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PubMed2006

"Crystal clear"-sonographic assessment of gout and calcium pyrophosphate deposition disease.

OBJECTIVES: To date, high-resolution ultrasound (US) has not been fully exploited in the field of crystalline arthropathy. Both gout and calcium pyrophosphate deposition (CPPD) disease are significant diseases within the purview of the rheumatologist. The aim of this pictorial review was to present the principal findings in patients with crystal deposition in gout and CPPD. METHODS: US pictures were obtained from 60 consecutive patients, 34 with CPPD disease and 26 with gout, whose diagnosis was confirmed by synovial fluid analysis. The US examinations were performed using the following US systems: Diasus (Dynamic Imaging, Livingstone, UK) and Logiq 9 (General Electric Medical Systems, Milwaukee, WI). RESULTS: Pictorial evidence of the principal US findings in gout includes monosodium urate (MSU) deposition on the surface of articular cartilage, various patterns within synovial fluid ranging from completely anechoic fluid to collections filled with aggregates of variable shape and echogenicity, microdeposition within tendons, and tophus formation. In CPPD, the hallmark US features include crystal deposition within articular cartilage, calcification of fibrocartilage, together with focal crystal deposition within tendons. CONCLUSION: US is an impressive imaging modality in crystalline arthropathy. The anatomical location of the crystal deposits, clearly depictable by US, allows differentiation between MSU and CPPD aggregates.

Arthritis, Gouty↗
PubMed2026

Co-occurrence of rheumatoid arthritis and calcium pyrophosphate deposition disease: A systematic literature review.

BACKGROUND: Rheumatoid arthritis (RA) and calcium pyrophosphate deposition (CPPD) disease are forms of inflammatory arthritis which may have similar presentations. There is growing recognition that these conditions can coexist, especially in elderly patients. This systematic literature review aims to examine the epidemiology and clinical characteristics of patients with both RA and CPPD disease. METHODS: A systematic literature search was performed from database inception to 31st January 2026 using the databases EMBASE, MEDLINE, Scopus, PubMed, CINAHL, and Cochrane. Keywords relating to RA, CPPD and chondrocalcinosis were used. Inclusion criteria were studies published in English and those that addressed the co-occurrence of RA and CPPD. RESULTS: The search yielded 24 studies comprising 12 cross-sectional studies, 2 case series, and 10 case reports published between 1965 and 2026. A total of 404 patients had both RA and CPPD, with 397/404 (98.3%) aged over 60 years old. Of 365 patients with serostatus data, 204/339 (60.2%) were seronegative for both rheumatoid factor (RF) and anti-citrullinated protein antibody (ACPA). Radiographic chondrocalcinosis was evident in 271/287 (94.4%). Of 271 patients with chondrocalcinosis, 162 (59.8%) were seronegative for both RF and ACPA. The most prescribed medications were methotrexate and prednisolone, in 75/205 (36.6%) and 64/205 (31.2%) patients, respectively. Colchicine was prescribed for 24/205 (11.7%). CONCLUSION: While the studies were small, RA, which is commonly seronegative, and CPPD can co-exist in the elderly. Higher-quality studies are required to determine the prevalence of co-existent RA and CPPD, thereby improving insight into the epidemiology and potentially enhancing outcomes of these patients.

Humans↗
PubMed1999

Can technetium 99m pyrophosphate be used to quantify myocardial injury in donor hearts?

BACKGROUND: There are no prospective methods available to quantify the myocyte injury in hearts prior to transplantation. The potential of the isotope labeled infarct marker 99m Technetium pyrophosphate (TcPPT) being used in this role was investigated. METHODS: Brain death was induced by creating an extradural space occupying lesion in young adult swine after which hemodynamic changes were monitored and myocyte injury was quantified by histochemistry. TcPPT was administered 5 hours after induction of intracranial hypertension, and after hearts were harvested myocardial uptake was measured. These latter measurements were related to the histochemical assessment of myocyte injury. RESULTS: Sham animals (n = 4) maintained cardiovascular stability and experienced minimal myocyte injury, grades 0 to 3. BD animals (n = 10) exhibited varying patterns of hemodynamic change and myocyte injury, the latter was significant in 6, graded 4 to 11, p less than 0.05. Uptake of TcPPT by BD hearts was greater than twice the 90th centile sham value in 6. The sensitivity and specificity of greater uptake indicating the presence of myocyte injury was 83.3% and 75% respectively. CONCLUSIONS: TcPPT has the potential to quantify myocardial injury induced by brain death and its potential utility merits further investigation.

