The use of planar bone scintigraphy and HiSPECT for diagnosis of primary and concomitant flexor enthesopathy in the canine elbow

Objective: To investigate the possibilities and limitations of planar bone scintigraphy and high resolution single photon emission computed tomography (HiSPECT) to diagnose flexor enthesopathy and to distinguish primary flexor enthesopathy from the con: comitant form. Materials and methods: A prospective study of 46 dogs with primary flexor enthesopathy, concomitant flexor enthesopathy, medial coronoid disease, and normal elbows was performed. All dogs underwent planar bone scintigraphy and HiSPECT imaging. The obtained images were visually scored for increased radiopharmaceutical uptake in the, medial humeral epicondylar and medial coronoid process region using a score from 1-3. Results: Planar bone scintigraphy demonstrated increased radiopharmaceutical uptake in all diseased elbow joints, except for one. HiSPECT demonstrated increased radiopharmaceutical uptake of the medial humeral epicondyle in nearly all clinically affected joints with primary and concomitant flexor enthesopathy. Additional uptake of the medial coronoid process was recorded in all clinically affected joints with concomitant flexor enthesopathy and in six out of 18 with primary flexor enthesopathy. No difference in intensity of the uptake was noticed. Clinical significance: Planar bone scintigraphy allows the attribution of lameness to the elbow joint in cases of primary flexor enthesopathy with minimal or even absent radiographic changes. The more detailed HiSPECT enables the localization of pathology within the elbow joint and is a sensitive technique to detect flexor enthesopathy. However HiSPECT is insufficient to distinguish primary from concomitant flexor enthesopathy

Factor XIII Val34Leu mutation accelerates the development of fibrosis in patients with chronic hepatitis B and C

Aim: There is considerable variation in liver fibrosis stage and progression to cirrhosis among patients with chronic hepatitis B (CHB) or C (CHC). Coagulation pathway activity due to genetic variations could influence the rate of fibrosis. We investigated thrombotic risk factors and their association with the extent and progression of fibrosis in CHB or CHC patients. Methods: In total, 194 patients with CHB (n = 88) or CHC (n = 106) were included. Data on demographic and laboratory findings were collected. Liver biopsies were evaluated according to the Ishak classification system. Fibrosis progression rate (FPR), defined as ratio of fibrosis score to duration of infection, was determined for 131 patients. Prevalence of factor V Leiden, prothrombin G20210A, plasminogen activator inhibitor type-1 (PAI-1) 4G/5G and factor XIIIA Val34Leu mutations was evaluated. Results: Heterozygosity for factor V Leiden, prothrombin G20210A, PAI-1 4G/5G and factor XIIIA Val34Leu mutations was present in 3.1%, 2.1%, 49% and 28% of the patients, respectively. Factor XIII Val34Leu mutation was a risk for enhanced FPR (odds ratio 4.7; P = 0.01). In patients with both factor XIII Val34Leu and PAI-1 4G/5G mutations the risk of an accelerated FPR was further increased (odds ratio 5.0; P = 0.02). Mutations of the other thrombotic genes were not significantly associated with fibrosis stage and FPR. Conclusion: Our data show that factor XIII Val34Leu mutation alone or in combination with PAI-1 4G/5G mutation is a risk factor for an increased rate of liver fibrosis development in patients with CHB or CH