Pierre Lafforgue

Occult Osteoporotic Vertebral Fractures : Vertebral Body Fractures Without Radiologic Collapse

Study Design. Retrospective observational study. Objectives. We report our experience with patients who presented with osteoporotic vertebral fractures with no visible deformation of vertebral body. Summary of Background Data. The diagnosis of osteoporotic vertebral fractures largely relies on the observation of vertebral deformations on plain radiographs, termed vertebral collapses. There are no data on the characteristics, or indeed of the reality, of osteoporotic vertebral fractures with no significant deformation of the vertebral body. Methods. We retrospectively analyzed cases that presented with acute back pain with no initial deformation of the vertebral body on plain radiographs, and later proved to be fresh osteoporotic vertebral body fractures. All cases met each of the following criteria: 1) The incriminated vertebra appeared normal on initial radiographs (Genant’s Grade 0 deformation). 2) The diagnosis of fresh vertebral body fracture was confirmed by MRI. 3) The diagnosis of osteoporosis was made by the combination of established osteoporosis, ruling out of underlying disease, and follow-up. Results. We observed 21 fractures in 16 patients (11 female/5 male; mean age, 72 years). Most of these fractures affected the lumbar spine (14 of 21 occurred at L2–L5). Osteoporosis was known beforehand in 9 patients and newly diagnosed in 7 patients. At follow-up, radiographs were obtained for 19 of 21 fractures: in 15 cases, the vertebral fracture developed a vertebral collapse (Genant’s Grade ≥ 0.5) in a mean of 12.5 weeks (range, 4–24 weeks); in the 4 remaining cases, the vertebra remained normal. All cases had a clinically favorable outcome. Conclusion. Osteoporotic vertebral fractures with no sign of vertebral collapse on initial radiographs do indeed exist. They are analogous to occult stress fractures well known in other skeletal sites. They must not be misdiagnosed as malignant lesions.

Reflex sympathetic dystrophy syndrome and neuromediators

Concepts related to the pathophysiology of reflex sympathetic dystrophy syndrome (RSDS) are changing. Although sympathetic influences are still viewed as the most likely mechanism underlying the development and/or perpetuation of RSDS, these influences are no longer ascribed to an increase in sympathetic tone. Rather, the most likely mechanism may be increased sensitivity to catecholamines due to sympathetic denervation with an increase in the number and/or sensitivity of peripheral axonal adrenoceptors. Several other pathophysiological mechanisms have been suggested, including neurogenic inflammation with the release of neuropeptides by primary nociceptive afferents and sympathetic efferents. These neuromediators, particularly substance P, calcitonin gene-related peptide, and neuropeptide Y (NPY), may play a pivotal role in the genesis of pain in RSDS. They induce an inflammatory response (cutaneous erythema and edema) and lower the pain threshold. Neurogenic inflammation at the site of the lesion with neuromediator accumulation or depletion probably contributes to the pathophysiology of RSDS. However, no single neuromediator has been proved responsible, and other hypotheses continue to arouse interest.

Magnetic resonance imaging in reflex sympathetic dystrophy syndrome of the foot

OBJECTIVE The purpose was to analyze magnetic resonance imaging (MRI) abnormalities in reflex sympathetic dystrophy syndrome (RSDS) of the foot, with the goal of helping to meet the difficult diagnostic challenges raised by this condition. METHODS Retrospective study of 20 patients with RSDS of the foot, 15 at the warm phase and five at the dystrophic phase. RESULTS Of the 15 patients at the warm phase, seven had evidence of bone edema (low signal on T1-weighted images and high signal on T2, T2 STIR, and fat saturation images) and five had occult fractures (linear band of low signal on T1 and T2 weighted images with no enhancement after contrast injection). Other abnormalities included soft tissue changes in three patients, joint effusion in five, and synovial hypertrophy in one. Of the five patients at the dystrophic phase, one had a fracture with a joint effusion, one had isolated joint edema, and three had normal MRI findings. CONCLUSION Bone marrow edema is inconsistent at the warm phase of RSDS and is never present at the dystrophic phase. Thus, absence of bone edema does not rule out RSDS. Fractures may be visible by MRI in one-third of patients with RSDS and no clinical or plain radiography evidence of fracturing.

Emergence of Q Fever Arthritis in France

ABSTRACT Osteoarticular infection is an uncommon presentation of Q fever. Positron emission tomography (PET) scanning is a valuable tool for the diagnosis of Coxiella burnetii graft prosthesis infection and endocarditis. Our objective was to test a series of culture-negative osteoarticular samples using molecular assays for Coxiella burnetii. We tested for C. burnetii by molecular assays targeting the IS1111 and the IS30A spacer regions, using culture-negative osteoarticular samples obtained in our laboratory between January 2011and December 2012. We examine a total of 1,410 osteoarticular samples, and we observed two cases of arthritis and subacromial bursitis caused by C. burnetii. The infections were localized using PET scanning, and the diagnosis was confirmed through serology. For one, a C. burnetii strain with a multispacer sequence type 8 genotype was isolated from synovial fluid culture. Q fever articular infections could be undiagnosed because of the long evolution of articular attack, and patients with high antibody titers against C. burnetii should be tested using PET scanning to localize the site of infection.

