[Intermittent claudication of the lower limbs may mask another problem...!].
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Biomedical subjects
Publications and source records attributed to F Eulry.
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Thirty-nine patients with rheumatoid arthritis who had presented with tarsitis before, were investigated at the level of the rearfoot. The first 17 patients had CT with previous tenography when it was possible; the following 22 patients had MRI with gadolinium injection. Tendon involvement appeared in 52.9% of the cases on CT, and in 90% of the feet on MRI; therefore, in case of clinical or radiological signs of tarsitis, it appears that tendon involvement must be suspected. With the two procedures the tibialis posterior tendon lesions were very predominant. In the majority of the patients (31/39), there was associated involvement of two or more tendons. If there is a ruptured tendon, the authors think that one must be cautious with surgical tendinous transfer; indeed, the long-term results of this surgical procedure present a strong probability of being compromised in rheumatoid arthritis which is a progressive disease.
We report 16 cases of epiphyseal metatarsal stress fractures in 11 patients. Four patients had osteoporosis and two of these four were under fluoride therapy. Three of the fractures occurred upon resumption of weight-bearing. The fractures were distributed over the five rays; seven fractures were located to the second metatarsal. Manifestations were acute focal metatarsal pain, diffuse edema of the forefoot and inflammatory metatarsophalangeal arthropathy. Delayed, transient visualization of a linear area of epiphyseal sclerosis occurred in 14 cases. Radionuclide bone scans consistently showed early accumulation of the tracer in the metatarsal head. The focus of increased activity extended to the shaft in three cases. The main differential diagnoses are second ray syndrome, metatarsophalangeal arthritis, focal radial reflex sympathetic dystrophy of the foot and osteonecrosis of the metatarsal heads. The clinical and roentgenographic outcome was consistently favorable after one month without weight-bearing. These fractures can simulate, complicate, induce (two cases), reflex sympathetic dystrophy of the foot or occur concomitantly with (two cases).
Diffuse uniform vertebral osteosclerosis in vertebra affected by osteoporotic crush fracture, without osteonecrosis is reported. Multiple fissure-fractures were seen upon magnetic resonance imaging.
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The distribution of alpha-1-antitrypsin phenotypes was similar in 555 controls and 98 patients with ankylosing spondylitis: the MM phenotype (including "main" MM subtypes, i.e., M2M2 and M3M3, and "secondary" MM subtypes) was found in 86% of subjects and "rare" phenotypes combining M, F, S, and Z in 14%. Six per cent of the controls and none of the ankylosing spondylitis patients had the M4M4 phenotype (p < 0.01). Respiratory function tests were performed in 49 patients with axial ankylosing spondylitis and 30 controls matched on sex, age, body mass index, smoking status, nonsteroidal antiinflammatory drug use and distribution of "main" and "secondary" phenotypes (no subjects in this study had "rare" phenotypes); the significant reduction in chest expansion seen in the ankylosing spondylitis group (5.6 +/- 2.7 cm versus 8.7 +/- 1.2; p < 0.001) was correlated with total capacity (p < 0.04) and vital capacity (p < 0.001). Restrictive ventilatory dysfunction was seen in four ankylosing spondylitis patients versus no controls (p < 0.02). Proximal airway obstruction, pulmonary distension and decreases in the diffusing capacity for carbon monoxide were seen in similar proportions of ankylosing spondylitis patients and controls. In the ankylosing spondylitis group, evidence of pulmonary distension included increases in mean residual functional capacity and mean residual volume (105.6 +/- 21.2% versus 94.8 +/- 17.4, p < 0.03, and 100.3 +/- 22.8% versus 88.6 +/- 17.9, p < 0.04, respectively) and bullous emphysema in the lung bases in two patients (versus no controls). In the small subgroup of ankylosing spondylitis patients with lung distension or a decreased diffusing capacity for carbon monoxide, smokers and nonsmokers were evenly balanced but subjects with "secondary" phenotypes outnumbered those with "main" phenotypes (p < 0.02); in contrast, our data suggested that smoking may play the central role in the proximal airway obstruction. Our findings suggest that in addition to previously established causes of pulmonary involvement in ankylosing spondylitis a "secondary" MM phenotype (i.e., neither M2M2 nor M3M3) may be a risk factor for lung distension and impaired diffusing capacity for carbon monoxide.
