Comparison of the mechanical properties of different tension band materials and suture techniques.

OBJECTIVES: This study determined the tensile properties of 18-gauge stainless steel wire, 5-mm woven polyester (Mersilene) tape, and multiple loop configurations of No. 5 braided polyester suture (Ethibond). DESIGN: Mechanical property testing. INTERVENTION: Single loops of stainless steel wire, Mersilene, and Ethibond were tested to determine their mechanical properties. Ethibond was tested with different numbers of loops and different knot configurations. MAIN OUTCOME MEASURES: Stiffness, load at failure, and elongation at failure. RESULTS: One loop of Mersilene and two loops of Ethibond had similar loads at failure, but the load at failure was significantly higher for stainless steel wire. Four loops of Ethibond withstood a similar failure load to stainless steel wire, but the failure load of the Ethibond suture was greater than the yield load of stainless steel wire. Stainless steel wire had a higher stiffness than both Ethibond and Mersilene. No difference was found in the failure load between different Ethibond knot configurations. The individually tied suture configuration resulted in a higher stiffness than the single-knot configuration. The elongation at failure was not statistically different among the different knot configurations and materials, with the exception of Mersilene tape. Mersilene tape demonstrated a significant increase in elongation at failure as compared to the other materials and knot configurations. CONCLUSION: It appears that multiple loops of Ethibond can substitute for stainless steel wire in situations where a compliant repair is suitable (support of a patellar tendon repair), but may not be satisfactory for rigid fixation (tension band fixation of a fracture). There appears to be no significant difference in strength but a small decrease in stiffness between tying multiple suture loops in one knot as opposed to individual knots.

Fluoroquinolone-induced tendinopathy: what do we know?

Fluoroquinolones are relatively safe, effective antibiotics. As their use becomes more frequent, so will the adverse side effects. I highlight a rare but debilitating adverse reaction-fluoroquinolone-induced tendinopathy. Case reports and letters from 1987 to 1998 were identified by using Grateful Med and PubMed Internet accesses to the National Library of Medicine. Articles were reviewed for clinical practicality. There are few articles on fluoroquinolone-induced tendinopathy in the US literature targeting primary care physicians. This entity has been described in many case reports, but little has been done to isolate the causative agents. Incidence of this side effect is difficult to estimate, since no prospective studies are available for review or calculation of risk. Fluoroquinolone-induced tendinopathy appears more commonly in tendons under high stress. The cause is probably multifactorial. Risk factors for the development of fluoroquinolone-induced tendinopathy are age, renal failure, corticosteroid use, and previous tendinopathy from fluoroquinolones.

Plasma levels of gonadal steroids during final oocyte maturation of striped bass, Morone saxatilis L.

Levels of estradiol-17 beta (E2), testosterone (T), 17 alpha,20 beta-dihydroxy-4-pregnen-3-one (DHP), and 17 alpha,20 beta,21-trihydroxy-4-pregnen-3-one (20 beta-S) were measured by radioimmunoassay (RIA) in blood plasma of striped bass undergoing final oocyte maturation (FOM). Females were captured just prior to, or in the early stages of, FOM and induced to complete maturation and ovulation with injected human chorionic gonadotropin, synthetic salmon gonadotropin-releasing hormone analogue (sGnRHa; [D-Arg6-Pro9 NEt]-sGnRH), sGnRHa plus the dopamine receptor antagonist, domperidone (DOM), or OVAPRIM, a commercial preparation of sGnRHa + DOM. Their plasma levels of immunoreactive DHP and 20 beta-S were significantly greater at ovulation relative to the time of hormone injection, whereas the plasma levels of E2 and T were greatest at injection and decreased by ovulation and 24 hr thereafter. Plasma levels of 20 beta-S, but not DHP, were sustained at high levels after ovulation. Fish injected only with DOM did not undergo FOM, its associated changes in plasma steroid levels, or ovulation. In females captured at various natural stages of FOM, plasma levels of 20 beta-S and DHP were low during germinal vesicle migration (GVM), peaked coincident with germinal vesicle breakdown, and then decreased near the time of ovulation. Plasma levels of E2 and T were greatest during GVM and decreased as DHP and 20 beta-S levels increased. Analyses of conjugated versus free plasma steroids showed 64-79% of the various hormones to be in the free fraction. RIA of plasma fractionated by reversed-phase HPLC showed that half of the 20 beta-S immunoreactivity coeluted with 5 beta-pregnan-3 alpha,17,20 beta,21-tetrol, a putative 20 beta-S metabolite with 99.7% cross-reactivity in the 20 beta-S RIA. These results indicate that striped bass follow the typical profile of changing plasma steroid levels seen in other teleosts during FOM, with a clear shift from C18 and C19 steroids to C21 steroids. They suggest that both DHP and 20 beta-S, both potent inducers of striped bass FOM in vitro, may play a role in regulating FOM in this species.

Calcification of entheses associated with X-linked hypophosphatemic osteomalacia.

