Metabolism and inflammatory mediators in the peritendinous space measured by microdialysis during intermittent isometric exercise in humans. (1/488)

1. The metabolic processes that occur around the tendon during mechanical loading and exercise are undescribed in man. These processes are important for understanding the development of overuse inflammation and injury. 2. A microdialysis technique was used to determine interstitial concentrations of glycerol, glucose, lactate, prostaglandin E2 (PGE2) and thromboxane B2 (TXB2) as well as to calculate tissue substrate balance in the peritendinous region of the human Achilles tendon. Recovery of 48-62 % (range) at rest and 70-77 % during exercise were obtained for glycerol, glucose and PGE2. 3. Six young healthy humans were studied at rest, during 30 min of intermittent static plantar flexion of the ankle at a workload corresponding to individual body weight, and during 60 min of recovery. Microdialysis was performed in both legs with simultaneous determination of blood flow by 133Xe washout in the same area, and blood sampling from the radial artery. 4. With exercise, the net release of lactate as well as of glycerol from the peritendinous space of the Achilles tendon increased 2-fold (P < 0.05). Furthermore a 100 % increase in interstitial concentration of PGE2 and TXB2 was found, but it was only significant for TXB2(P < 0.05). As peritendinous blood flow increased 2- to 3-fold during intermittent static contractions, this indicates also that the output of these substances from the tissue increased during exercise. 5. This study indicates that both lipid and carbohydrate metabolism as well as inflammatory activity is accelerated in the peritendinous region of the human Achilles tendon with dynamic loading.  (+info)

Sonographic incidence of tendon microtears in athletes with chronic Achilles tendinosis. (2/488)

OBJECTIVE: To assess the number and distribution of tendon microtears in asymptomatic controls and athletes with chronic Achilles tendinitis or partial thickness tears using high resolution ultrasound. METHODS: The mean number of microtears in three random tendon cross sections were recorded per tendon third in 19 asymptomatic volunteers, 16 athletes with symptomatic chronic Achilles tendinitis, and eight athletes with partial Achilles tendon rupture. RESULTS: Microtears were most numerous in the middle third section of the Achilles tendon. Some 67% of tendons in the control group had no microtears, and 28% showed a single microtear. Only 18% of the athletes with chronic Achilles tendinitis and none of the athletes with partial tendon rupture were without microtears in the middle third of their Achilles tendon. Of the tendons with chronic tendinitis, 13% had more than three microtears per section which increased to 87% in tendons exhibiting partial rupture. CONCLUSIONS: There appears to be an association between microtear formation and Achilles tendon rupture.  (+info)

Safe relief of rest pain that eases with activity in achillodynia by intrabursal or peritendinous steroid injection: the rupture rate was not increased by these steroid injections. (3/488)

A history of morning and rest pain that eases with activity was found to improve after anti-inflammatory injections around the paratenon or within the Achilles bursae. The reduction in pain morbidity was significant, and the peritendinous steroid injections did not increase the rupture rate.  (+info)

Negative interstitial pressure in the peritendinous region during exercise. (4/488)

In the present study, tissue pressure in the peritendinous area ventral to the human Achilles tendon was determined. The pressure was measured during rest and intermittent isometric calf muscle exercise at three torques (56, 112, and 168 Nm) 20, 40 and 50 mm proximal to the insertion of the tendon in 11 healthy, young individuals. In all experiments a linear significant decrease in pressure was obtained with increasing torque [e.g., at 40 mm: -0.4 +/- 0.3 mmHg (rest) to -135 +/- 12 mmHg (168 Nm)]. No significant differences were obtained among the three areas measured. On the basis of these observations, microdialysis was performed in the peritendinous region with a colloid osmotic active substance (Dextran 70, 0.1 g/ml) added to the perfusate with the aim of counteracting the negative tissue pressure. Dialysate volume was found to be fully restored (100 +/- 4%) during exercise. It is concluded that a marked negative tissue pressure is generated in the peritendinous space around the Achilles tendon during exercise in humans. Negative tissue pressure could lead to fluid shift and could be involved in the increase in blood flow previously noted in the peritendinous tissue during exercise (H. Langberg, J. Bulow, and M. Kjaer. Acta Physiol. Scand. 163: 149-153, 1998; H. Langberg, J. Bulow, and M. Kjaer. Clin. Physiol. 19: 89-93, 1999).  (+info)

Atraumatic bilateral Achilles tendon rupture: an association of systemic steroid treatment. (5/488)

A case of bilateral Achilles tendon rupture associated with steroid use is reported. This case illustrates the importance of taking a thorough drug history in cases of tendon rupture. In lower limb tendon rupture all patients, especially those on steroids, should be warned of the increased risk of contralateral injury.  (+info)

Achilles tendinitis associated with fluoroquinolones. (6/488)

