; SPECT images were positive in 33 patients. In "Q wave" myocardial infarctions planar images were positive in 13 out of 15 patients, whereas SPECT images were positive in all subjects; in "non-Q wave" myocardial infarctions planar images were positive in 6 out of 22 patients whereas SPECT images were positive in 16 patients (p less than 0.005); in 2 patients with left bundle branch block both planar and SPECT images were positive. A bidimensional echocardiogram was carried out on 38 patients: an alteration of left ventricular regional wall motion was present in 30 subjects; in one patient diffuse hypokinesia was present.(ABSTRACT TRUNCATED AT 250 WORDS)