Strength Measurements in Acute Hamstring Injuries: Intertester Reliability and Prognostic Value of Handheld Dynamometry

Study Design Cohort study, repeated measures. Background Although hamstring strength measurements are used for assessing prognosis and monitoring recovery after hamstring injury, their actual clinical relevance has not been established. Handheld dynamometry (HHD) is a commonly used method of measuring muscle strength. The reliability of HHD has not been determined in athletes with acute hamstring injuries. Objectives To determine the intertester reliability and the prognostic value of hamstring HHD strength measurement in acute hamstring injuries. Methods We measured knee flexion strength with HHD in 75 athletes at 2 visits, at baseline (within 5 days of hamstring injury) and follow-up (5 to 7 days after the baseline measurement). We assessed isometric hamstring strength in 15° and 90° of knee flexion. Reliability analysis testing was performed by 2 testers independently at the follow-up visit. We recorded the time needed to return to play (RTP) up to 6 months following baseline. Results The intraclass correlation coefficients of the strength measurements in injured hamstrings were between 0.75 and 0.83. There was a statistically significant but weak correlation between the time to RTP and the strength deficit at 15° of knee flexion measured at baseline (Spearman r = 0.25, P = .045) and at the follow-up visit (Spearman r = 0.26, P = .034). Up to 7% of the variance in time to RTP is explained by this strength deficit. None of the other strength variables were significantly correlated with time to RTP. Conclusion Hamstring strength can be reliably measured with HHD in athletes with acute hamstring injuries. The prognostic value of strength measurements is limited, as there is only a weak association between the time to RTP and hamstring strength deficit after acute injury. Level of Evidence Prognosis, level 4. J Orthop Sports Phys Ther 2016;46(8):689-696. Epub 12 May 2016. doi:10.2519/jospt.2016.636

Parathyroid hormone analogues in the treatment of osteoporosis

Osteoporosis is characterized by the occurrence of fragility fractures. Over the past years, various treatment options have become available, mostly antiresorptive agents such as bisphosphonates. However, antiresorptive therapy cannot restore bone mass and structure that has been lost due to increased remodeling. In this case, recombinant human parathyroid hormone (PTH) analogues-the full-length PTH(1-84) or the shortened molecule PTH(1-34), which is also known as teriparatide-present the possibility of increasing the formation of new bone substance by virtue of their anabolic effects. The bone formation induced by PTH analogues not only increases BMD or bone mass but also improves the microarchitecture of the skeleton, thereby leading to improved strength of bone and increased mechanical resistance. Controlled trials have shown that both analogues significantly reduce the incidence of vertebral fractures, and PTH(1-34) also reduces the risk of nonvertebral fractures. The need for daily self-injection and the higher cost compared with other forms of treatment limit the widespread use of PTH analogues. Nevertheless, treatment with PTH analogues should be considered in postmenopausal women and men with severe osteoporosis, as well as in patients on established glucocorticoid treatment with a high fracture risk. Concurrent therapy with antiresorptive agents should be avoided, but sequential therapy with these agents might consolidate the beneficial effects on the skeleton

Maintenance of Hypertensive Hemodynamics Does Not Depend on ROS in Established Experimental Chronic Kidney Disease

While the presence of oxidative stress in chronic kidney disease (CKD) is well established, its relation to hypertensive renal hemodynamics remains unclear. We hypothesized that once CKD is established blood pressure and renal vascular resistance (RVR) no longer depend on reactive oxygen species. CKD was induced by bilateral ablation of 2/3 of each kidney. Compared to age-matched, sham-operated controls all ablated rats showed proteinuria, decreased glomerular filtration rate (GFR), more renal damage, higher mean arterial pressure (MAP), RVR and excretion of oxidative stress markers and hydrogen peroxide, while excretion of stable nitric oxide (NO) metabolites tended to decrease. We compared MAP, RVR, GFR and fractional excretion of sodium under baseline and during acute Tempol, PEG-catalase or vehicle infusion in rats with established CKD vs. controls. Tempol caused marked reduction in MAP in controls (96±5 vs.79±4 mmHg, P<0.05) but not in CKD (130±5 vs. 127±6 mmHg). PEG-catalase reduced MAP in both groups (controls: 102±2 vs. 94±4 mmHg, P<0.05; CKD: 118±4 vs. 110±4 mmHg, P<0.05), but did not normalize MAP in CKD rats. Tempol and PEG-catalase slightly decreased RVR in both groups. Fractional excretion of sodium was increased by both Tempol and PEG-catalase in both groups. PEG-catalase decreased TBARS excretion in both groups. In sum, although oxidative stress markers were increased, MAP and RVR did not depend more on oxidative stress in CKD than in controls. Therefore reactive oxygen species appear not to be important direct determinants of hypertensive renal hemodynamics in this model of established CKD