AIMS: To determine whether there is an association between use of fluoroquinolones and tendinitis in a large population under everyday circumstances. METHODS: A retrospective cohort study was carried out in a dynamic population. Data came from the IPCI-database which consists of all data on consultations, morbidity, prescriptions and other interventions, as registered by GPs in a source population of approximately 250 000 persons. For this study data were collected from 41 general practices in the period from January 1st, 1995 through December 31st, 1996. All persons treated with either fluoroquinolones, amoxicillin, trimethoprim, cotrimoxazole or nitrofurantoin were followed from the first day of treatment until the outcome of interest, death, transfer to another practice, or end of the study period, whichever came first. The risk window was defined as the legend duration +1 month. Potential cases were defined as a registration of a tendinitis or tendon rupture. Patients with a history of tendinitis or tendon rupture, preceding trauma or inadequate diagnoses were excluded on the basis of a review of the patient profiles and additional clinical data, blinded as to the exposure status. Results were adjusted for age, gender, concurrent corticosteroid exposure and number of GP visits. RESULTS: There were 1841 users of fluoroquinolones and 9406 users of the other antibacterial drugs with an average duration of 9 and 7 days, respectively. Tendinitis or tendon rupture was registered in 97 profiles, but after review only 22 complied with the case definition. The adjusted relative risk of tendinitis to fluoroquinolones was 3. 7 (95%CI: 0.9-15.1) for Achilles tendinitis and 1.3 (95%CI: 0.4-4.7) for other types of tendinitis. Achilles tendinitis to ofloxacin had a relative risk of 10.1 (95%CI: 2.2-46.0) and an excess risk of 15 cases per 100 000 exposure days. CONCLUSIONS: Although the numbers in our study are small, our results suggest that some fluoroquinolones may increase the risk of Achilles tendinitis, and that this risk increase is highest for ofloxacin.  (+info)

Percutaneous repair of the ruptured tendo Achillis. (7/488)

Percutaneous repair of the ruptured tendo Achillis has a low rate of failure and negligible complications with the wound, but the sural nerve may be damaged. We describe a new technique which minimises the risk of injury to this nerve. The repair is carried out using three midline stab incisions over the posterior aspect of the tendon. A No. 1 nylon suture on a 90 mm cutting needle approximates the tendon with two box stitches. The procedure can be carried out under local anaesthesia. We reviewed 27 patients who had a percutaneous repair at a median interval of 35 months after the injury. They returned to work at four weeks and to sport at 16. One developed a minor wound infection and another complex regional pain syndrome type II. There were no injuries to the sural nerve or late reruptures. This technique is simple to undertake and has a low rate of complications.  (+info)

Teasing out the truth about collagen. (8/488)

Of all of the non-mineral constituents of the mammalian body there is more collagen than anything else except water and possibly fat. Nevertheless our understanding of the physiology of collagen is rudimentary. All cells and tissues are supported by a network of collagen fibres, the arrangement of which appears to be specifically site adaptive. We know a lot about the biochemistry of collagen, and its many subtypes: for example, all collagen molecules are made within fibroblasts (or modifications of them such as osteocytes), then the oversized collagen molecule is secreted in a soluble form, with hydrophilic ends which are enzymatically cleaved to leave the insoluble core collagen (tropocollagen) beached in the extracellular space. We know that collagen is made relatively immortal by being cross-linked and rather impervious to proteolysis. However, we do not know much about what governs collagen synthesis or its breakdown in the human body. It is important to know, not simply because like Everest, collagen presents a large unignorable mass. We need to understand collagen metabolism in order to understand how we grow, adapt to the environment, maintain our adult shapes and then wrinkle and crumble as we age. Collagen diseases are relatively common and almost certainly if we knew more about how, for example, the collagen framework of bone is laid down and turned over we would understand much more about osteopenia of old age. The problem in finding out has been that collagen is so difficult to study. It turns over relatively slowly, and that part of it that is cross-linked and forms mature collagen is, it seems, with us for life come hell, high-water or famine. The body reduces to mainly skin and bone-collagen in extremis. Because the system as a whole is so sluggish, it is difficult to see changes in indices of collagen metabolism. However, not all the body collagen seems to be as fixed, and indeed collagen in some tissues must turn over, enabling remodelling and adaptation, rather quickly. Think about the stiffness and discomfort that accompanies un-accustomed exercise, which not only abates with time but ceases to occur once the exercise has become customary. What is happening to collagen protein turnover in these circumstances? One obvious way to study protein turnover, even of collagen, is to follow the incorporation of stable isotope markers such as proline into the tissue (although the breakdown is harder to quantify), but this is technically difficult and requires biopsy of the tissue in question. Another way is to follow the appearance in biological fluids of markers of collagen turnover. Since the propeptides which make collagen soluble are cleaved as collagen is deposited extracellularly, their concentration is an index of the rate of collagen synthesis; similarly when tropocollagen is degraded by extracellular proteases, specific N- and C-terminal fragments are released, the amount of which scales with the rate of collagen breakdown. These bits of collagen find their way into the blood. However, assaying them there introduces non-specificity and dilution, rendering interpretation difficult. The ideal would be to measure them in the extracellular fluid at the site of production. This of course is not easy in vivo. One of the delights of the paper by Langberg and colleagues in this issue of The Journal of Physiology (Langberg et al. 1999) is the sheer cheek with which the authors decided to use the microdialysis technique to do this. Microdialysis is a technique whereby a slowly perfused, thin-walled membranous tube is introduced into the extracellular space and the collected fluid assayed for molecules which have diffused into it. Until now the idea of using microdialysis to measure concentrations of molecules much bigger than 300 Da would be regarded as ludicrous. (ABSTRACT TRUNCATED)  (+info)