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PubMed1988

Calcium pyrophosphate dihydrate crystal deposition disease in the cervical ligamentum flavum.

The authors describe three cases of cervical radiculomyelopathy caused by calcium pyrophosphate dihydrate crystal deposition disease (CPPDcdd). Radiological investigations revealed nodular calcifications, 5 to 7 mm in diameter, in the cervical ligamentum flavum compressing the spinal cord. Light microscopic, scanning electron microscopic, and x-ray diffraction studies were performed on all three surgical specimens obtained by laminectomy. In two of the cases x-ray microanalysis and transmission electron microscope studies were also performed. This study defined the presence of two patterns of crystal deposition in the ligamentum flavum. One is a nodular deposit, in which hydroxyapatite crystals are seen in the central part of the nodules, with calcium pyrophosphate dihydrate (CPPD) being distributed thinly around them. The other pattern is a linear deposit seen in multiple ligaments and composed of pure CPPD, which causes minimal thickening of the ligaments. A transitional pattern between the two types was also observed. This study revealed details of the nodular deposition of crystals in the ligamentum flavum and demonstrates that CPPDcdd and so-called "calcification of the ligamentum flavum" are the same disease: namely, CPPDcdd. Hydroxyapatite is assumed to have been transformed from CPPD.

Aged↗
PubMed1975

Enzymic formation of thiamine pyrophosphate in plants.

Evidence was presented by paper chromatographic analysis on the occurrence of an enzyme capable of catalyzing a pyrophosphate transfer from ATP to thiamine in green leaves of various plants. The exclusive localization of the enzyme activity in the 105,000 X g supernatant (in a soluble form) was demonstrated by differential centrifugation of a cell homogentae in 0.25 M sucrose. The enzyme was purified by column chromatography with DEAE-cellulose and by gel filtration with Sephadex G-150. The partially pruified preparation, while contaminated with detectable activity of acid phosphatase, lost the ability of utilizing thiamine monophosphate as the substrate in place of thiamine. These findings lead to the conclusion that thiamine pyrophosphate is formed in green leaves of plants through a direct pyrophosphorylation of thiamine in the presence of ATP and Mg.

Acid Phosphatase↗
PubMed2000

[A case of sarcoid myopaty with external ocular muscle involvement--diagnosis and follow-up study with 99mTc pyrophosphate scintigraphy].

A 62-year-old woman was admitted to our hospital because of diplopia and muscular weakness. She had been diagnosed as having sarcoidosis histologically by skin biopsy 5 years before. Although neither CT nor MRI could detect the granulomas, 99mTc-pyrophosphate scintigraphy successfully detected the involvement of sarcoidosis not only in the skeletal muscles but also in the external ocular muscles. After treatment with prednisolone, the symptoms markedly subsided and increased uptake of radionucleotide disappeared. Although 67Ga scintigraphy is also known to be useful in investigating the sites affected by sarcoidosis throughout the body, it was not effective in detecting the involvement of external ocular muscle due to the physiological uptake of 67Ga to the lacrimal grands. While the granulomas are frequently observed histologically in skeletal muscles, usually they are not associated with muscle symptoms. In our study 99mTc-pyrophosphate scintigraphy has proven to be useful in investigating the nodular lesions in skeletal muscles of sarcoidosis than 67Ga scintigraphy.

Female↗
PubMed2002

Reduced serum concentrations of riboflavine and ascorbic acid, and blood thiamine pyrophosphate and pyridoxal-5-phosphate in geriatric patients with and without pressure sores.

BACKGROUND: Patients with pressure sores have as part of their treatment been reefed with energy and proteins with varying result. It has been uncertain, however, to what an extent these patients also were depleted of micronutrients which might be critical for ulcer healing. OBJECTIVE: To study the nutritional intake and nutritional status of a number of micronutrients in geriatric pressure sore patients and in matched controls. DESIGN: The nutritional intake and nutritional status as anthropometric measures, serum conc. of albumin, zinc, and of vitamins (ascorbic acid, riboflavin, calcidiol), were measured. Thiamin pyrophosphate and pyridoxal-5-phosphate were determined in whole blood from 11 geriatric in-patients with pressure sores and 11 matched controls. RESULTS: The serum conc. of ascorbic acid was significantly (p< 0.05) more reduced in pressure sore patients (mean+/-S.D.) 4.2+/-3.4 (ug/ml) than in control patients 7.4+/-5.4 (ug/ml) which still was lower than in a reference group (10.9+/-1.9) (ug/ml). In all the geriatric patients compared to the reference group, the conc. of serum-riboflavin was reduced to about 15 %, thiamine-pyrophosphate and pyridoxine-5-phosphate in whole blood and serum calcidiol to about 50 %, without any differences between the pressure sore patients and the matched controls. CONCLUSION: Refeeding of pressure sore patients who often are catabolic and have increased needs for protein and energy, should include micronutrients not only to cover recommended dietary allowances, but sufficient to reach normal nutritional status for the individual micronutrient.

