Reduced tonicity stimulates an inflammatory response in nucleus pulposus tissue that can be limited by a COX‐2‐specific inhibitor

In intervertebral disc herniation with nucleus pulposus (NP) extrusion, the elicited inflammatory response is considered a key pain mechanism. However, inflammatory cytokines are reported in extruded herniated tissue, even before monocyte infiltration, suggesting that the tissue itself initiates the inflammation. Since herniated tissue swells, we investigated whether this simple mechanobiological stimulus alone could provoke an inflammatory response that could cause pain. Furthermore, we investigated whether sustained‐release cyclooxygenase‐2 (COX2) inhibitor would be beneficial in such conditions. Healthy bovine NP explants were allowed to swell freely or confined. The swelling explants were treated with Celecoxib, applied either as a bolus or in sustained‐release. Swelling explants produced elevated levels of interleukin‐6 (IL‐6) and prostaglandin E₂ (PGE₂) for 28 days, while confined explants did not. Both a high concentration bolus and 10 times lower concentration in sustained release completely inhibited PGE₂ production, but did not affect IL‐6 production. Swelling of NP tissue, without the inflammatory system response, can trigger cytokine production and Celecoxib, even in bolus form, may be useful for pain control in extruded disc herniation. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:1724–1731, 2015.     

Cardiac insufficiency in acromegaly. Apropos of a case

The authors report the case of a patient with acromegaly. The clinical history was dominated by left ventricular failure, for which acromegaly was the only evident cause. The cardiac index, pulmonary arterial pressure and the average pulmonary capillary pressure were measured before ablation of the hypophyseal tumour; the measurements were repeated 3 months and 8 years later. The postoperative course followed two phases: transient improvement of the haemodynamic parameters, then relapse of cardiac failure. This case confirms the possibility of a true cardiomyopathy during acromegaly; but the fact that the cardiac failure did not regress despite the decreased growth hormone levels was unusual and raises several physiopathological hypotheses.