Analysis of complications in 97 periprosthetic Vancouver B2 fractures treated either by internal fixation or revision arthroplasty.

INTRODUCTION: The treatment of Vancouver B2 periprosthetic fractures after hip arthroplasty is still a matter of debate. Revision Arthroplasty (RA) was long thought to be the treatment of choice, however several recent papers suggested that Open Reduction and Internal Fixation (ORIF) is a viable option for selected B2 fractures. Complication rates of 14-26% have been reported following surgical treatment of B2 fractures. No significant difference between RA and ORIF in the complication rates nor in the functional outcome was observed. METHOD: We conducted a retrospective analysis of 97 consecutive Vancouver B2 fractures treated according to the algorithm at our institution from 2007 to 2020 and recorded complications and patient specific data. RESULT: From the 97 patient, 45 fractures were treated with RA while 52 fractures were treated with ORIF. Thirteen patients in the RA group had a complication that needed revision (28%) and 11 patients in the ORIF group needed revision (21%). There was no significant difference between complication rates. The reason for failure in the 13 RA patients were infection (n = 4), stem subsidence (n = 1), refracture after a new fall (n = 3), secondary dislocation of the greater trochanter (n = 1) and dislocation (n = 4). The reason for failure in the 11 ORIF patients that were revised were infection (n = 5), persistent symptomatic stem loosening (n = 3) and refracture (n = 3) after a new fall. CONCLUSION: ORIF can be used to revise cemented and non-cemented shafts in more than half of Vancouver B2 fractures with no difference in complication rates when compared to RA. A periprosthetic fracture around the hip has a 21-28% risk of a re-operation after revision surgery with infection and re-fracture after a new fall being the most frequent cause of re-operation.

[Reconstruction of osseous defects using the Masquelet technique]. / Rekonstruktion ossärer Defekte mit der Masquelet-Technik.

The Masquelet procedure or induced membrane technique presents a treatment option for relatively large osseous defects, e.g. after trauma, tumour resection or osteomyelitis even in the presence of unfavourable soft tissues. Initially developed at the end of the last century by the French surgeon Masquelet, the technique relies on a bioactive membrane that forms a foreign body reaction around a cement spacer. This spacer is implanted in the residual defect after rigorous debridement of bone and soft tissue during a first-stage procedure. A second-stage intervention is performed 1-2 months later with removal of the spacer under preservation of the membrane that has since formed around the cement. The membrane acts as an internal bioreactor exerting its effect via a rich vascularization and secretion of growth and differentiation factors. The void within the membrane is filled with an autologous cancellous graft. After adequate stabilisation using standard techniques, a gradual corticalisation of the graft can be observed over the duration of several months, with remodelling in the long-term course.The following article describes the original technique, our preferred approach including indication, surgical technique and postoperative follow-up. Additionally, the biological background and clinical tips and tricks are presented.

Three-dimensional microstructural properties of regenerated mineralizing tissue after PTH (1-34) treatment in a rabbit tibial lengthening model.

UNLABELLED: Since the approval of parathyroid hormone (PTH) as treatment for osteoporosis, PTH has increasingly been investigated for bone repair and regeneration. The aim of the study was to investigate the effects of intermittent PTH treatment on the microstructure of regenerated mineralizing tissue after distraction osteogenesis in rabbits. After tibial mid-diaphyseal osteotomy the callus was distracted 1 mm/day for 10 days. 72 rabbits were divided in to 3 groups, which daily received a PTH (1-34) 25 microg/kg injection for 30 days; a saline injection for 10 days and a PTH injection for 20 days; or a saline injection for 30 days. The microstructure of the regenerate was assessed by micro computed tomography (microCT). In all 51 obtained specimens were evaluated morphometrically using three different volumes of interests. The results showed that treatment with PTH during distraction osteogenesis resulted in a significantly higher trabecular number, a more isotropic trabecular orientation, a higher connectivity density, and a higher mineralizing tissue mass. We also found that distraction calluses treated with PTH were more mature than the non-treated. CONCLUSION: treatment with PTH resulted in an enhanced microstructure of the newly regenerated mineralizing tissue indicating that PTH has a potential role as a stimulating agent during distraction osteogenesis.

Recombinant human vascular endothelial growth factor enhances bone healing in an experimental nonunion model.