Bilateral symmetric polyarthralgia revealing Fanconi’s syndrome

We report the case of a 45-year-old woman who presented with a six-year history of diffuse polyarthralgia responsible for major disability. She reported bilateral symmetric arthralgia in nearly every joint, as well as back pain. Muscle wasting predominating in the roots of the limbs was found. Laboratory tests showed hypocalcemia, severe hypophosphatemia, hypokalemia, alkaline phosphatase elevation, aminoaciduria, and hyperphosphaturia, with no glycosuria. Radiographs disclosed osteolysis of the pubic symphysis, multiple pelvic fractures, vertebral compression fractures, and diffuse demineralization. A bone scan visualized symmetric foci of hyperactivity in nearly all joints and fracture sites. Dramatic improvements in clinical and radiographic abnormalities were noted after six months of treatment with phosphate and calcitriol. This is a case of incomplete Fanconi syndrome, with no glycosuria. The clinical presentation of Fanconi syndrome can be misleading. Fanconi syndrome should be borne in mind as a possible cause of polyarthralgia to avoid diagnostic delay, which in our patient led to a picture of pseudomyopathy with multiple fractures.

Bone infarcts: Unsuspected gray areas?

There is agreement to label as bone infarcts avascular necrosis (AVN) occurring in the metaphyses or diaphyses of long bones, the terms AVN or osteonecrosis being used at the epiphyses. One might expect bone infarction to hold no mysteries. Oddly enough, however, scientific evidence about bone infarcts is extraordinarily scant. The prevalence of bone infarcts is unknown. The main sites of involvement are the distal femur, proximal tibia, and distal tibia. In patients without sickle cell disease or Gauchers disease, involvement of the upper limbs and lesions confined to the diaphysis are so rare as to warrant a reappraisal of the diagnosis. Although widely viewed as a generally silent event, bone infarcts causes symptoms in half the cases. Standard radiographs are normal initially then show typical high-density lesions in the center of the marrow cavity. A periosteal reaction is common and may be the first and only radiographic change. Magnetic resonance imaging consistently shows typical features and therefore, in principle, obviates the need for other investigations. Bone infarcts are multifocal in over half the cases and, when multifocal, are usually accompanied with multiple foci of epiphyseal avascular necrosis. Thus, bone infarcts, whose prognosis is good per se (with the exception of the very low risk of malignant transformation), are usually a marker for systemic avascular necrosis. Consequently, patients with bone infarcts must be investigated both for known risk factors and for other foci of avascular necrosis, which may, in contrast, have function-threatening effects.

Are Ultrasound Findings Similar in Patients with Axial Spondyloarthritis and in Athlete Entheses

Objective. Enthesitis is the spondyloarthritis (SpA) landmark, but can also be seen after entheses overuse, such as during intensive sport. Methods. We aimed to compare entheses ultrasound (US) findings in a prospective cross-sectional study of 30 axial SpA cases, 30 athletes, and 29 controls. Results. Mean (SD) MAdrid Sonographic Enthesis Index (MASEI) score was 26.3 (13), 12.2 (7), and 10.4 (6) in patients with SpA, athletes, and non-athlete control groups, respectively (p < 0.0001). Conclusion. The MASEI score was significantly higher in patients with SpA compared with healthy controls, athletes, and non-athletes, and can be of value to distinguish SpA from healthy subjects, whatever their physical activity.

Hallux metastasis revealing occult pulmonary squamous cell carcinoma

Joint Bone Spine - In Press.Proof corrected by the author Available online since vendredi 1 juillet 2011

Comments on Ahn et al. case report entitled "Periosteal reaction in systemic lupus erythematosus".

A 23-year-old woman was referred to our department in February 2008 for a 3-week history of abdominal pain. In August 2002, she had been admitted for a decline in general health with a fever and asthenia; tests had shown inflammatory anemia (hemoglobin, 6 g/dl) and mediastinal lymphadenopathy visible by computed tomography (CT). Ultrasonography and CT established the diagnosis of Takayasu arteritis involving the descending thoracic aorta, left common carotid artery, and pulmonary artery. Systemic pulse glucocorticoid therapy was given, followed by oral glucocorticoid therapy with tapering of the dosage over several years. She was monitored closely with physical examinations, laboratory tests, and imaging studies including Doppler ultrasonography of the aortic arch branches and renal arteries at 6-month intervals. Positron emission tomography performed in 2004 showed moderately hypermetabolic foci in the root of the ascending thoracic aorta, left subclavian artery, and abdominal artery proximal to the root of the celiac artery. In 2006, tests showing moderate inflammation, together with a desire to reduce her glucocorticoid exposure, prompted the initiation of add-on methotrexate therapy. At admission, she reported continuous epigastric pain radiating posteriorly, of increasing severity since the onset 3 weeks earlier. She had episodes of stabbing pain at night. The epigastric area was tender to palpation, with rebound tenderness. Laboratory tests at admission showed severe inflammation (Creactive protein, 110 mg/l). Tests for liver and pancreatic function were normal. CT angiography of the abdomen disclosed hypodense circumferential thickening of the abdominal aortic wall, with contrast enhancement. The thickening extended from the diaphragm to below the renal arteries and involved the renal artery ostia, being more marked on the right where a long inflammatory stenotic lesion reduced the renal artery lumen by about 80%. The appendix was normal. Findings from endoscopy of the upper gastrointestinal tract were unremarkable, with no evidence of peptic ulcer. Her glucocorticoid dosage was brought up to 0.5 mg/kg and her methotrexate dose was increased also. The pain resolved completely, indicating that the cause was a flare of aortic inflammation due to Takayasu disease. Another case of dull aortic pain related to inflammatory aortic involvement by Takayasu disease was reported recently [1]. In our patient, the aortic pain served as a valuable warning sign and allowed us to detect an 80% stenosis of the right renal artery, which was normal on the last Doppler ultrasonogram 5 months earlier. It is to be hoped that this patient with extremely severe Takayasu disease from the outset will benefit from recent therapeutic advances.