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Results for “Calcium Pyrophosphate”

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At least 289 records · Page 16Linked to original sources
PubMed1999

Exclusion of the gene for human cartilage intermediate layer protein in currently mapped calcium pyrophosphate dihydrate deposition syndromes.

OBJECTIVE: To map the gene for human cartilage intermediate layer protein (CILP) in order to assess its involvement in some familial forms of calcium pyrophosphate dihydrate (CPPD) deposition disease. METHODS: A radiation hybrid panel was analyzed for chromosomal assignment of the CILP gene within a 1-cM limit of resolution. The location of the gene for CILP was confirmed to reside at the observed radiation hybrid locus by fluorescence in situ hybridization. RESULTS: The human CILP gene resides at chromosome 15q21. CONCLUSION: This map location definitively excludes mutations in the CILP gene as the cause of certain familial forms of CPPD deposition disease that have been genetically mapped to chromosomes 8q and 5p.

Base Sequence↗
PubMed1976

Pseudotumor of temporomandibular joint: destructive calcium pyrophosphate dihydrate arthropathy.

The clinical and pathological features of a tumor of the temporamandibular joint occurring in a 55 year old man, and subsequently identified as a calcium pyrophosphate dihydrate (CPPD) arthropathy, are reported. Crystalline deposits were identified by compensated light microscopy and confirmed with X-ray diffraction, transmission, and scanning electron microscopy. The relationship of this unique case to other clinical presentations of CPPD deposition disease and the implications of the histological features to the pathogenesis of pseudogout are discussed. This case demonstrates that CPPD arthropathy should be included in the differential diagnosis of an arthrosis or of a tumor involving the temporomandibular joint.

Arthritis↗
PubMed2005

Foraminal deposition of calcium pyrophosphate dihydrate crystals in the thoracic spine: possible relationship with disc herniation and implications for surgical planning. Report of two cases.

The authors report two cases of nodular calcium pyrophosphate dihydrate (CPPD) crystal deposition close to the thoracic neural foramen, which caused chronic radiculopathy. Preoperatively, the lesions were interpreted as calcified disc herniations. Both patients underwent surgery in which an extended transfacet pedicle-sparing approach was used. Incision of the posterior longitudinal ligament released soft degenerated material. In both cases, histological examination showed abundant degenerative debris along with CPPD crystals. Spinal CPPD deposition is a comparatively rare disease that almost invariably involves the posterior aspect of the spinal canal, typically the ligamentum flavum. The exceptional foraminal location of the lesions reported here, combined with the surgical findings, indicated that the CPPD crystals were deposited on a laterally herniated disc fragment. A distinctive feature in both cases was the soft consistency of the resected tissue. The consistency of the disc material and the location of the lesion in the axial plane (that is, median compared with lateral) are key factors in determining the optimal surgical approach to thoracic disc herniations. In describing consistency, terms such as "calcified" and "hard" have been used interchangeably in the literature. In the cases reported here, what appeared on computerized tomography and magnetic resonance imaging studies to be densely calcified lesions were shown intraoperatively to be soft herniations. The authors' experience underscores that not all densely calcified herniated discs are hard. Although detection of this discrepancy would have left surgical planning for the lateral disc herniations unchanged, it could have altered planning for centrally or centrolaterally located disc herniations.

Adult↗
PubMedDate not supplied

Management of a patient with calcium pyrophosphate deposition disease and meniscal tear of the knee: a case report.

OBJECTIVE: To describe the chiropractic management of a patient suffering from a right lateral meniscus tear concurrent with calcium pyrophosphate dihydrate (CPPD) deposition disease. CLINICAL FEATURES: A 51-yr-old bus driver suffered from right knee pain (7 on a 1-10 pain scale). The onset of the pain was gradual and increased during braking and accelerating. Palpatory tenderness was noted at the right lateral knee joint line and the inferior lateral margin of the patella. Active resistive range of motion (ROM) in the knee during extension was painful throughout the full ROM, whereas passive ROM was restricted in flexion at 110 degrees. A positive McMurray's test reproduced pain at the knee. Radiographic analysis revealed CPPD deposition disease, and magnetic resonance imaging revealed a probable "parrot's beak" tear in the posterior horn of the right lateral meniscus. INTERVENTION AND OUTCOME: The patient was treated conservatively. He was instructed not to put weight on the knee and not to return to work for 5 days. Initial treatments involved the use of ice and interferential electrical stimulation along with glucosamine sulfate supplements. Bicycling, weight lifting for general fitness and general knee strengthening exercises were prescribed. Approximately 5 months after initial treatment, the patient was lost to follow-up; 12 months later, he returned for treatment because of a recurrence. Physical examination at that time revealed knee pain rated at 3/10 but there was no pain upon palpation, McMurray's test was negative and right knee ROM was full without pain. CONCLUSION: A patient suffering from CPPD can be managed by conservative means. The pathophysiology, clinical features and management considerations in the treatment of the patient's condition(s) are also discussed.

Chiropractic↗
PubMed1995

Calcium pyrophosphate dihydrate crystal deposition disease: a review of the literature and a light and electron microscopic study of a case of the temporomandibular joint with numerous intracellular crystals in the chondrocytes.

