Author(s):  
Donald E.G. Griesdale ◽  
Mike Boyd ◽  
Ramesh L. Sahjpaul

AbstractBackground:Calcium pyrophosphate dihydrate deposition in the cervical spine is infrequently symptomatic. This is especially true at the craniocervical junction and upper cervical spine.Case Report:A 70-year-old previously healthy woman presented with a progressive cervical myelopathy of four months duration.Results:Examination revealed sensorimotor findings consistent with an upper cervical myelopathy. Radiological studies (plain radiographs, computed tomography, and magnetic resonance imaging) revealed C1-2 instability, and a well-defined extradural 3cm x 1cm retro-odontoid mass causing spinal cord compression. Transoral resection of the mass was performed followed by posterior C1-2 stabilization. Histological examination of the mass confirmed calcium pyrophosphate dihydrate deposition. Follow-up examination showed marked clinical and radiological improvement.Conclusion:Although uncommon, calcium pyrophosphate dihydrate deposition disease should be considered in the differential diagnosis of extradural mass lesions in the region of the odontoid.


Neurosurgery ◽  
1995 ◽  
Vol 37 (2) ◽  
pp. 335-339 ◽  
Author(s):  
Christopher I. Shaffrey ◽  
Edwin L. Munoz ◽  
Curtis L. Sutton ◽  
Sebastian R. Alston ◽  
Mark E. Shaffrey ◽  
...  

Neurosurgery ◽  
1995 ◽  
Vol 37 (2) ◽  
pp. 335???339 ◽  
Author(s):  
Christopher I. Shaffrey ◽  
Edwin L. Munoz ◽  
Curtis L. Sutton ◽  
Sebastian R. Alston ◽  
Mark E. Shaffrey ◽  
...  

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1765.1-1765
Author(s):  
D. Khalifa ◽  
K. Baccouche ◽  
N. El Amri ◽  
H. Zeglaoui ◽  
E. Bouajina

Background:Calcium pyrophosphate dihydrate crystal-deposits (CPPD) is a common crystal disease affecting men and women equally. It is normally seen in peripheral joints. Spine involvement is rare and may mislead the diagnosis.Objectives:To describe clinical, radiological and therapeutic findings of CPPD of the spine.Methods:A retrospective descriptive study was conducted in the rheumatology department of Farhat Hached Hospital, including patients diagnosed with CPPD of the spine over a period of 20 years (1998-2018). Data concerning clinical, radiological and therapeutic aspects of CPPD of the spine were callected from their medical files.Results:Twelve patients had a spinal localisation of CPPD. The mean age was 59.91±16.21 years. Patients were mainly women with a sex ratio men/women of 1:3. Mean duration of symptoms before the diagnosis was 27.08±25.69 months. Spinal presentation was the revealing symptom of CPPD in 45.5% of the cases. It affected the cervical spine in 66.7% and the lumbar spine in 33.3% of the cases. Spinal localisation of CPPD was associated with a peripheral arthropatyhy in 75% of the cases (the knees in 41.7%, wrists and hands in 66.6%, shoulders in 25% and the hips in 16.7%). Discovery of spinal CPPD was coincidental on plain radiographs in 16.7% of the cases. When symptomatic, the disease manifested itself as inflammatory pain in 72.7%, mechanical pain in 9.1% and both diurnal and nocturnal pain in 18.2% of the cases. Physical examination revealed stiffness of the spine in 58.3% of the patients. Fever was noted in 8.3% and deterioration of general condition with anorexia was reported in 25% of the patients. Neurological complications were represented by cervical myelopathy in 25%, sciatica in 8.3% and a case of unilateral ulnar nerve neuropathy was reported. Laboratory tests revealed inflammation in 50% of the cases. However, crystals were present in synovial fluid in only 25% of the patients. Spinal CPPD was visible on plain radiographs in 83.3% of the cases, showing calcified discs in 75% and signs of destruction in 16.7% of the cases. Peripheral calcifications were present in the wrists in 33.3% and the knees in 58.3% of the cases. Crow dens syndrome was reported in 16.7% of the patients. CT-scan helped the diagnosis of calcifications and crown dens syndrome when performed. MRI was prescribed in 58.3% of the patients and characterized the cervical myelopathy. Treatment relied on analgesics in all patients, NSAIDS were prescribed in 83.3%, colchicine in 66.7% and general corticosteroids in 25% of the cases. Spinal immobilization was recommended in 25% of the cases for a short period. Spinal CPPD was idiopathic in 75%, secondary to hyperparathyroidism in 8.3% of the cases and familial cases were detected in 16.7% of the patients.Conclusion:Axial CPPD is rare and is an under-recognized entity that should be considered in elderly patients with neck or back pain. It can involve the discs or ligaments. The crown dens syndrome is quite suggestive of the diagnosis. If spinal CPDD is suspected, colchicine therapy could be a good therapeutic test and would avoid unnecessary further tests.References:[1]Ferrone C, Andracco R, Cimmino MA. Calcium pyrophosphate deposition disease: clinical manifestations. Reumatismo. 19 janv 2012;63(4):246‑52.[2]Feydy A, Lioté F, Carlier R, Chevrot A, Drapé J-L. Cervical spine and crystal-associated diseases: imaging findings. Eur Radiol. févr 2006;16(2):459‑68.Disclosure of Interests:None declared