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The lumbar spine bone density (BMD) was assessed by single energy quantitative tomography in 16 young patients with non traited Klinefelter's syndrome (19 +/- 2.2 yr) and in 16 age weight- and height-matched control males. The BMD were significantly lower in the patients than in the control group (175 +/- 26 mg/cm3 K2HPO4 vs 204 +/- 26; p < 0.02). The authors found a significant correlation between BMD and plasmatic levels of testosterone and estradiol suggesting the hormonal origin of the osteopenia whereas no correlation was found with serum calcium, phosphorus or prolactin levels or hydroxy-proteinuria. Such osteopenia in young patients with Klinefelter's syndrome supports early androgenic treatment of these patients.
The foot is among the sites most often affected in spondyloarthropathies, whose diagnostic criteria include heel pain and sausage-like swelling of the toes. Few studies have systematically analyzed foot manifestations in reactive arthritides. We retrospectively reviewed 143 patients fulfilling Amor's criteria. One hundred five patients (73%) exhibited inflammatory involvement of one (n = 47) or both feet. In 8 cases no other articular sites were affected. Heel pain was reported by 36% of patients (52/143), within the first six months in half the cases. Both heels were painful in 26 patients. Heel pain was plantar in 36 cases, posterior in 7 cases, and bipolar in 4 cases. Roentgenographic calcaneal changes were found in 54 cases overall but in only 31 of the patients with heel pain. Sixteen patients had asymptomatic calcaneitis. Seventeen patients had involvement of the transverse tarsal joint, usually with no other affected joints. Involvement of the subtalar joint was rare (6 cases). Metatarsophalangeal manifestations were found in 44% of patients (64/143) and were symmetrical in 17 cases; 17 patients had changes of the great toe suggestive of gout. Interphalangeal arthritis was seen in 22% (32/143) of cases; in half these cases the first two rays were affected and sausage-like digital swelling was seen in 28 patients (20%). Permanent roentgenological damage was uncommon.
Plasma levels of cholesterol, triglyceride, HDL-cholesterol, and apolipoproteins A1 and B were assayed in ninety patients (sixty-four male and twenty-six female) with reflex sympathetic dystrophy and in ninety controls matched for age, sex, and body mass index (BMI). No significant differences were found between the two groups for the proportions of patients with increased plasma cholesterol levels (6.6% versus 4.4%) or increased plasma triglyceride levels (40% versus 30%), as defined by Turpin's age and sex-specific criteria, or for mean values of these parameters. In the 38 patients with reflex sympathetic dystrophy of less than 3.5 months duration, plasma triglyceride levels were significantly higher than in the 38 matched controls (1.24 + 0.57 g/l versus 1.02 +/- 0.91; p = 0.04). In patients (n = 52) with disease of more than four months duration (range 4-39), plasma triglyceride levels were similar in the two groups. Lipidemia was similar in patients and controls regardless of age, sex, topography of the disease, clinical manifestations, and whether or not the disease was due to an injury. This study, in contrast to previous reports, failed to disclose an association between reflex sympathetic dystrophy and hyperlipidemia. Transient hypertriglyceridemia may occur during the first 3 1/2 months of the disease as a result of initial immobilization.
To appreciate hyperlipidaemia as a contributing factor to reflex sympathetic dystrophy (RSD), we have evaluated basal lipidic values (cholesterol, HDL-cholesterol, triglycerides, apolipoproteins A1, B) and frequency of hypertriglyceridaemia (Turpin's diagnosis criteria) in 75 cases of RSD and in 75 paired controls. No difference exists in both groups with regard to frequency of hypertriglyceridaemia or basal lipidic values. These values seem independent of age, sex, duration of localization or etiology (traumatic or nontraumatic) of RSD. Hyperlipidaemia does not seem a contributing factor to RSD.
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