Animals↗
PubMed2003

Pyruvate:NADP+ oxidoreductase is stabilized by its cofactor, thiamin pyrophosphate, in mitochondria of Euglena gracilis.

Pyruvate:NADP(+) oxidoreductase (PNO) is a thiamin pyrophosphate (TPP)-dependent enzyme that plays a central role in the respiratory metabolism of Euglena gracilis, which requires thiamin for growth. When thiamin was depleted in Euglena cells, PNO protein level was greatly reduced, but its mRNA level was barely changed. In addition, a large part of PNO occurred as an apoenzyme lacking TPP in the deficient cells. The PNO protein level increased rapidly, without changes in the mRNA level, after supplementation of thiamin into its deficient cells. In the deficient cells, in contrast to the sufficient ones, a steep decrease in the PNO protein level was induced when the cells were incubated with cycloheximide. Immunofluorescence microscopy indicated that most of the PNO localized in the mitochondria in either the sufficient or the deficient cells. These findings suggest that PNO is readily degraded when TPP is not provided in mitochondria, and consequently the PNO protein level is greatly reduced by thiamin deficiency in E. gracilis.

Animals↗
PubMed1999

Further characterization of ATP-initiated calcification by matrix vesicles isolated from rachitic rat cartilage. Membrane perturbation by detergents and deposition of calcium pyrophosphate by rachitic matrix vesicles.

Although membrane associated enzymes such as ATPase, alkaline phosphatase, and NTP pyrophosphohydrolase in matrix vesicles (MVs) may underlie the mechanisms of ATP-promoted calcification, prior to the current investigation, the role of the MV membrane in calcification had not been addressed. In this study, various perturbations were introduced to the MV membrane in in vitro calcification systems to determine ideal conditions for ATP-initiated calcification by MVs isolated from rachitic rat epiphyseal cartilage. Membrane integrity appears to be required, since the rupture of the vesicular membrane by vigorously mixing with 10% butanol abolished calcification. In contrast, a mild treatment of MVs with low concentrations (e.g., 0.01%, which is much below the critical concentration for micelle formation) of either neutral Triton X-100 or anionic deoxycholate stimulated calcification by >2-fold, without inducing obvious changes in vesicular appearance. Fourier transform infrared spectroscopic studies were done to identify the mineral phase formed in these experiments. For the first time, rachitic MVs were shown to induce the formation of a calcium pyrophosphate dihydrate-like phase after their exposure to calcifying medium with 1 mM ATP. The integration of spectral areas indicated that calcification was enhanced by Triton X-100. The detergent effect was reversible and appeared to be not mediated through activation of ATPase, alkaline phosphatase, or ATP pyrophosphohydrolase. In contrast to neutral Triton X-100 and anionic deoxycholate, cationic cetyltrimethylammonium bromide inhibited both ATPase activity (I50=10 microM) and ATP-initiated calcification. These observations suggest that membrane perturbations can affect calcification and that the presence of NTP-pyrophosphohydrolase in MVs may play a role in the deposition of CaPPi in rachitic cartilage.

Adenosine Triphosphate↗
PubMed1999

Selective inhibition of protein kinase C, mitogen-activated protein kinase, and neutrophil activation in response to calcium pyrophosphate dihydrate crystals, formyl-methionyl-leucyl-phenylalanine, and phorbol ester by O-(chloroacetyl-carbamoyl) fumagillol (AGM-1470; TNP-470).

