Can local corticosteroid injection in the retrocalcaneal bursa lead to rupture of the Achilles tendon and the medial head of the gastrocnemius muscle?

PURPOSE: The purpose of the study is to explain the cause-effect relationship in three patients who reported combined ruptures of the Achilles tendon and the gastrosoleus complex 6 months after they had received corticosteroids injections for the management of retrocalcaneal bursitis. METHODS: Three cryopreserved cadavers (three men, three left legs) were examined to assess the anatomic connection between the retrocalcaneal bursa and the Achilles tendon (distal and anterior fibers). Blue triptan medium contrast was injected. RESULTS: An unexpected connection between the retrocalcaneal bursa and the anterior fibers of the Achilles tendon was found in all instances. CONCLUSIONS: Local corticosteroid injection of the retrocalcaneal bursa may help the symptoms of retrocalcanear bursitis, but pose a risk of Achilles tendon rupture. This risk-benefit has to be taken into account when corticosteroid injections are prescribed to professional and high-level athletes.

Apunts. Medicina de l'Esport: una revista internacional / Apunts. Medicina de l'Esport: an international journal

No disponible

Central aponeurosis tears of the rectus femoris: practical sonographic prognosis.

OBJECTIVE: This study is a statistical analysis to establish whether a correlation exists between the level and degree of rectus femoris (RF) central tendon injury and the amount of time that an athlete is unable to participate subsequently, referred to as "sports participation absence" (SPA). DESIGN: Causal-comparative study. PATIENTS: 35 players from two high-level Spanish soccer teams with an injury to the central tendon of the RF based on clinical and ultrasound criteria. MAIN OUTCOME MEASURE: Ultrasound examination was performed with an 8-2 MHz linear multifrequency transducer. All studies included both longitudinal and transverse RF sections. RESULTS: At the proximal level the SPA time is 45.1 days when the injury length is 4.0 cm. This value increases by 5.3 days with each 1 cm increase in the length of injury. In the case of distal level injury, SPA time is 32.9 days when the injury length is 3.9 cm. This value increases by 3.4 days with each 1 cm increase. In the total representative sample, SPA time when the injury length is 4.2 cm corresponds to 39.1 days. This value increases by 4.2 days per length unit. CONCLUSIONS: RF central tendon injury at the proximal level is associated with a greater SPA time than at the distal level. Patients with a grade II injury have an SPA time longer than those with a grade I injury whether the injury is located proximal or distal.

Fast and slow myosins as markers of muscle injury.

OBJECTIVE: The diagnosis of muscular lesions suffered by athletes is usually made by clinical criteria combined with imaging of the lesion (ultrasonography and/or magnetic resonance) and blood tests to detect the presence of non-specific muscle markers. This study was undertaken to evaluate injury to fast and slow-twitch fibres using specific muscle markers for these fibres. METHODS: Blood samples were obtained from 51 non-sports people and 38 sportsmen with skeletal muscle injury. Western blood analysis was performed to determine fast and slow myosin and creatine kinase (CK) levels. Skeletal muscle damage was diagnosed by physical examination, ultrasonography and magnetic resonance and biochemical markers. RESULTS: The imaging tests were found to be excellent for detecting and confirming grade II and III lesions. However, grade I lesions were often unconfirmed by these techniques. Grade I lesions have higher levels of fast myosin than slow myosin with a very small increase in CK levels. Grade II and III lesions have high values of both fast and slow myosin. CONCLUSIONS: The evaluation of fast and slow myosin in the blood 48 h after the lesion occurs is a useful aid for the detection of type I lesions in particular, since fast myosin is an exclusive skeletal muscle marker. The correct diagnosis of grade I lesions can prevent progression of the injury in athletes undergoing continual training sessions and competitions, thus aiding sports physicians in their decision making.

Subcutaneous administration of CAMPATH-1H: clinical and biological outcomes.

OBJECTIVE: A 24 week study of subcutaneous (sq) dosing with titration of CAMPATH-1H (C1H) dose against the circulating CD4+ T cell count in patients with rheumatoid arthritis (RA) was undertaken to examine the safety, biologic activity, and clinical efficacy of this approach. METHODS: All patients met American Rheumatism Association (ARA) criteria for active RA. Patients received either 0.5 or 1.0 mg of C1H subcutaneously twice per week; dosing could be doubled after the first 8 weeks of treatment and subsequently following 4 week dose intervals for lack of clinical efficacy, but was discontinued any time the CD4+ T cell count fell below 400/mm3. Patients were evaluated weekly for 2 weeks and then biweekly for clinical and laboratory variables of safety, biological activity, and disease activity. RESULTS: Ten patients were treated, 6 in the 0.5 mg cohort and 4 in the 1.0 mg cohort. Four of ten patients had a 20% modified Paulus response (2 in each cohort) while taking drug; there were minimal side effects, primarily limited to local reaction at the injection site. All patients had a > 50% drop in circulating CD4+ T cells within the first 2 weeks of therapy, with no further significant reduction; only 1/6 patients in the 0.5 mg cohort had dose limiting CD4+ T cell depression vs 2/4 in the 1.0 mg cohort. All patients developed antibodies to C1H. Appearance of anti-C1H was temporarily associated with a halt in further reduction of CD4+ T cell count despite continued C1H administration. CONCLUSION: Subcutaneous administration of C1H in low doses (0.5 mg biweekly) was well tolerated and did not result in dose limiting CD4+ T cell depletion in 5 of 6 patients. Clinical efficacy was observed in some patients but could not be maintained, possibly due to the production of anti-C1H antibodies.