Giant cell arteritis and polymyalgia rheumatica: two different but often overlapping conditions.

Genetic markers of disease susceptibility and severity in giant cell arteritis and polymyalgia rheumatica.

Diagnosis and classification of adult Still's disease

Osteoporosis is the most common contributing factor of spinal fractures, which characteristically are not generally known to produce spinal cord compression symptoms. Recently, an increasing number of medical reports have implicated osteoporotic fractures as a cause of serious neurological deficit and painful disabling spinal deformities. This has been corroborated by the present authors as well. These complications are only amenable to surgical management, requiring instrumentation. Instrumenting an osteoporotic spine, although a challenging task, can be accomplished if certain guidelines for surgical techniques are respected. Neurological deficits respond equally well to an anterior or posterior decompression, provided this is coupled with multisegmental fixation of the construct. With the steady increase in the elderly population, it is anticipated that the spine surgeon will face serious complications of osteoporotic spines more frequently. With regard to surgery, however, excellent correction of deformities can be achieved, by combining anterior and posterior approaches. Paget's disease of bone (PD) is a non-hormonal osteometabolic disorder and the spine is the second most commonly affected site. About one-third of patients with spinal involvement exhibit symptoms of clinical stenosis. In only 12–24% of patients with PD of the spine is back pain attributed solely to PD, while in the majority of patients, back pain is either arthritic in nature or a combination of a pagetic process and coexisting arthritis. In this context, one must be certain before attributing low back pain to PD exclusively, and antipagetic medical treatment alone may be ineffective. Neural element dysfunction may be attributed to compressive myelopathy by pagetic bone overgrowth, pagetic intraspinal soft tissue overgrowth, ossification of epidural fat, platybasia, spontaneous bleeding, sarcomatous degeneration and vertebral fracture or subluxation. Neural dysfunction can also result from spinal ischemia when blood is diverted by the so-called "arterial steal syndrome". Because the effectiveness of pharmacologic treatment for pagetic spinal stenosis has been clearly demonstrated, surgical decompression should only be instituted after failure of antipagetic medical treatment. Surgery is indicated as a primary treatment when neural compression is secondary to pathologic fractures, dislocations, spontaneous epidural hematoma, syringomyelia, platybasia, or sarcomatous transformation. Five classes of drugs are available for the treatment of PD. Bisphosphonates are the most popular antipagetic drug and several forms have been investigated.

Principles of management of osteometabolic disorders affecting the aging spine.

Adult onset Still disease is an unusual multisystem inflammatory disorder of unknown etiology and pathogenesis. Among its protean manifestations is pericarditis which occurs in approximately 30-40% of patients. Cardiac tamponade is a rare complication of pericarditis occurring in the context of Still disease. We conducted a review of the English literature pertaining to the occurrence of pericardial tamponade in Still disease. We searched relevant journals and the PubMed Medline databases. A total of eighteen reported cases were identified; ten among children and eight in adults. Treatment of pericardial tamponade was medical therapy alone in two cases versus combined modality, medical and surgical drainage in the remainder of the cases. Outcomes were death among four of the ten children and there was no recurrence of tamponade in the remaining child and adult series. This review re-emphasizes the importance of considering Still disease in the differential diagnosis of the life-threatening emergency of pericardial tamponade.

Cardiac tamponade in Still disease: a review of the literature.

Pericarditis is a common manifestation of adult still's diseases (ASD), observed in 20% to 3% cases. Pericardial tamponade is more seldom, less than ten cases have been reported in the literature. We reported two observations of patients with ASD and pericardial tamponade above a series of 18 patients with ASD, in one case revealed the disease. The first patient was a 32-year-old women and had fever, arthritis, high white blood cell count and developed pericardial tamponade. The evolution was favourable with bolus of methylprednisolone. In the second case, cardiac tamponade occurred several years after the onset of the disease. Surgical drainage was first required (800 ml) because of inefficacity of oral prednisone. A dramatic improvement was observed after bolus of methylprednisolone. In conclusion pericardial tamponade is a seldom but sometimes the first manifestation of ASD and may required in first intention bolus of methylprednisolone.