The effect of O-(chloroacetyl-carbamoyl) fumagillol (AGM-1470; TNP-470) was investigated on protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) activation in neutrophils stimulated by plasma-opsonized crystals of calcium pyrophosphate dihydrate (triclinic) [CPPD(T)], formyl-Met-Leu-Phe (fMLP), and phorbol 12-myristate 13-acetate (PMA). Neutrophil respiratory burst responses also were determined in AGM-1470-pretreated cells stimulated with the same agonists, using chemiluminescence and superoxide anion generation assays. AGM-1470 (5 microM) effectively inhibited PKC activation in cells treated with CPPD(T) crystals (50 mg/mL, 2 min) and fMLP (1 microM, 1 min), but had no effect on PMA-treated cells (0.5 microM, 5 min). AGM-1470 blocked MAPK activity completely and reduced neutrophil activation induced by fMLP and PMA but not by CPPD(T). The degree of inhibition of the respiratory burst plateaued at approximately 46+/-9 and 54+/-3% in fMLP- and PMA-treated cells, respectively. These data indicate that activation of neutrophil respiratory burst activity may be mediated through the MAPK pathway. AGM-1470 pretreatment did not inhibit CPPD(T) crystal- or fMLP-stimulated phosphatidylinositol 3-kinase (PI 3-kinase) activity. These findings, coupled with further observations that the PI 3-kinase inhibitor wortmannin (10 nM) inhibited fMLP- and CPPD(T) crystal-induced but not PMA-induced chemiluminescence, indicate that at least two distinct signaling pathways (mediated by PI 3-kinase or MAPK) lead to neutrophil respiratory burst responses. PKC may also be required in the MAPK-stimulated pathway. We propose that the inhibitory effect of AGM-1470 on the neutrophil respiratory burst may be due to its ability to inhibit PKC and MAPK activation.

Calcium Pyrophosphate↗
PubMed1978

Apparent stability constants of H+ and Mg2" complexes of 5-phosphoribosyl alpha-1-pyrophosphate.

Apparent Mg2+ and H+ stability constants of 5-phosphoribosyl alpha-1-pyrophosphate (ligand, L) complexes were determined from pH titration data at 25 degrees C with an average of 0.17 M NaCl or KCl and 0.20 M ionic strength. The logarithms of calculated macroscopic overall stability constants are: 3.2 (MgL3-), 4.8 (Mg2L-), 6.5 (HL4-), 12.4 H2L3-), 9.4 (Mg HL2-), and 11.0 (MgH2L). Comparison of the stepwise Mg2+ stability constants (log k = 3.2 and 1.6) with those of MgADP- and MgAMP or Mg-hexose-1-P suggests that the first and second Mg2+ bind to the 1-PP and 5-P groups of the ligand, respectively. Reasonable assumptions about relative microscopic constants indicate that several of the microscopic isomers do not achieve significant concentrations over a large range of conditions. Judging from other data on organophosphate complexes, it is likely that the constants of this study may be extrapolated with little error to other conditions of ionic strength 0.1--0.2 M) and temperature (e.g., 15--35 degrees C), and widely different monovalent ion concentrations.

Chemical Phenomena↗
PubMed1998

Cyclic AMP decreases the availability of 5-phosphoribosyl-1-pyrophosphate and decelerates de novo purine synthesis in rat hepatocytes.

Cyclic adenosine monophosphate (cAMP) was found to decrease the availability of 5-phosphoribosyl-1-pyrophosphate (PRPP) and to decelerate the rate of de novo purine synthesis in suspensions of adult rat hepatocytes. Glucagon did not affect these parameters. The glucagon antagonist des-His1[Glu9]glucagon amide (DHGA), and the protein kinase C activator 1,2-dioctanoyl-sn-glycerol (DOG) were also found to lower PRPP availability. Incubation of the hepatocytes with dbcAMP or with DHGA, did not alter the activity of PRPP synthetase in the hepatocyte lysates, indicating that the above effects are not mediated through the activity of this enzyme. The possibility that the decrease in PRPP availability reflects increased consumption associated with accelerated pyrimidine synthesis is discussed. The decelerated rate of de novo purine synthesis is probably secondary to the decreased PRPP availability.

Animals↗
PubMed2002

An improvement in sintering property of beta-tricalcium phosphate by addition of calcium pyrophosphate.

The sintering behavior of calcium pyrophosphate (CPP, Ca2P2O7)-doped beta-tricalcium phosphate [TCP, Ca3(PO4)2], prepared by solid state reaction, was investigated in-situ, using dilatometry. Pure beta-TCP undergoes phase transition to alpha-TCP at about 1200 degrees C; hence pure beta-TCP ceramics should be sintered bclow 1200 degrees C. Pure beta-TCP sintered body can achieve a relative density of only 86% when sintered at 1150 degrees C. However, the addition of CPP in the range of 0.5-3 wt% delays phasc transition of beta-TCP and enables sintering of beta-TCP at 1200 degrees C without a phase transformation to alpha-TCP. Due to this effect of CPP added to TCP, CPP-doped beta-TCP ceramics with relative density over 95% could be obtained when sintered at 1200 degrees C for 2 h.

Bone Cements↗
PubMed1997

Subcutaneous extensor tendon rupture associated with calcium pyrophosphate dihydrate crystal deposition disease of the wrist.

