Dislocations and the femoral head size in primary total hip arthroplasty.

The dislocation rate of 3197 Charnley prostheses with 22 mm head in which the surgery was done between 1979 and 1991 in 2 orthopaedic centers was compared with that of 2875 Lubinus prostheses with 32 mm head in which the surgery was done between 1980 to 1991 in 3 other centers. A 1-year followup showed an equal rate of dislocation (2.4%-2.5%) in the 2 groups and included 75% of the 201 dislocated hips. Almost all of the late dislocations occurred with the Charnley prosthesis, resulting in a total dislocation rate of 3.7% compared with 2.9% with the Lubinus prosthesis. Regardless of the type of prosthesis used, there was a higher risk of dislocation in patients with nonhealed hip fractures and in arthroplasties performed by less experienced surgeons. When these 2 variables were removed, the small femoral head was not associated with an increased risk of dislocation. However, there were 77 of 118 (65%) recurrent dislocations in the Charnley group, compared with 37 of 83 (45%) in the Lubinus group, and the relative risk of a dislocated hip arthroplasty becoming recurrent increased by 2.3 times if the small femoral head was used. The number of reoperations also were doubled in this group. Almost 4 times as many dislocations were documented within 2 weeks after surgery after any type of prosthesis inserted through a posterior approach compared with the transtrochanteric approach, but there was no increase in rate of recurrence or revision.

Migration of press-fit cups fixed with poly-L-lactic acid or titanium screws: a randomized study using radiostereometry.

The early migration of porous acetabular cups was studied in 43 patients with osteoarthrosis. The patients were randomly allocated to additional fixation of the cup with either biodegradable poly-L-lactic acid screws or titanium screws. Radiostereometric evaluation was done during the first 2 years after the procedure in 43 hips (23 with poly-L-lactic acid screws and 20 with titanium screws). At the 2-year follow-up, cups fixed with poly-L-lactic acid screws had migrated significantly more in the proximal-distal (p < 0.05) and medial-lateral (p < 0.05) directions. Cups with titanium screws displayed more pronounced rotations around the longitudinal axis (p < 0.05). Postoperatively, on the lateral view, there was an increased occurrence of radiolucencies at the dome of the cups fixed with poly-L-lactic acid screws (p < 0.05). The clinical result did not differ between the two groups. Inferior implant-bone contact in the poly-L-lactic acid group, local changes of the bone quality, and diminishing support of the poly-L-lactic acid screws caused by their degradation with time could be reasons for the different pattern of migration observed.

Bone and wound fluid concentrations of cephalosporins. Oral cefadroxil and parenteral cefuroxime compared in 52 patients with a trochanteric fracture.

We performed a prospective and randomized study in 52 patients to compare the concentrations in cancellous bone and wound fluid of antibiotics, given orally (cefadroxil) or intravenously (cefuroxime) as prophylaxis in trochanteric fracture surgery. Oral cefadroxil resulted in adequate antibiotic levels in 22 of 26 patients in wound fluid and cancellous bone, while parenteral cefuroxime resulted in sufficient antibiotic levels in all 26 patients. The concentrations in bone varied greatly between the subjects.

Prophylaxis with oral cefadroxil versus intravenous cefuroxime in trochanteric fracture surgery. A clinical multicentre study.

