Search

Objectives Patients with acromegaly appear to be at increased risk of vertebral fractures despite normal bone mineral density. We investigated the prevalence of vertebral fractures in a cohort of acromegalic patients under 80 years of age. Methods Monocentric cross-sectional study performed at Nantes University Hospital from 1988 to 2018. Fifty patients (18 females, 32 males) with a median age of 52.3 years (range: 27–78) were included. Radiological vertebral fractures were evaluated on conventional lumbar and thoracic spine radiographs using Genant's semiquantitative fracture assessment. We studied qualitative abnormalities of the spine using three criteria: osteophytes, disc-space narrowing and wedge-shaped vertebrae. We analysed bone mineral density and endocrine status. Results Three patients (6%) had a vertebral fracture: one grade 1 and two grade 2 according to Genant's assessment, with two osteoporotic and one osteopenic patients. They had no unsubstituted pituitary deficiency. Considering the frank deformations (osteophyte or disc narrowing ≥ grade 2 or wedge-shaped), the thoracic spine was deformed in 22 patients (44%) and the lumbar spine in 21 patients (42%). Conclusion Acromegalic patients had a low prevalence of vertebral fractures but had a significant amount of vertebral deformations. We speculate that this high prevalence of frank deformations could explain the previously reported high prevalence of vertebral fractures.

This narrative review gathers current evidence for a contribution of rheumatoid arthritis (RA) HLA-DRB1, PTPN22 and CTLA4 polymorphisms to the gut dysbiosis observed in RA, especially at its onset (transient excess of Prevotella). The gut microbiome contains elements which are 30% heritable, including genera like Bacteroides and Veillonella, and to a lesser extent Prevotella. The first months/year seems a critical period for the selection of a core of microbiota, that should be considered as a second self by the immune system, and tolerized by regulatory T and B cells. Imperfect tolerization may increase the risk of RA following further repeated silent translocations of various gut microorganisms, including Prevotella copri, from gut to joints (fostered by a concurrent loss in gut mucosa of protective bacteria like Faecalibacterium prausnitzii). Genetics studies confirmed that Prevotella copri was partly heritable, and strong associations were observed between the overall microbial composition of stools and the HLA-DRB1 RA risk allele, either in a US cohort (P=0.00001), or the Twins UK cohort (P=0.033). This finding also stands for persons still free from RA, and was replicated in the Swiss SCREEN-RA cohort. Gene variants of PTPN22 also modify intestinal microbiota composition, compromise granulocyte-mediated antibacterial defence in gut, and reduce the suppressive effect of gut regulatory B cells. CTLA4 variants may similarly contribute to RA dysbiosis, since immunotherapy by CTLA-4 blockade depends on microbiota, and CTLA4 activates T follicular regulatory cells to reduce immune responses to segmented filamentous bacteria. Suggestions for future works are made.

Hip labral tears are found in 22-55% of individuals with hip pain, but labral tears without cysts are usually not responsible for hip pain, which originates mostly from other structures than the torn labrum, like osteochondral, but also tendinous injuries (rectus femoris, gluteus minimus, iliopsoas) or capsulo-ligamentous tears (iliofemoral ligaments, ligament teres). Those lesions are mainly the consequences of underlying unrecognized functional acetabular dysplasia, and/or femoroacetabular impingements. Although the early repair of labral tears in young sportsmen induces a marked and lasting relief, and might delay the onset of osteoarthritis, the microinstability fostered by labral damages seems less important than underlying dysplasias/impingements. This narrative review details recent findings on: (i) the various mechanisms of pain associated with labral tears; (ii) few evidence for hip microinstability induced by isolated labral tears; (iii) how to best detect labral tears, both clinically (including through IROP test) and on imaging (MRI, MRA, computed tomography arthrography, ultrasound). Some authors suggested to use pull-out tests during surgery, but pulling of hips do not seem to increase much diagnostic performances of ultrasounds. Ultrasound-guided intra-articular and peri-articular injections may tell how often hip pain is exclusively induced by peri-capsular injuries secondary to the acetabular dysplasia/femoro-acetabular impingements already responsible for labral tears. Further works could tell whether labral repair, tendinous debridement, plication of capsule, and/or focal denervation, may induce lasting reliefs of pain induced by the chronic contraction of surrounding muscles (rectus femoris, gluteus minimus, psoas), whose deep aponeuroses mix with the superficial fibres of the thick hip capsule.

Compression of roots/nerves can disrupt some of their functions, but does not necessarily cause pain. This is illustrated by the frequency of nearly asymptomatic spinal stenosis or disc herniations. In fact, pain of radiculopathies (and nerve entrapments) may mostly be the consequence of intraneural oedema induced by microscopical venous stasis around roots/spinal ganglia (or nerves) not or poorly shown by imaging. This narrative review first lists arguments for a role of congestion of vasa-nervorum in the pathophysiology of radiculopathies, including those induced by disc herniation and spinal stenosis, but also other sources of overpressures in spinal venous plexuses (pregnancy, vena cava atresia and thrombosis, portal hypertension, epidural varices, arterio-venous fistula, vertebral hemangioma or hemangioblastoma). It also details sources of venous congestion around nerves outside the spine, from pelvis (May-Thurner syndrome, Nut-cracker syndrome) to buttocks (superior and inferior gluteal veins), and even thighs and legs. A better recognition of a preeminent role of venous congestion in radiculopathies, plexopathies, and nerve entrapments, should have major consequences: (i) discard the dogma that compression is mandatory to induce root/nerve suffering, since root/nerve adherences in two locations can impair blood flow in vasa-nervorum through root/nerve stretching; (ii) implementation of sensitive techniques to visualise impingement of blood flow around or within roots and nerves; (iii) better prevention of roots/nerves adherence, or arachnoiditis induced by extravascular fibrin deposition secondary to venous stasis.; (iv) optimizing treatments dampening clot formation and/or extravascular fibrin leakage in the intradural/peridural spaces, or around roots/nerves, like guided injection of tissue plasminogen activator.

International audience