Ten commercially available parathormone (PTH) assays were competitively validated, using dilutional parallelism, intra-assay and interassay coefficients of variation, and sensitivity and measured responses of 2 dogs to calcium and EDTA infusions. A 2-site immunoradiometric assay for intact human-PTH was superior to the others for estimating canine-PTH, met the criteria for validity, and was further investigated. A series of sample-handling studies was performed. Serum and plasma samples stored at 24 C lost 15% (n = 5; P less than 0.05) of PTH between 2 and 24 hours. This did not occur at 6 C. The mean PTH concentration of sera from blood samples clotted at 24 C was 6% (P less than 0.05) higher than equivalent EDTA samples. Serum samples stored at 6 and 37 C deteriorated 35% and 100% (n = 5; P less than 0.05), respectively, after 1 week, whereas samples stored at -20 and -70 C for 4 weeks did not deteriorate. There was no significant deterioration of PTH in samples frozen (-40 C) and thawed up to 7 times (n = 5). Parathyroid function testing was investigated by use of 2-hour infusions of disodium EDTA (25 mg/kg/h), 10-minute infusions of calcium gluconate (3 mg of elemental calcium/kg/10 min), and physiologic saline controls (n = 8). Renal function was monitored before and after EDTA infusion by exogenous creatinine clearance. Infusion of disodium EDTA increased mean PTH concentration from 67 (time 0) to 317 and 235 pg/ml at 90 and 180 minutes, respectively (P less than 0.001). Infusion of calcium gluconate decreased mean PTH concentration from 84 (time 0) to 14 and 12 pg/ml at 15 and 60 minutes, respectively (P less than 0.005). There were no observable side effects of the infusions in normal conscious dogs and no differences in exogenous creatinine clearance after EDTA infusion.

An 8-year-old, castrated male, Schnauzer dog was presented for evaluation of gradually worsening erythematous papules. Physical examination revealed multiple erythematous papules having a firm, gritty texture located in bilateral ears, dorsal midline, perianal and inguinal area. Skin biopsy revealed aberrant structure, characterized by atrophic epidermal-dermal layer structure with granular materials which was presumed as calcinosis cutis secondary to iatrognic hyperadrenocotricism. By initiating minocycline for 14 days, there was reduction in size, number of calcium deposit with remarkably decreased erythema. This case report presents the clinical trial of minocycline as a potential agent in treating dogs with calcinosis cutis.

Of 143 Greyhounds necropsied consecutively, 6 (4%) had chondrocalcinosis of the scapulohumeral joint; lesions were identified in 6 additional dogs. Lesions were seen exclusively in the humeral head, mainly in the plateau region. The lesions in the dogs of the initial group were unilateral, but 2 of the 6 additional dogs had bilateral lesions. Focal mineralization of articular cartilage appeared as a white raised nidus, sometimes surrounded by a translucent halo in the opaque cartilage. Circular, small translucent cartilage foci, with or without beginning mineralization, were adjacent to definitive chondrocalcinosis lesions. Chondrocyte necrosis and matrix degradation were considered to antedate appearance of matrical mineral granules; mineralization of the cartilage was considered a secondary process, but not necessarily an epiphenomenon. Scanning electron microscopy indicated that the chondrocalcinosis lesion was composed of deposits of irregularly fused stone material that, in scanning and transmission electron micrographs, was composed of irregular spheroids, 0.05 to 0.5 micrometer in diameter. The spheroids contained poorly formed needle-like crystals of apatite. Sparse transformation of the mineral phase into hydroxyapatite was considered to be attributable to a biological mechanism that inhibited phase transition. Cartilage degeneration and chondrocalcinosis of the plateau region of the humeral head appear to be unique lesions that develop in young Greyhounds. It is possible that these lesions are the result of the biomechanical stress of training and racing.

Ten commercially available parathormone (PTH) assays were competitively validated, using dilutional parallelism, intra-assay and interassay coefficients of variation, and sensitivity and measured responses of 2 dogs to calcium and EDTA infusions. A 2-site immunoradiometric assay for intact human-PTH was superior to the others for estimating canine-PTH, met the criteria for validity, and was further investigated. A series of sample-handling studies was performed. Serum and plasma samples stored at 24 C lost 15% (n = 5; P less than 0.05) of PTH between 2 and 24 hours. This did not occur at 6 C. The mean PTH concentration of sera from blood samples clotted at 24 C was 6% (P less than 0.05) higher than equivalent EDTA samples. Serum samples stored at 6 and 37 C deteriorated 35% and 100% (n = 5; P less than 0.05), respectively, after 1 week, whereas samples stored at -20 and -70 C for 4 weeks did not deteriorate. There was no significant deterioration of PTH in samples frozen (-40 C) and thawed up to 7 times (n = 5). Parathyroid function testing was investigated by use of 2-hour infusions of disodium EDTA (25 mg/kg/h), 10-minute infusions of calcium gluconate (3 mg of elemental calcium/kg/10 min), and physiologic saline controls (n = 8). Renal function was monitored before and after EDTA infusion by exogenous creatinine clearance. Infusion of disodium EDTA increased mean PTH concentration from 67 (time 0) to 317 and 235 pg/ml at 90 and 180 minutes, respectively (P less than 0.001). Infusion of calcium gluconate decreased mean PTH concentration from 84 (time 0) to 14 and 12 pg/ml at 15 and 60 minutes, respectively (P less than 0.005). There were no observable side effects of the infusions in normal conscious dogs and no differences in exogenous creatinine clearance after EDTA infusion.