We undertook a retrospective analysis of 26 patients with X-linked hypophosphatemic osteomalacia (or rickets), whose ages ranged from 1 to 62 years and who were from 11 different kindreds, to determine the prevalence and clinical characteristics of a unique disorder of the entheses (tendons, ligaments, and joint capsules). We found a generalized involvement of the entheses, with exuberant calcification of tendon and ligament insertions and of joint capsules, in 69 per cent of the subjects. The prevalence and extent of disease increased with age but were not correlated with sex. Commonly affected sites included the hand and sacroiliac joints. Histologic evaluation in a selected patient revealed intratendinous lamellar bone but no inflammatory cells. Our observations indicate that this disorder is an integral part of X-linked hypophosphatemic osteomalacia and exhibits clinical, radiographic, and histologic characteristics that differentiate it from degenerative disorders of these tissues and seronegative spondyloarthropathies.

Healing of bone disease in X-linked hypophosphatemic rickets/osteomalacia. Induction and maintenance with phosphorus and calcitriol.

Although conventional therapy (pharmacologic doses of vitamin D and phosphorus supplementation) is usually successful in healing the rachitic bone lesion in patients with X-linked hypophosphatemic rickets, it does not heal the coexistent osteomalacia. Because serum 1,25-dihydroxyvitamin D levels are inappropriately low in these patients and high calcitriol concentrations may be required to heal the osteomalacia, we chose to treat five affected subjects with high doses of calcitriol (68.2 +/- 10.0 ng/kg total body weight/d) and supplemental phosphorus (1-2 g/d) performing metabolic studies and bone biopsies before and after 5-8 mo of this therapy in each individual. Of these five patients, three (aged 13, 13, and 19 yr) were receiving conventional treatment at the inception of the study and therefore showed base-line serum phosphorus concentrations within the normal range. The remaining two untreated patients (aged 2 and 37 yr) displayed characteristic hypophosphatemia before calcitriol therapy. All five patients demonstrated serum calcitriol levels in the low normal range (22.5 +/- 3.2 pg/ml), impaired renal phosphorus conservation (tubular maximum for the reabsorption of phosphate per deciliter of glomerular filtrate, 2.13 +/- 0.20 mg/dl), and osteomalacia on bone biopsy (relative osteoid volume, 14.4 +/- 1.7%; mean osteoid seam width, 27.7 +/- 3.7 micron; mineral apposition rate, 0.46 +/- 0.12 micron/d). On high doses of calcitriol, serum 1,25-dihydroxyvitamin D levels rose into the supraphysiologic range (74.1 +/- 3.8 pg/ml) with an associated increment in the serum phosphorus concentration (2.82 +/- 0.19 to 3.78 +/- 0.32 mg/dl) and improvement of the renal tubular maximum for phosphate reabsorption (3.17 +/- 0.22 mg/dl). The serum calcium rose in each patient while the immunoactive parathyroid hormone concentration measured by three different assays remained within the normal range. Most importantly, repeat bone biopsies showed that high doses of calcitriol and phosphorus supplements had reversed the mineralization defect in all patients (mineral apposition rate, 0.88 +/- 0.04 micron/d) and consequently reduced parameters of bone osteoid content to normal (relative osteoid volume, 4.1 +/- 0.7%; mean osteoid seam width, 11.0 +/- 1.0 micron). Complications (hypercalcemia and hypercalciuria) ensued in four of these five patients within 1-17 mo of documented bone healing, necessitating reduction of calcitriol doses to a mean of 1.6 +/- 0.2 micrograms/d (28 +/- 4 ng/kg ideal body weight per day). At follow-up bone biopsy, these four subjects continued to manifest normal bone mineralization dynamics (mineral apposition rate, 0.88 +/-0.10 micrometer/d) on reduced doses of 1.25-dihydroxyvitamin D with phosphorus supplements (2 g/d) for a mean of 21.3 +/- 1.3 mo after bone healing was first documented. Static histomorphometric parameters also remained normal (relative osteoid volume, 1.5 +/- 0.4%; mean osteoid seam width, 13.5 +/- 0.8 micrometer). These data indicate that administration of supraphysiologic amounts of calcitriol, in conjunction with oral phosphorus, results in complete healing of vitamin D resistant osteomalacia in patients with X-linked hypophosphatemic rickets. Although complications predictably require calcitriol dose reductions once healing is achieved, continued bone healing can be maintained for up to 1 yr with lower doses of 1,25-dihydroxyvitamin D and continued phosphorus supplementation.

Renal vascular lesions after chemotherapy with vinblastine, bleomycin, and cisplatin.

A 30 year old man with metastatic embryonal carcinoma became hypertensive during vinblastine, bleomycin, and cisplatin therapy. Three months after completion of therapy, accelerated hypertension occurred (blood pressure 210/140 mm Hg). Nitroprusside failed to control the hypertension, but captopril resulted in a prompt and sustained normalization of the blood pressure. The plasma renin activity was markedly elevated before therapy. Renal biopsy disclosed "onionskin" narrowing of the interlobular arteries and fibrin thrombosis of a majority of the afferent arterioles. A form of drug-induced renovascular hypertension is suggested.