1998 ◽  
Vol 39 (3) ◽  
pp. 269-272
Author(s):  
H. Mizutani ◽  
S. Ohba ◽  
M. Mizutani ◽  
S. Sasaki ◽  
K. Ando ◽  
...  

2021 ◽  
Vol 9 (7) ◽  
pp. e002716
Author(s):  
Sang T. Kim ◽  
Jean Tayar ◽  
Siqing Fu ◽  
Danxia Ke ◽  
Elliot Norry ◽  
...  

With durable cancer responses, genetically modified cell therapies are being implemented in various cancers. However, these immune effector cell therapies can cause toxicities, including cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS). Pseudogout arthritis is an inflammatory arthritis induced by deposition of calcium pyrophosphate dihydrate crystals. Here, we report a case of pseudogout arthritis in a patient treated with MAGE-A4 directed T cell receptor T cells, for fallopian tube cancer. The patient developed CRS and ICANS 7 days after infusion of the T cells. Concurrently, the patient newly developed sudden onset of left knee arthritis. Synovial fluid analyses revealed the presence of calcium pyrophosphate dihydrate crystal. Notably, the pseudogout arthritis was resolved with tocilizumab, which was administered for the treatment of CRS and ICANS. Immunoprofiling of the synovial fluid showed that the proportion of inflammatory interleukin 17 (IL-17)-producing CD4+ T (Th17) cells and amount of IL-6 were notably increased, suggesting a potential role of Th17 cells in pseudogout arthritis after T-cell therapy. To the best of our knowledge, this is the first reported case of pseudogout arthritis after cell therapy. Clinicians, especially hematologists, oncologists and rheumatologists, should be aware that pseudogout arthritis can be associated with CRS/ICANS.


2020 ◽  
Vol 22 (1) ◽  
pp. 262
Author(s):  
Nobuyuki Onai ◽  
Chie Ogasawara

Calcium pyrophosphate dihydrate (CPPD) crystals are formed locally within the joints, leading to pseudogout. Although the mobilization of local granulocytes can be observed in joints where pseudogout has manifested, the mechanism of this activity remains poorly understood. In this study, CPPD crystals were administered to mice, and the dynamics of splenic and peripheral blood myeloid cells were analyzed. As a result, levels of both granulocytes and monocytes were found to increase following CPPD crystal administration in a concentration-dependent manner, with a concomitant decrease in lymphocytes in the peripheral blood. In contrast, the levels of other cells, such as dendritic cell subsets, T-cells, and B-cells, remained unchanged in the spleen, following CPPD crystal administration. Furthermore, an increase in granulocytes/monocyte progenitors (GMPs) and a decrease in megakaryocyte/erythrocyte progenitors (MEPs) were also observed in the bone marrow. In addition, CPPD administration induced production of IL-1β, which acts on hematopoietic stem cells and hematopoietic progenitors and promotes myeloid cell differentiation and expansion. These results suggest that CPPD crystals act as a “danger signal” to induce IL-1β production, resulting in changes in course of hematopoietic progenitor cell differentiation and in increased granulocyte/monocyte levels, and contributing to the development of gout.


2004 ◽  
Vol 71 (5) ◽  
pp. 365-368 ◽  
Author(s):  
Patrick Netter ◽  
Thomas Bardin ◽  
Arnaud Bianchi ◽  
Pascal Richette ◽  
Damien Loeuille

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