The re-establishment of vascularity is an early event in fracture healing; upregulation of angiogenesis may therefore promote the formation of bone. We have investigated the capacity of vascular endothelial growth factor (VEGF) to stimulate the formation of bone in an experimental atrophic nonunion model. Three groups of eight rabbits underwent a standard nonunion operation. This was followed by interfragmentary deposition of 100 microg VEGF, carrier alone or autograft. After seven weeks, torsional failure tests and callus size confirmed that VEGF-treated osteotomies had united whereas the carrier-treated osteotomies failed to unite. The biomechanical properties of the groups treated with VEGF and autograft were identical. There was no difference in bone blood flow. We considered that VEGF stimulated the formation of competent bone in an environment deprived of its normal vascularisation and osteoprogenitor cell supply. It could be used to enhance the healing of fractures predisposed to nonunion.

Effects of simvastatin on lipoprotein (a) and lipoprotein composition in patients with nephrotic syndrome.

The influence of simvastatin, a competitive inhibitor of 3-hydroxy-3-methyl glutaryl coenzyme A reductase, on quantitative and qualitative changes in lipoprotein metabolism was investigated in 18 patients (group I, 10 with primary kidney disease and group II, 8 with diabetic nephropathy) with nephrotic syndrome. Nephrotic patients exhibited severe hyperlipidemia (serum cholesterol 390 +/- 17 mg/dl and triglyceride 335 +/- 42 mg/dl; mean +/- SEM) and had significantly higher lipoprotein (a) [Lp(a)] levels (54 +/- 12 mg/dl; median 31 mg/dl, p < 0.01) compared with 20 healthy subjects (mean 12 +/- 1.8 mg/dl; median 7 mg/dl). Fifty-six percent of the patients and 15% of the controls had values greater than 30 mg/dl. Treatment with simvastatin in increasing doses over a period of three months (13 patients received 40 mg/day and 5 patients 20 mg/day at the end of the third month) reduced LDL-cholesterol in both groups of patients (35% and 54%) as well as apolipoprotein B (apoB) (31% and 46%) significantly, but Lp(a) levels were not influenced (57 +/- 21 vs 59 +/- 20 and 50 +/- 14 vs 53 +/- 16 mg/dl, respectively). On the other hand a complex change in lipoprotein composition occurred. The ratio of LDL apoB/LDL cholesterol-ester increased significantly (0.75 +/- 0.03 to 0.84 +/- 0.03 and 0.80 +/- 0.03 to 1.02 +/- 0.1, respectively) and cholesterol concentration in VLDL (64 +/- 16 to 39 +/- 7 and 74 +/- 18 to 55 +/- 74 mg/dl, respectively) was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium antagonists increase the amount of mRNA for the low-density lipoprotein receptor in skin fibroblasts.

The effects of calcium antagonists on the amount of LDL-receptor (LDL-R) mRNA in cultured human fibroblasts was examined by hybridization with a fragment of LDL-R cDNA. In a 'Northern' blot the fragment hybridized to a 5,3-kilobase RNA, as expected for LDL-R mRNA. The concentration of this RNA was increased in preparations from cells that were treated with Verapamil or Diltiazem. The selectivity of the increase was established by using a probe for beta-actin mRNA. In dot-blot hybridization it was observed that the calcium antagonists cause 2-3-fold relative increase in the amount of LDL-R mRNA. The increase in the amount of LDL-R mRNA is paralleled by elevated high binding and uptake of [125J] LDL by cells pretreated with the calcium entry blocker. Studies in several types of animal models especially cholesterol-fed rabbits, have shown that calcium channel blockers can reduce the accumulation of atherogenic lesion components and thus apparently decrease the progression of lesions (Weinstein, D. B., 1988). Verapamil has been proposed to be effective in early stages of atherogenic lesion formation to decrease aortic lesion area in cholesterol fed rabbits (Sievers R., et al., 1987). There are essentially no effects of calcium antagonists on lipoprotein composition or concentrations (Trost et al., 1987). It does not appear, therefore, that calcium antagonists are working by reducing lipid levels. Interactions of calcium channel blockers, however, with lipoprotein metabolic pathways cannot be ignored as a major potential mechanism for altering cholesterol accumulation and the atherogenic state (Weinstein D. B., 1988). It could be shown that Verapamil and Diltiazem could decrease the rate of low density lipoprotein (LDL) degradation in human skin fibroblast cultures (Ranganathon S., et al., 1982) and that Verapamil increased receptor mediated clearance of LDL from cell surfaces but also caused a delay in lysosomal degradation of LDL (Stein O., et al. 1985). How does an calcium blocker lead to an increase of LDL-receptor activity in fibroblasts? We have suggested that calcium antagonists increase the LDL-receptor activity by eliciting an increase in the mRNA for LDL-receptors. It has now become possible to test this hypothesis through the use of cDNA probes for the LDL-receptor (Ma, et al., 1986). We have shown that both calcium entry blockers Verapamil and Diltiazem increase the apparent rate of the synthesis and the endocytic capacity of the LDL-receptors in human skin fibroblasts (Filipovic et al., 1986a).(ABSTRACT TRUNCATED AT 400 WORDS)