Complications cardiaques de la maladie de Still de l'adulte : de la péricardite à la tamponade parfois révélatrice

Cardiac tamponade is very seldom complication of adult onset-Still's disease. We reported 2 cases; it was the first manifestation of the disease in one case.

[Cardiac complication of adult-onset Still's disease: from pericarditis to tamponade, sometimes a manifestation of the disease].

Resume La pathogenie de la pseudopolyarthrite rhizomelique (PPR) et de la maladie de Horton (MH) est probablement multifactorielle, ce qui explique en particulier la diversite des resultats des etudes du genotype HLA DR. Toutefois, ces facteurs genetiques pourraient rendre compte de la diversite des formes cliniques d'une meme maladie comme la PPR par rapport a la Symptomatologie d'arterite temporale au cours de la MH. But de l'etude Etude comparative des antigenes HLA DRB1 au cours de la PPR et de la MH. Malades et methodes

Étude du polymorphisme HLA DRB1 au cours de la pseudopolyarthrite rhizomélique et de la maladie de Horton

Osteoporotic vertebral crush fractures with neurologic complications are rarely reported in the literature. We report six new cases particularly severe in which death occurred in two cases. The study group included four women and two men with a mean age of 75 years (range: 72-79). Vertebral collapse causing neurological deficit was T5, T9, T11 in two cases, L1 and L3. The mean number of vertebral collapses was three per patient (range: 1-9). Back pain appeared without traumatism 6 weeks before admission (range: 1-24). Neurological complications appeared 2.5 weeks after back pain (range: 1-8). One patient suffered from a paraplegia, three from a paraparesia with bladder dysfunction (n = 1). In one case there was a severe weakness of the levator muscles of the foot and in another a L3 femoral neuralgia with severe bowel and bladder dysfunction. X-rays demonstrated backwards displacement of the posterior cortex in three cases, an intravertebral vacuum phenomenon in two cases and a heterogeneous appearance suggesting a malignancy in two cases. Computed tomography, performed in four patients and tomography in one patient, demonstrated fragmentation of the vertebral body in all the cases and vacuum phenomenon in four cases. Magnetic resonance imaging performed in four cases has confirmed the absence of epiduritis and a compression due to bony structures in two cases. A vertebral biopsy was performed in three cases. Osteoporosis was observed in all the cases and in two cases there was also an osteonecrosis. Surgical treatment was performed in three cases and conservative medical treatment in the other cases. After surgical treatment we have observed an absence of improvement of neurological complications in one case, an improvement in another and finally a full recovery in the last case. After conservative treatment we have noted in two cases an absence of improvement of neurological complications and in one case an improvement of neurological deficit. Two patients died (one after medical treatment and another after surgical treatment).

Tassements vertébraux ostéoporotiques avec complications neurologiques sévères. À propos de six observations

Resume La polychondrite atrophiante est une maladie inflammatoire revelee une t'ois sur deux par une chondrite caracteristique auriculaire ou nasale, plus rarement par des manifestations beaucoup moins evocatrices comme une polyarthrite, une Symptomatologie respiratoire ou laryngee, une episclerite qui retardent toujours le diagnostic. A partir d'une serie de 15 cas de polychondrite atrophiante, revelee de maniere classique, les auteurs analysent, a partir du premier signe, le delai diagnostique: il est en moyenne de 3 ans et 6 mois (extremes de 3 mois a 17 ans) meme en cas de symptome initial evocateur (chondrite visible). Deux fois seulement le diagnostic est fait des la premiere poussee. Ce retard diagnostique a des consequences socioeconomiques et expose aux risques de complications graves, notamment laryngotracheales.

Manifestations révélatrices et retard diagnostique dans la polychondrite chronique atrophiante: à propos d'une série de 15 malades

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