Aged↗
PubMed2002

[Myocardial pyrophosphate uptake in cardiac amyloidosis: report of case].

We report a previously healthy 73 years old woman, who was hospitalised with increasing dyspnea and signs of congestive heart failure. Echocardiography showed a normal left ventricular cavity with increased echogenicity of its walls and severe pulmonary hypertension. A lung ventilation/perfusion scintigraphy concluded that there was a low probability for pulmonary embolism. Coronary angiography was normal. A restrictive cardiomyopathy due to amyloid deposits was suspected. Myocardial pyrophosphate scintigraphy showed intense pyrophosphate uptake in the left ventricle wall. An abdominal fat tissue biopsy was positive for amyloid deposits.

Aged↗
PubMed1992

Tumoral calcium pyrophosphate dihydrate deposition disease. Report of a case with a review of the literature.

In a 56-year-old female patient with a mass at the proximal end of the left third finger for 22 years, the lesion enlarged obviously during the last 4 years. Initial diagnosis was chondroma with malignant change, and disarticulation of the finger was performed. Pathological diagnosis was "secondary chondrosarcoma". Microscopically, the mass contained a large amount of amorphous basophilic phosphate deposits surrounded by fibrous capsule. The pyrophosphate deposits consisted of birefringent needle shaped or rhomboid crystals which can be identified by polarizing microscope. It can be distinguished as tumoral calcium pyrophosphate dihydrate deposition disease, differing from tophaceous pseudogout, tumoral calcinosis and chondrocalcinosis. Nine cases were collected from the literature and the clinical, radiological and pathological features were discussed.

Calcinosis↗
PubMed1992

[Clinical and prognostic value of myocardial scintigraphy using technetium Tc 99m pyrophosphate in patients with unstable stenocardia].

The clinical and predictive value of 99mTc pyrophosphate myocardial scintigraphy was studied in 164 patients with various clinical courses of unstable angina pectoris. Some patients with the unstable anginal syndrome proceeding with prolonged pain attacks were shown to have irreversible myocardial lesions detectable by 99mTc pyrophosphate myocardial scintigraphy. However, the study indicated that the presence of small myocardial necrotic foci in this case was of insignificant predictive value.

Adult↗
PubMed1991

Synovial fluid ATP: a potential substrate for the production of inorganic pyrophosphate.

The enzyme nucleoside triphosphate pyrophosphohydrolase (NTPPPH) is present in all joint fluids and on intraarticular cells. It generates inorganic pyrophosphate (PPi) from nucleoside triphosphate substrate, thus serving as a potential source of the PPi which forms in the cartilages of patients with calcium pyrophosphate dihydrate (CPPD) crystal deposition. NTPPPH is also important in matrix vesicle induced calcification with basic calcium phosphate (BCP) crystals. An articular substrate for this enzyme was sought. ATP was measured in the joint fluids from 107 patients with various forms of arthritis. Synovial fluid ATP levels were higher in patients with CPPD deposits than in osteoarthritis (p less than 0.02) or rheumatoid arthritis (p less than 0.002). ATP also correlated with PPi concentration (p less than 0.05) and with the presence of BCP crystals (p less than 0.05), but not with cellularity of the fluid, NTPPPH activity, or age of the donor. This substrate for NTPPPH may contribute to CPPD crystal deposition by generating PPi and may stimulate matrix vesicle induced formation of BCP crystals in several forms of arthritis.

Adenosine Triphosphate↗
PubMed1991

Alkaline phosphatase dissolves calcium pyrophosphate dihydrate crystals.