[Diagnosis of muscle function in hereditary muscular dystrophies]. / Muskelfunktionsdiagnostik bei hereditären Muskeldystrophien.

The evaluation of musclefunction im myopathies has been done upto now only by clinical trial. But in contrast in the field of medicine in sports has been proved the method of dynamometry of the muscles for a longer time which are necessary for objectivation of musclefunktion in myopathies. In this paper we present first results of health children and children suffering from Duchenne myopathy.

Lovastatin versus bezafibrate: efficacy, tolerability, and effect on urinary mevalonate.

Lovastatin and benzafibrate have proved effective in lowering low-density-lipoprotein (LDL) cholesterol and elevating high-density-lipoprotein (HDL) cholesterol. We compared their tolerability, safety, and effects on lipoproteins and urinary mevalonate excretion in a short-term study. Forty patients with primary hypercholesterolemia were enrolled in a single-blind randomized study with a diet/placebo period of 8 weeks and a treatment period of 12 weeks. Twenty patients received lovastatin (final average dose 70.5 mg/day), and 20 patients received bezafibrate 400 mg/day. LDL cholesterol was lowered by 35% (from 323 to 208 mg/dl) with lovastatin and by 8% (from 289 to 264 mg/dl) with benzafibrate. HDL cholesterol increased by 21 and 20% with lovastatin and benzafibrate, respectively. Twenty-four-hour urinary mevalonic acid output decreased by 37% during treatment with lovastatin and by 2% during treatment with bezafibrate. Thus, the lowering of cholesterol by lovastatin, but not by bezafibrate, can be attributed to inhibition of HMG CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase. Both lovastatin and bezafibrate are well tolerated.

Calmodulin antagonists increase the amount of mRNA for the low-density-lipoprotein receptor in skin fibroblasts.

The effects of calmodulin antagonists on the amount of LDL receptor (LDL-R) mRNA in cultured human fibroblasts was examined by hybridization with a fragment of LDL-R cDNA. In a 'Northern' blot the fragment hybridized to a 5.3-kilobase RNA, as expected for LDL-R mRNA. The concentration of this RNA was increased in preparations from cells that were treated with trifluoperazine or W-7 [N-(6-aminohexyl)-5-chloronaphthalene-1-sulphonamide]. The selectivity of the increase was established by using a probe for beta-actin mRNA. In dot-blot hybridization it was observed that the calmodulin antagonists cause 2-4-fold relative increase in the amount of LDL-R mRNA.

Analysis of polymorphonuclear leukocyte respiratory burst activity in uremic patients using whole-blood chemiluminescence.

The respiratory burst activity of peripheral leukocytes from 17 patients with chronic renal failure and 12 healthy individuals was assessed using the technique of whole-blood chemiluminescence (CL). Luminol- and lucigenin-dependent CL was measured in two dilutions of venous blood following stimulation with serum-treated zymosan or phorbol myristate acetate, and the CL peaks associated with a polymorphonuclear leukocyte count of 10(4)/ml were calculated. The mean CL peaks for the patients were significantly higher than those for the controls in all experimental designs (p less than 0.05). This enhanced leukocyte respiratory burst activity was not associated with the underlying renal abnormality or with the type of dialysis treatment, but may have been related to the induction of tissue enzymes which is known to occur in uremia.