| A 66-year-old woman, diagnosed with chronic thyroiditis at age 63, presented with anorexia and fatigue. Therapy for the chronic thyroiditis consisted of levothyroxine sodium (100 microg/day). Her symptoms were attributed to the insufficient supply of levothyroxine sodium. Following a dosage increase to 150 microg/day, she suffered from an acute attack of pseudogout. Clinical features were complicated by sjogren's syndrome, which appeared after treatment onset. Pseudogout was effectively treated by colchicine after administration of diclofenac sodium failed to alleviate the symptoms. Pseudogout is a recognized complication of thyroid replacement therapy, but association with sjogren's syndrome has not been previously reported. ( info) |
| A case of pseudogout occurring in the temporomandibular joint of a 76-year-old man is reported. The diagnostic work-up and its differential diagnosis is discussed. ( info) |
| In this retrospective study of 57 patients with primary hyperparathyroidism who underwent parathyroidectomy, the overall incidence of chondrocalcinosis was 40%. Neither joint symptoms nor chondrocalcinosis regressed after the operation. In several patients the condition appeared to deteriorate both clinically and radiologically after the operation, while in a few both the chondrocalcinosis and the associated symptoms first appeared some time after the operation. ( info) |
4/186. Posterior interosseous nerve syndrome due to pseudogout. Posterior interosseous nerve palsy associated with pseudogout of the elbow joint in a 71-year-old woman is described. Local steroid injection and administration of a nonsteroidal anti-inflammatory drug was effective in treatment. ( info) |
5/186. Destructive tophaceous calcium hydroxyapatite tumor of the infratemporal fossa. Case report and review of the literature. Tophaceous pseudogout is one of the rarest forms of crystal deposition disease, typically presenting as a destructive and invasive mass involving the temporomandibular joint or the infratemporal fossa region in the absence of any other articular manifestations. Previous cases have been assumed to be caused by calcium pyrophosphate dihydrate (CPPD) crystal deposition, based on finding weakly birefringent crystals in the involved tissues. The authors present the unique case of a 65-year-old woman with a destructive and invasive facial mass extending to the middle cranial fossa with microscopic and clinical features consistent with tophaceous pseudogout. High-resolution x-ray crystallographic powder diffraction and Fourier transformed infrared spectroscopy subsequently revealed that the crystals were composed of calcium hydroxyapatite without CPPD. The patient was later found to have primary hyperparathyroidism and mild hypercalcemia. This case demonstrates that tissue deposits of calcium hydroxyapatite can cause a destructive and invasive mass containing weakly birefringent crystals and raises the question of whether previous cases attributed to tophaceous pseudogout resulting from CPPD actually were composed of birefringent calcium hydroxyapatite. ( info) |
6/186. Acute sacroiliitis as a manifestation of calcium pyrophosphate dihydrate crystal deposition disease. While radiographic lesions of the sacroiliac joint (SIJ) are common in patients with calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, they are rarely accompanied by clinical symptoms. We report the case of a 69-year-old woman who presented with an acute sacoiliitis and a linear calcification in the right SIJ on CT scan. The patient recovered well after intra-articular steroid injections. ( info) |
| The term chondrocalcinosis is often used to describe the radiological or pathological features of calcified joint cartilage, and it usually indicates the deposition in cartilage of calcium pyrophosphate dihydrate. The prevalence of chondrocalcinosis increases with age, with dramatic increases occurring in the decades past age 60. In younger patients with chondrocalcinosis, either clinical evidence of associated metabolic diseases leading to the chondrocalcinosis or familial disease occurrence usually can be detected. We report a 42-year-old Chinese woman with ankylosing spondylitis and arthritis involving multiple peripheral joints. Severe chondrocalcinosis was detected incidentally in this patient, however, subsequent studies revealed no associated metabolic disease or familial susceptibility and the clinical features of this patient were different from those of ankylosing chondrocalcinosis (pseudoankylosing spondylitis). The cause of chondrocalcinosis in this patient remains unknown, but joint damage and repair could have been initiating or aggravating factors of the chondrocalcinosis. ( info) |
8/186. calcium pyrophosphate dihydrate deposition disease causing thoracic cord compression: case report. OBJECTIVE AND IMPORTANCE: calcium pyrophosphate dihydrate (CPPD) deposition disease is being increasingly recognized. Spinal involvement in CPPD deposition disease is rare. When involved, the cervical and lumbar regions are commonly affected. We report a rare case of CPPD deposition disease that caused thoracic cord compression. CLINICAL PRESENTATION: A 45-year-old woman presented with clinical features suggestive of thoracic cord compression. Radiographic findings were consistent with calcification of the ligamenta flava in the lower thoracic levels causing cord compression. Calcification of the ligamentum flavum is commonly attributed to CPPD deposition disease. Evaluation for conditions that might be associated with CPPD deposition disease proved to be negative. INTERVENTION: laminectomy with removal of the calcified ligamenta flava was performed. Histopathological examination of the excised ligaments revealed evidence of CPPD crystals. Postoperatively, the patient's spasticity decreased and sensations improved, with no significant improvement in motor power. CONCLUSION: Calcification of the ligamenta flava due to CPPD deposition disease is a rare cause of thoracic cord compression. CPPD deposition disease should be entertained in the differential diagnosis of thoracic cord compression. ( info) |
9/186. Acute adrenal crisis in a patient treated with intraarticular steroid therapy. Intraarticular therapy with corticosteroids can cause systemic effects such as decreased concentration of plasma cortisol, but whether this might place a patient at risk from stress induced acute adrenal failure is not known. We describe a patient who presented with lethargy, hyponatremia, and then with acute abdomen. The diagnosis of acute adrenal crisis was related to suppression of the hypothalamic-pituitary-adrenal axis by intraarticular use of corticosteroid. This was confirmed by a low basal cortisol concentration and by a short Synacthen test that elicited an increase in plasma cortisol concentration from 36 to 481 nmol/l. Within 24 h of receiving 37.5 mg of hydrocortisone, the patient rapidly improved. ( info) |
| A case of calcium pyrophosphate dihydrate (CPPD) crystal deposition arthropathy of the temporomandibular joint is reported. The patient presented a 10-year history of swelling and pain of the left preauricular region. Magnetic resonance imaging showed a calcified mass filling the joint space and destroying the roof of the joint. Radiographs showed chondrocalcinosis of other joints. The authors discuss the diagnosis of this arthropathy and the reason why the temporomandibular joint is more affected than the other joints in the patient reported. ( info) |