The pathogenesis of calcium pyrophosphate dihydrate (CPPD) crystal deposition disease of synovial joints is still unclear, although overproduction of extracellular pyrophosphate (PPi) is thought to play a key role. We studied the light and electron microscopic appearances of a case of CPPD crystal deposition disease of the temporomandibular joint (TMJ) in search of new clues for its pathogenesis. Light microscopic examination of CPPD-containing material from the joint space revealed cartilaginous nodules with various degrees of crystallization. Transmission electron microscopic examination revealed numerous extra- as well as intracellular crystals and crystal shaped spaces in the chondrocytes. Other striking ultrastructural features of the chondrocytes included the presence of many mitochondria, frequently containing crystalline material, and the presence of highly dilated rough endoplasmic reticulum and large glycogen islands. The presence of intramitochondrial crystals may hypothetically imply a derangement in mitochondrial adenosine triphosphate or PPi metabolism. The finding of intracellular CPPD crystals in chondrocytes points to the existence of an intracellular pathway of CPPD crystal formation in CPPD crystal deposition disease of the TMJ and possibly in CPPD crystal deposition disease in general.

Cartilage, Articular↗
PubMed1998

Serum nucleotide pyrophosphohydrolase activity; elevated levels in osteoarthritis, calcium pyrophosphate crystal deposition disease, scleroderma, and fibromyalgia.

OBJECTIVE: Quantification of serum nucleotide pyrophosphohydrolase (NTPPHase) activity in healthy subjects and in patients with various rheumatic diseases or with quad/hemiplegia, hemodialysis, or renal transplant. METHODS: Colorimetric assay of enzyme activity in serum. RESULTS: Serum NTPPHase activity in 85 healthy subjects was independent of age or sex and was highly reproducible in each individual. The biologic and methodologic coefficients of variation were nearly identical. Elevated enzyme levels were found in sera from patients with osteoarthritis/spondylosis, calcium pyrophosphate dihydrate (CPPD) crystal deposition, scleroderma, fibromyalgia, or hemodialysis. Renal transplant patients receiving cyclosporine had the highest enzyme activity of any group, whereas transplant patients not taking this drug had normal levels. Histograms of values in all groups showed a normal distribution. CONCLUSION: Serum NTPPHase activity levels were significantly elevated in patients with degenerative arthritis whether or not CPPD crystals were present, in patients with either scleroderma or fibromyalgia, and in patients receiving hemodialysis therapy or taking cyclosporine.

Chondrocalcinosis↗
PubMed2005

Rehabilitation of orthopedic and rheumatologic disorders. 4. Rheumatoid arthritis and calcium pyrophosphate deposition disease.

UNLABELLED: This self-directed learning module highlights a clinical vignette of 2 patients: (1) a woman with bilateral, distal, upper-limb pain assessed by differential diagnosis, laboratory work-up, and treatment of rheumatologic disorders frequently seen in the physiatric practice setting and (2) a 57-year-old man with an acute recurring monoarthritis of the knee and addresses clinical presentation, assessment, medical management, and rehabilitation approaches. It is part of the chapter on rehabilitation of orthopedic and rheumatologic disorders in the Self-Directed Physiatric Education Program for practitioners and trainees in physical medicine and rehabilitation. This article specifically focuses on 2 aspects: (1) the differential diagnosis of polyarthralgia, distal upper-limb pain, criteria for classification of rheumatoid arthritis, synovial fluid analysis, and comprehensive treatment of rheumatoid arthritis, both pharmacologic and nonpharmacologic and (2) the differential diagnosis, clinical diagnostic considerations, current pharmacotherapy, invasive procedure options, and orthotic and exercise interventions for a patient with calcium pyrophosphate dehydrate-induced monoarthritis of the knee. OVERALL ARTICLE OBJECTIVES: (a) Clinical evaluation, diagnosis, management, and rehabilitation strategies in persons with initial presentations of inflammatory distal upper-limb pain and (b) clinical evaluation of an individual with crystal-induced monoarthritis and differentiation of the pathophysiology, assessment, and treatment of chondrocalcinosis.

Adult↗
PubMed1986

The deposition of calcium pyrophosphate by NTP pyrophosphohydrolase of matrix vesicles from fetal bovine epiphyseal cartilage.

About 5 mumol CaPPi/mg protein was deposited within 3 h in the presence of the reaction mixtures containing 1 mM ATP, 2 mM Ca2+, 1 mM Pi, and 17 micrograms of purified NTP pyrophosphohydrolase. At 1 mM ATP, 50% of the deposition was inhibited by 0.5-1 mM of various substrate and product analogues including AMP, ADP, and ethylene hydroxyl diphosphonate. The magnitude of inhibition on NTP pyrophosphohydrolase activity was in the order of AMP = CMP = ADP greater than adenosine greater than adenine greater than NAD = NADP. AMP, CMP, ADP, and adenosine are competitive inhibitors. The modes of inhibition by adenine, NAD, and NADP differ from the competitive inhibition. Ribose, 3'-AMP, 2'-AMP, and cAMP did not inhibit the enzyme activity.

Adenosine Triphosphate↗