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P Priollet

Publications and source records attributed to P Priollet.

At least 91 records · Page 5Linked to original sources
PubMed1988

[Reestablishment of the clinical diagnosis in vascular acrosyndromes].

Raynaud's phenomenon (RP) is very frequent with a prevalence of 4% in a general population. Its evaluation has to be simple noninvasive and cheap. The only difficulty is to differentiate early primary RP from secondary RP that may evolve principally to a connective tissue disorder. Two questions have to be solved 1--Is it a primary or a secondary RP? 2--In case of secondary RP how to obtain a more precise diagnosis? Clinical examination alone is able to give a response for question 1 with 76% of reliability. Information has to be collected about sex, age at onset, occupation, uni or bilaterality of the disability, thumb involvement and drug consumption. Physician has to examine skin carefully, pulses, arterial bruits, heart, lungs, the time of return of color of digits after squeezing the blood out of the hand by clenching with and without compression of the radial and/or the cubital artery. Inquiries should be made about visceral involvement: oesophageal dysfunction, dyspnea, sicca syndrome, thyroiditis or polyneuritis that rule out a primary form of Raynaud's phenomenon.

Auscultation↗
PubMed1987

How to classify Raynaud's phenomenon. Long-term follow-up study of 73 cases.

Raynaud's phenomenon without an underlying cause was diagnosed in 96 consecutive patients in 1978 to 1979. Seventy-three patients were available for long-term follow-up. They were classified on initial evaluation as having primary Raynaud's phenomenon (49 patients) when no clinical, laboratory, or serologic abnormality was detected, and as having suspected secondary Raynaud's phenomenon when at least one finding was abnormal. Re-evaluation was performed in 1984 to 1985 after an average duration of Raynaud's phenomenon of 14.9 +/- 12 years. The average duration of the follow-up from initial to final evaluation was 4.7 +/- 1 years. On final evaluation, none of the 49 patients with an initial diagnosis of primary Raynaud's phenomenon had evidence of secondary Raynaud's phenomenon, whereas 14 of the 24 patients with suspected secondary Raynaud's phenomenon had a definite diagnosis. Among them, there were 13 connective tissue diseases. The study proved that Raynaud's phenomenon without an underlying cause must be followed up for more than two years, contrary to what was recommended previously, before it can be rightly diagnosed as primary Raynaud's phenomenon. Moreover, the results suggested that, in order to distinguish early primary Raynaud's phenomenon from suspected secondary Raynaud's phenomenon, a simple and noninvasive evaluation is sufficient. In this study, the evaluation included history and clinical examination, tests for antinuclear antibodies, radiography of hands, chest roentgenography, and nailfold capillary microscopy.

Adult↗
PubMed1987

A new cold test for the diagnosis of Raynaud's phenomenon.

An objective test for the diagnosis of Raynaud's phenomenon is useful for three reasons: 1. the phenomenon may not be evident at the time of the clinical examination, 2. proof of diagnosis is required by insurance companies when an occupational origin is suspected, and 3. to assess drug induced improvement. Most cold tests in the medical literature are either complex and expensive or unreliable for routine clinical use. We studied cold induced post-ischemic reactive hyperemia in 14 patients with Raynaud's disease and in 15 healthy controls. The hand was immersed in a stirred water bath at 13 degrees C, and ischemia was induced by placing an inflatable tourniquet around a finger for five minutes. Afterwards the tourniquet was deflated while the hand remained in the cold water bath. The temperature of the finger with the deflated tourniquet was compared with that of an adjacent finger serving as control. Hyperemia was the increase in differential temperature between these two fingers after tourniquet release minus the difference in temperature existing before deflating the tourniquet. With a normal lower limit of 0.7 degrees C for hyperemia, 13 of the 14 patients with Raynaud's phenomenon were abnormal (93% sensitivity), and 14 of the 15 controls were normal (93% specificity). All these 14 controls were also normal at a second examination done to assess test reproducibility. A false-positive healthy control was still positive at the second examination. This new, simple and inexpensive cold test can reliably diagnose Raynaud's phenomenon. Further studies are necessary to establish its reliability in monitoring the effectiveness of treatment in prospective trials.