We report a patient with rupture of the ring extensor tendon associated with calcium pyrophosphate dihydrate crystal deposition disease of the wrist. Crystal deposits were noted in synovium and the triangular fibrocartilage complex. Histological examination revealed chronic synovitis with foreign body giant cell reaction to crystals. The cause of the tendon rupture was synovitis due to crystal deposition.

Aged↗
PubMed1983

Hand and wrist involvement in calcium pyrophosphate dihydrate crystal deposition disease.

The clinical records and hand and wrist radiographs of 51 patients with calcium pyrophosphate dihydrate crystal deposition disease have been analyzed, and symptomatology and radiologic abnormalities have been correlated. Characteristic roentgenographic features included cartilage and synovial calcification and arthropathy of the metacarpophalangeal joints and the radiocarpal compartment of the wrist, including scapholunate dissociation. Clinical-radiologic correlation revealed many asymptomatic patients with calcification and arthropathy and many symptomatic patients with normal radiographs. Thorough radiologic evaluation may reveal many patients with this disorder before the onset of clinical symptoms.

Aged↗
PubMed2000

Kelley-Seegmiller syndrome due to a unique variant of hypoxanthine-guanine phosphoribosyltransferase: reduced affinity for 5-phosphoribosyl-1-pyrophosphate manifested only at low, physiological substrate concentrations.

A male child, who presented at the age of 3.5 years with acute renal failure, was diagnosed as having partial deficiency of hypoxanthine-guanine phosphoribosyltransferase (HPRT; EC 2.4.2.8). The underlying HPRT mutation was unique in that the specific activity of HPRT in erythrocyte and in fibroblast lysates was normal, but the rate of uptake of hypoxanthine into nucleotides of intact cultured fibroblasts was markedly reduced (23% of normal). The low functioning of HPRT in the intact fibroblasts was associated with decreased utilization of endogenously generated hypoxanthine and with decreased utilization of the cosubstrate 5-phosphoribosyl-1-pyrophosphate (PRPP). The non-utilized hypoxanthine was excreted into the incubation medium. The accumulation of PRPP was indicated by the 2.3-fold increase in the rate of uptake of adenine into intact cell nucleotides and by the 7. 5-fold enhancement of the rate of de novo purine synthesis. Kinetic studies of HPRT activity in fibroblast lysates revealed reduced affinity of the enzyme for PRPP (apparent K(m) 500 microM in comparison to 25 microM in control lysates), manifested in low activity at low (physiological), but not at high PRPP concentrations. The apparent K(m) for hypoxanthine was normal (23 microM in comparison to 14.2 microM in control lysates). With allopurinol treatment, our patient has had no problems since presentation, and is developing normally at 5 years of age.

Acute Kidney Injury↗
PubMedDate not supplied

Combined thallium 201/technetium 99m-labeled pyrophosphate tomography for identification of the "culprit" vessel in acute myocardial infarction.

BACKGROUND: Many previous investigations have used the presence of transient ischemic 201Tl perfusion defect to localize coronary artery stenosis. This study reports the results of 201Tl tomography alone and combined 201Tl/99mTc-labeled pyrophosphate (99mTc PYP) tomography employed to identify the infarct-related vessel in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: All short-axis images were evaluated by dividing each left ventricular slice into eight equal sectors. In addition, for combined 201Tl/99mTc PYP tomography, two sectors were added to evaluate involvement of the right ventricle. In a preevaluation phase of the study, the sectors were assigned to the supplying coronary arteries in 75 patients with single chronic myocardial infarction related to the left anterior descending coronary artery (LAD), left circumflex artery (LCX), or right coronary artery (RCA). In this pilot phase, 201Tl tomograms were reviewed in conjunction with the angiographic data. This assignment was then tested prospectively in 117 patients with AMI. As confirmed by angiography, the AMI was related to the LAC, LCX, and RCA in 54, 17, and 46 patients, respectively. Sensitivity and specificity for 99mTc PYP accumulation on combined 201Tl/99mTc PYP tomography were 98% a nd 100% for the LAD, 88% and 99% for the LCX, and 98% and 96% for the RCA, respectively. For 201Tl tomography, sensitivity and specificity for identification of the culprit vessel were 94% and 89% for the LAD, 82% and 91% for the LCX, and 72% and 96% for the RCA, respectively. CONCLUSION: This prospective study demonstrates that combined 201Tl/99mTc PYP tomography is highly accurate for identification of the infarct-related artery in AMI, even in patients with multivessel disease. Positive contrast visualization of myocardial necrosis in both the left and right ventricle allows for reliable differentiation between AMI related to the LCX or RCA territory. In comparison, for 201Tl tomography the sensitivity to detect the culprit vessel, particularly the LCX and RCA, appears to be lower than for 201Tl 99mTc PYP imaging, particularly in patients with prior infarction or right dominant coronary artery.