A prospective, randomized study was performed in 559 patients to compare two doses of oral cefadroxil with three doses of intravenous cefuorxime as antibiotic prophylaxis in intra- and subtrochanteric hip fracture surgery. Antibiotic concentrations in the wound fluid were determined at the start and at the end of the operation. The first dose of cefadroxil was given about 2 h before surgery and cefuroxime about 30 min before operation. In 226/242 (93%) patients randomized to oral cefadroxil, the concentration in the wound during surgery was on average 15 micrograms/ml, i.e., well above the minimum inhibitory concentration (MIC-90) for Staphylococcus aureus. In the cefuroxime group, antibiotic levels in the wound exceeded the MIC-90 for S. aureus in 204/210 (97%) of the patients at the start and/or at the end of surgery. All patients were followed up for 4 months. One deep and five superficial infections occurred in the cefuroxime group and no deep but one superficial infection in the cefadroxil group (P = 0.07). S. aureus was cultured in three of the infected cases while cultures were negative in four patients. Four of the seven infected patients had adequate levels of antibiotic in the wound during surgery, and in three patients no antibiotic assay was performed. The infected patients did not differ in age, sex, operation time, bleeding or any other basic variable compared with patients who healed without complications. Two doses of cefadroxil seems to be practical and as effective as intravenously administered cefuroxime as antibiotic prophylaxis in trochanteric hip fracture surgery.

Piroxicam and indomethacin suppositories for painful coxarthrosis.

Six orthopaedic clinics in Sweden made a comparison of the effects and side effects of Piroxicam (20 mg) and Indomethacin (100 mg) suppositories in 261 patients with painful coxarthrosis on the waiting list for total hip replacement (THR). The study was designed as a single blind study over 4 weeks. Amount of pain and range of motion was registered before the trial and compared with findings after 4 weeks, including reported side effects. Both drugs gave satisfactory pain relief without any appreciable variation on weightbearing or at rest. On the other hand, the trial showed a significant difference (p = 0.0033, Student's-test) between the two drugs as regards the frequency of side effects from the lower gastrointestinal tract, where piroxicam had a lower rate compared with indomethacin. No serious complications occurred; 16 patients dropped out, 8 in each group.

Hepatic and extrahepatic uptake of intravenously injected lipoprotein lipase.

Rats were injected intravenously with 125I-labeled bovine lipoprotein lipase. The lipase disappeared within minutes from the blood due to uptake both in the liver (about 50% of the injected dose) and in extrahepatic tissues. Lipase enzyme activity disappeared in parallel to the 125I radioactivity. Thus, there was no inactivation of lipase in the circulating blood. Similar results were obtained when lipoprotein lipase purified from guinea pigs was injected into guinea pigs. Using supradiphragmatic rats we could show that the extrahepatic uptake was saturable and that the amounts of lipase that could be bound far exceeded the amounts of endogenous lipase expected to be present on the endothelium. When the lipase was denatured before injection, its removal in supradiaphragmatic rats became slower, and in intact rats the fraction of the uptake that occurred in extrahepatic tissues was much decreased. It is concluded that recognition by the extrahepatic receptors depends on the native conformation of the lipase. The extrahepatic uptake was strongly impeded by injection of heparin prior to injection of the lipase, and the uptake could to a large extent be reversed by injection of heparin after the lipase. Even after 1 h lipase that had been taken up by extrahepatic tissues reappeared immediately in the blood on injection of heparin. This was true both for enzyme activity and for enzyme radioactivity. Thus, internalization-inactivation-degradation occur only slowly in extrahepatic tissues. It is possible that the extrahepatic binding occurs to the enzyme's physiological receptors. The hepatic uptake was not dependent on the native conformation of the lipase, was less sensitive to heparin, could not be reversed by heparin and was not saturable. The enzyme was not rapidly inactivated after uptake; its activity could be detected in liver homogenates even after 1 h. Degradation to acid-soluble products in the liver was relatively slow; the t1/2 for native lipase was about 1 h. In comparison, in parallel experiments asialofetuin was degraded with a t1/2 of about 15 min.

Activity of lipoprotein lipase in thyroidectomized rats.