We have shown that yeast pyrophosphatase dissolves calcium pyrophosphate dihydrate (CPPD) crystals in solutions. In this investigation we demonstrate that alkaline phosphatase (ALP) effectively dissolves CPPD crystals in vitro. CPPD dissolution by ALP had a pH optimum of 7.4, which is the optimum pH for its pyrophosphatase (PPiase) activity. The CPPD dissolution and PPiase activity by ALP are magnesium dependent, whereas its phosphoester hydrolytic activity is not. Calcium, which inhibited the enzymatic CPPD dissolution and PPiase activity of ALP had no effect on its phosphoester hydrolytic activity. These data indicate that PPiase activity of ALP is responsible for CPPD dissolution and not its phosphoester hydrolytic activity. Matrix molecules such as proteoglycans and chondroitin sulfate had no effect on the enzymatic and nonenzymatic dissolution of CPPD crystals. ALP acted more effectively on CPPD crystals than on soluble pyrophosphate relative to yeast PPiase. Our data suggest that chondrocyte ALP may play an important role in the dissolution of CPPD crystals in cartilage.

Alkaline Phosphatase↗
PubMed1991

[Technetium-99m-pyrophosphate myocardial scintigraphy in polymyositis--a case report].

A patient with polymyositis who had cardiac involvement underwent myocardial scan with technetium-99m-pyrophosphate. We used Activity Index for evaluating myocardial uptake of technetium-99m-pyrophosphate, which correlated with the degree of serum creatine phosphokinase elevation. Our findings indicate that these examinations may be helpful for identifying patients who have cardiac involvement and evaluating their response to the treatment with corticosteroids or immunosuppressants.

Cardiomyopathies↗
PubMed1991

Myocardial distribution of indium-111-antimyosin Fab in acute inferior and right ventricular infarction: comparison with technetium-99m-pyrophosphate imaging and histologic examination.

In a postmortem study of a 69-yr-old female patient who had suffered 2 yr previously a non-Q-wave anterior infarction and who had sustained just seven days earlier a left inferior and right ventricular infarction, the distribution of 111In-antimyosin Fab was compared to the results of 99mTc-pyrophosphate imaging and histologic examination. Indium-111-antimyosin Fab imaging could not be performed because of cardiogenic shock. However, postmortem gamma scintillation counting revealed increased activities of antimyosin Fab in the inferoapical and right ventricular infarcted regions in which 99mTc-pyrophosphate positive imagings were observed; in contrast, a histologically confirmed old subendocardial anterior infarction had no definite activity. Thus, the myocardial distribution of 111In-antimyosin Fab corresponded well to the results of 99mTc scintigrams and histologic examinations in a human heart, suggesting that this technique could be useful in vivo for detecting several-day-old myocardial infarction of the right ventricle as well as the left ventricle. Tissue from the 2-yr-old infarction was not identified by this technique.

Aged↗
PubMed1991

Effects of pyrophosphatase on dissolution of calcium pyrophosphate dihydrate crystals.

Understanding the dissolution mechanisms involved in calcium pyrophosphate dihydrate (CPPD) crystals may prove important for the development of therapy for CPPD arthropathy. We demonstrate that yeast pyrophosphatase effectively dissolved CPPD crystals in solutions. Maximum enzymatic dissolution of CPPD crystals was achieved at neutral pH and when the enzyme had access to the crystal surface. The enzymatic dissolution of CPPD crystals was highly dependent on ambient [Mg++] and [Ca++]. The stimulating effects of Mg++ on crystal dissolution in the presence of the enzyme is due to stimulation of pyrophosphatase activity and to enhanced direct release of pyrophosphate ions from the crystal surface. The inhibiting effect of Ca++ on crystal dissolution by the enzyme is mainly due to the suppression of pyrophosphatase activity.

Calcium↗
PubMed1990

[Myocardial 99mTc-pyrophosphate scintigraphy during bicycle ergometry as a method of evaluating the severity of chronic ischemic heart disease].

The time course of myocardial 99mTc-pyrophosphate accumulation 1 hour after a bicycle ergometric test versus the resting scintigraphic findings was correlated with the severity of chronic coronary heart disease (CHD) and long-term prognosis. A group of the patients who had higher radiotracer accumulation following the exercise showed the most severe disease and unfavorable prognosis (in this group 19.4% deaths were observed during a three-year follow-up). A single administration of 99mTc-pyrophosphate followed by scintigraphy 2 hours after bicycle ergometry and repeated scintigraphy 1 hour later allows one to assess the time course of myocardial radiotracer accumulation and to judge how the myocardium is supplied by blood.

Adult↗
PubMed1990

[Myocardial 99mTc-pyrophosphate scintigraphy in acute heart infarct].