Adolescent↗
PubMed1987

An abnormal antithrombin III (AT III) with low heparin affinity: AT III Clichy.

We have identified an inherited qualitative deficiency of antithrombin III (AT III) in a family with apparently no increased incidence of venous thrombosis. Plasma antithrombin and anti-Xa activities were normal, but the interaction with heparin, heparan sulphate and low molecular weight heparin was uniformly decreased. An immunoblotting technique performed in plasma showed normal complex formation with thrombin. By using heparin-Sepharose affinity chromatography and crossed immunoelectrophoresis, the variant could be separated: at least two fractions of low affinity AT III were obtained. A minor one had no antiprotease activity; the other one was further purified to homogeneity and found to have normal specific activity in absence of heparin and a 50% decreased activity in presence of heparin. We propose to call this new variant AT III Clichy.

Adult↗
PubMed1987

[Update on the treatment of systemic scleroderma].

Renewed clinical trials of drugs used for many years and the availability of new symptomatic therapies allows selection of appropriate treatment for progressive systemic sclerosis. Colchicine damages intracytoplasmic microtubules and when administered at a dose of at least 1.5 mg per day during early stages of the disease reduces cutaneous sclerosis without improving other manifestations of scleroderma. D-penicillamine inhibits bridge formation during collagen maturation, acting mainly on cutaneous infiltration with more uncertain effects on visceral localizations of the disease. It can be effective against pulmonary lesions but, as with colchicine, must be prescribed early. Its action is delayed and its side effects limit its use. Corticoids are of very limited efficiency and although they may be useful for relief of muscular and articular localizations they have been accused of precipitating onset of renal insufficiency. Immunodepressants have until now been assessed as ineffective. The demonstration in patients with progressive systemic sclerosis of abnormal activation of immunity system cells suggested the use in this collagen disease of a new immunosuppressive agent, cyclosporine A, but clinical utility of this drug remains to be demonstrated. In systemic sclerosis efficacy of plasma exchange is mainly directed against vasomotor disorders and digital ulcerations, but study results are difficult to assess because of associated therapies. Constraints and risks of this treatment also considerably reduce its interest. The coagulation factor XIII acts as a stabilizing factor of collagen. It reduces cutaneous infiltration but its efficacy is based on results of a single controlled trial and its use is limited by the need for repeated intravenous injections.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1986

Nailfold capillary microscopy in mixed connective tissue disease. Comparison with systemic sclerosis and systemic lupus erythematosus.

Nailfold capillary microscopy patterns in 22 patients with mixed connective tissue disease (MCTD) were compared with those of 21 patients with systemic lupus erythematosus (SLE) and 30 patients with systemic sclerosis (scleroderma [SD]). Microvascular data were classified blindly as follows: normal, nonspecific abnormalities, SD pattern, and SLE pattern, with special attention to the presence of dystrophic, branched "bushy" capillary formations. Of the 22 patients with MCTD, 63.6% had an SD pattern, 22.7% had an SLE pattern, 13.6% had nonspecific abnormalities, and 72.7% had bushy capillary formations. Compared with SLE microangiopathy, MCTD microangiopathy exhibited significantly greater capillary loss (P less than 0.05), more frequent SD patterns (P less than 0.001), and more frequent bushy capillaries (P less than 0.001). Compared with SD patients, MCTD patients displayed less frequent SD patterns (P less than 0.02) and more frequent bushy capillary formations (P less than 0.01). The presence of bushy capillaries was suggestive of MCTD. For diagnostic purposes, bushy capillaries displayed 72% sensitivity, 80% specificity, and 87.2% negative predictive value. The quantitative and qualitative expressions of microangiopathy were different in MCTD and SLE, respectively. This supports the hypothesis that each disease is a distinct entity. Nevertheless, there were many resemblances between MCTD and SD, which implies that MCTD is possibly a clinical form of SD.

Adult↗