Coronary Vessels↗
PubMed2003

A novel point mutation (I137T) in the conserved 5-phosphoribosyl-1-pyrophosphate binding motif of hypoxanthine-guanine phosphoribosyltransferase (HPRTJerusalem) in a variant of Lesch-Nyhan syndrome.

We identified a novel point mutation (I137T) in the hypoxanthine-guanine phosphoribosyltransferase (HPRT; EC 2.4.2.8) encoding gene, in a patient with partial deficiency of the enzyme (variant of Lesch-Nyhan syndrome). The mutation, ATT to ACT, resulting in substitution of isoleucine to threonine, occurred at codon 137 (exon 6), which is within the region encoding the binding site for 5-phosphoribosyl-1-pyrophosphate (PRPP). We suggest the mechanism by which the mutation-induced structural alteration of HPRT reduced the affinity of the enzyme for PRPP.

Amino Acid Motifs↗
PubMed1995

The crystal structure of the orotate phosphoribosyltransferase complexed with orotate and alpha-D-5-phosphoribosyl-1-pyrophosphate.

The three-dimensional structure of Salmonella typhimurium orotate phosphoribosyltransferase (OPRTase) in complex with the ribose 5-phosphate donor alpha-D-5--phosphoribosyl-1-pyrophosphate (PRPP) and the nitrogenous base orotic acid has been solved and refined with X-ray diffraction data extending to 2.3 A resolution to a crystallographic R-factor of 18.7%. The complex was generated by carrying out catalysis in the crystal. Comparison of this structure with the previously reported structure of the orotidine 5'-monophosphate (OMP) complex [Scapin, G., Grubmeyer, C., and Sacchettini, J. C. (1994) Biochemistry 33, 1287-1294] revealed that the enzyme backbone undergoes only small movements. The most significant differences occur near the active site, at Ala71-Gly74, with the largest difference involving the side chains of Lys73, Val127-Ala133, the 5'-phosphate binding loop, and a long, solvent-exposed loop at the dimer interface. The position of the ribose moiety is, on the other hand, very different in the OMP and PRPP.orotate complexes, with its anomeric carbon moving approximately 7 A across the binding cavity. In the PRPP.orotate complex the highly conserved acidic side chain of Asp124 interacts with the ribose of PRPP, whereas there are no interactions of this aspartate with the substrate in the OMP complex.

Binding Sites↗
PubMed1986

Pyruvate dehydrogenase and 3-fluoropyruvate: chemical competence of 2-acetylthiamin pyrophosphate as an acetyl group donor to dihydrolipoamide.

The pyruvate dehydrogenase component (E1) of the pyruvate dehydrogenase complex catalyzes the decomposition of 3-fluoropyruvate to CO2, fluoride anion, and acetate. Acetylthiamin pyrophosphate (acetyl-TPP) is an intermediate in this reaction. Incubation of the pyruvate dehydrogenase complex with 3-fluoro[1,2-14C]pyruvate, TPP, coenzyme A (CoASH), and either NADH or pyruvate as reducing systems leads to the formation of [14C]acetyl-CoA. In this reaction the acetyl group of acetyl-TPP is partitioned by transfer to both CoASH (87 +/- 2%) and water (13 +/- 2%). When the E1 component is incubated with 3-fluoro[1,2-14C]pyruvate, TPP, and dihydrolipoamide, [14C]acetyldihydrolipoamide is produced. The formation of [14C]acetyldihydrolipoamide was examined as a function of dihydrolipoamide concentration (0.25-16 mM). A plot of the extent of acetyl group partitioning to dihydrolipoamide as a function of 1/[dihydrolipoamide] showed 95 +/- 2% acetyl group transfer to dihydrolipoamide when dihydrolipoamide concentration was extrapolated to infinity. It is concluded that acetyl-TPP is chemically competent as an intermediate for the pyruvate dehydrogenase complex catalyzed oxidative decarboxylation of pyruvate.

Carbon Radioisotopes↗