50 consecutive patients hospitalized because of suspected myocardial infarction were examined by 99mTc-pyrophosphate scintigraphy. The scans were interpreted blind by one of the authors. There were positive results in 17 of 21 patients with myocardial infarction (sensitivity 0.81). However, scintigraphy was also positive in 13 patients with no evidence of myocardial infarction as assessed by ECG and enzyme criteria (specificity 0.55). We conclude that, in our hospital, 99mTc-pyrophosphate myocardial scintigraphy did not contribute valuable information to the routine diagnosis of myocardial infarction.

Humans↗
PubMed1989

A histological study of calcium pyrophosphate dihydrate crystal-deposition disease.

Synovial, meniscal, articular cartilage, and other connective tissue from fifty-seven patients who had calcium pyrophosphate dihydrate crystal-deposition disease was examined by light microscopy, electron microscopy, and electron-probe microanalysis. Safranin O-positive hypertrophic chondrocytes that contained proteoglycans were observed in the tissues of each patient. Microcrystals that were suggestive of early precipitation of crystals were found in the degenerating matrix surrounding hypertrophic chondrocytes. The matrix contained electron-dense amorphous material, including proteoglycans and debris of cellular components. The microcrystals were often seen in contact with degenerating collagen fibers. There was never any histological evidence of formation of crystal in the areas that had no hypertrophic chondrocytes. Chondrocytes of this kind, surrounded by characteristic degenerating matrix, were never observed in the articular tissue from sixty-one patients who had only osteoarthritis. On the basis of our results, we speculate that electron-dense amorphous material containing proteoglycans and debris of cellular components, and the degenerating collagen fibers that were seen around the hypertrophic chondrocytes, may play important roles in the formation of calcium pyrophosphate dihydrate crystals.

Adult↗
PubMed1988

Calcium pyrophosphate crystal deposition: the effect of soluble iron in a kinetic study using a gelatin matrix model.

The kinetics of calcium pyrophosphate dihydrate (CPPD) crystal growth was studied by allowing calcium and pyrophosphate (PPi-4) ions to diffuse through a denatured collagen matrix (biological grade gelatin) in the presence of either ferric or ferrous ions. Ferric and, to some extent, ferrous ions blocked the migration of the PPi-4 diffusion gradient. This retardation in the [PPi-4] gradient led to numerous changes in the patterns of CPPD crystal formation. At the initial stages of crystal growth, the iron ions induced more crystal growth compared to control. At later incubation times, ferrous and ferric ions enhanced crystal growth at the expense of crystal nucleation. The presence of both ferrous and ferric ions resulted in the more rapid formation of the two crystals observed in vivo, triclinic CPPD and monoclinic CPPD. Further, both ferrous and ferric ions also reduced the solubility of the crystalline material in the broad diffuse band which formed when the Ca+2 and PPi-4 gradients first met. In this system, the presence of either ferrous or ferric ions increased the amount of hydroxyproline included in the crystalline precipitates. Iron was also incorporated into the crystals, particularly into the triclinic CPPD and monoclinic CPPD crystals.

Calcinosis↗
PubMed1988

Calcium pyrophosphate crystal deposition: the effect of monosodium urate and apatite crystals in a kinetic study using a gelatin matrix model.

The kinetics of calcium pyrophosphate dihydrate (CPPD) crystal growth was studied by allowing calcium and pyrophosphate (PPi-4) ions to diffuse through a denatured collagen matrix (biological grade gelatin) in the presence of either monosodium urate monohydrate (MSU) or hydroxyapatite (HA) crystals. In this in vitro model system, MSU crystals significantly altered the kinetics of PPi-4 ionic diffusion through the gelatin matrix by allowing the [PPi-4] gradient to fall off much more rapidly, suggesting an increased level of scavenging of PPi-4 ions into crystalline materials. Even more significantly, the presence of MSU crystals markedly influenced the crystal growth morphology of triclinic CPPD, producing that observed in vivo. A large number of epitaxially dimensional matches between MSU and triclinic (t) and monoclinic (m) CPPD were identified, suggesting that MSU crystals can epitaxially induce CPPD crystal growth. This finding supports the hypothesis that the association of urate gout and CPPD crystal deposition disease is based on the nucleating potential of MSU crystals for CPPD crystal growth. In contrast, the HA crystal structure did not appear to serve as a nucleating agent for CPPD crystals. However, HA crystals did serve as effective traps for PPi-4 ions and their presence led to more stable CPPD crystal growth.

Apatites↗