Total plasma postheparin lipolytic activity as well as lipoprotein lipase activity in plasma was higher after heparin injection in thyroidectomized rats than in controls. In contrast, the activity of liver lipase was lower in thyroidectomized rats. Adipose tissue from thyroidectomized rats contained more lipoprotein lipase activity than adipose tissue from controls as measured both in extracts of tissue homogenates and medium from in vitro incubations of tissue pieces. There were no differences between control and hypothyroid rats in the disappearance of intravenously injected 125I-labeled lipoprotein lipase, but when a low dose of heparin was injected before the labeled enzyme, the disappearance of 125I-labeled lipoprotein lipase was more retarded in thyroidectomized rats. The elimination of heparin itself was slightly retarded by thyroidectomy.

Purification and properties of lipoprotein lipase in guinea pig milk.

Lipoprotein lipase was purified from guinea pig milk by chromatography on heparin-Sepharose followed by chromatography on an immobilized preparation of heparin that had been N-desulphated and then acetylated. This second step was necessary to separate a plasma protein, presumably antithrombin, from the lipase. The guinea pig enzyme turned out to be quite similar to lipoprotein lipase from bovine milk with respect to composition and molecular size. Furthermore, the specific activities and the dose-response relations for activation by apolipoprotein C-II were quite similar for the two enzymes. Antibodies raised against the guinea pig milk enzyme inhibited not only this enzyme but also the lipoprotein lipase activity in post-heparin plasma and in homogenates from adipose tissue and heart.

Demonstration of hepatic heparin-releasable lipase in the guinea-pig.

It was recently reported by Yamada et al. (Yamada, N., Murase, T., Akanuma, Y., Ikakura, H. and Kosaka, K. (1979) Biochim. Biophys. Acta 575, 128-134) that the guinea-pig has no hepatic heparin-releasable lipase. We have, however, found a low but definite lipase activity in guinea-pig post-heparin plasma with the characteristics of the hepatic lipase. This activity, as measured in our assay, is only about one-tenth of that in rat post-heparin in plasma. Although the activity is thus much lower than in some other animals, its presence demonstrates that the guinea-pig is not qualitatively but only quantitatively different in this respect.

Guinea pig very low density lipoproteins are a good substrate for lipoprotein lipase.

In contrast to plasma from most other animals, guinea pig plasma causes little or no stimulation of lipoprotein lipase activity. Very low density lipoproteins (VLDL) isolated by ultracentrifugation of guinea pig serum caused a definite stimulation of lipase activity, whereas the infranatant inhibited the activity. Gel filtration in 5 M guanidinium hydrochloride of delipidated VLDL demonstrated that the activation was caused by a low molecular weight protein. The VLDL themselves were hydrolized at similar rates as human VLDL both by guinea pig and by bovine lipoprotein lipases. Thus, guinea pig VLDL contain an activator for lipoprotein lipase analogous to that in other animals and there is enough of the activator to support rapid hydrolysis of the VLDL lipids by the lipase.

Rapid removal to the liver of intravenously injected lipoprotein lipase.

Lipoprotein lipase was purified from bovine milk and labeled with 125I. After intravenous injection to rats the labeled lipase rapidly disappeared from the blood. The initial half-life was about 1 min and more than 70% of the radioactivity was found in the liver at 10 min. 30 min after the injection about 10% of the injected radioactivity was present in acid-soluble form in blood, indicating that the enzyme had been rapidly degraded. Injection of asialofetuin, ribonuclease B or mannan in amounts known to block the hepatic receptors for glycoproteins with exposed galactose, N-acetylglucosamine or mannose residues did not retard the removal of the lipoprotein lipase. Thus, some other, as yet undefined, receptor is implicated. Lipoprotein lipase is known to bind to heparin and some related polysacchrides. Heparin injected before the enzyme delayed its removal and heparin injected after the enzyme caused an immediate increase in blood radioactivity, signifying return from tissues to blood of labeled enzyme. Lipoprotein lipase is present at the endothelium in several extrahepatic tissues and is rapidly turned over. Its presence in blood in appreciable amounts would cause a derangement of lipid transport. The efficient hepatic removal of the enzyme may thus serve an important physiological purpose in keeping the blood levels of this enzyme low.