Primary Raynaud's phenomenon. Age of onset and pathogenesis in a prospective study of 424 patients.
ABSTRACT Many authors consider that late onset is a suspect criterion for differentiating primary Raynaud's phenomenon (Raynaud's disease, RD) from Raynaud's syndrome (RS). However, many cases of late-onset Raynaud's phenomenon in patients over forty years of age remain without etiologic diagnosis and therefore deserve the designation "late-onset RD." One hundred and ninety-four patients with RD (143 women, 51 men) were selected among 424 patients with Raynaud's phenomenon, according to Allen and Brown's criteria with negative serologic investigations and normal capillaroscopy. The purpose of the study was to consider the possible discriminant value of age of onset in distinguishing between RD and RS. The following epidemiologic features were studied: age of onset, sex, family history of Raynaud's phenomenon and migraine, and smoking and working habits. Microcirculation was assessed by capillaroscopy and strain-gauge plethysmography. Maximal digital flow at 45 degrees C and reactivity to cold were determined for each patient. Results were related to age of onset. The existence of true cases of late-onset RD in patients over forty years of age was confirmed (prevalence 27%), showing a correlation with a family history of Raynaud's phenomenon inferior to that found in early-onset cases (p < 0.0001). Microcirculation studies generally indicated a strong correlation between reactivity to cold, familial RD, and early onset, whereas no correlation was found with migraine or smoking. Nor was there any clinical or plethysmographic evidence for arteritis as a possible pathogenetic factor in late-onset RD. These results indicate that late-onset RD is a valid designation and that its pathogenesis seems less dependent on genetic sensitivity to cold than that of early-onset cases. In the absence of underlying arteritis, neurovascular dysfunction or a hemorheologic mechanism may be suggested as plausible causes of late-onset RD.
[show abstract] [hide abstract]
ABSTRACT: The objective was to assess the management, and short- and longer-term outcome of patients presenting with an acute blue finger. This was a retrospective, case-note review and prospective follow-up by telephone and general practitioner enquiry. All patients who presented with sudden onset blue discolouration of a finger within the previous 72 h, with normal radial and ulnar pulses, were included. From 2000 to 2006, 22 patients, 15 female, 7 male, were reviewed. Median age was 56 years (range, 19-88 years). Median time from onset of blue finger was 6 days (range 1 day to 3 months). In most cases (17), no underlying cause was identified. Five patients had an underlying cause; two had symptoms compatible with Raynaud's phenomenon, one patient had signs (later confirmed on MRA) of arterial thoracic outlet syndrome and two had polycythaemia (haemoglobin > 17 g/dl). Otherwise, all laboratory investigations were normal. Upper limb duplex, echocardiogram and 24-h cardiac tapes were normal in all cases. Median follow-up was 19 months. Three patients had recurrent symptoms in the finger. No patient suffered tissue loss or loss of digit(s), and none had stroke or arterial embolisation. The acute blue finger is a benign condition not suggestive of arterial embolisation. Tissue or digit loss is not a threat and, in the longer term, there is no threat of embolisation to other vascular sites.Annals of The Royal College of Surgeons of England 09/2008; 90(7):557-60. · 1.23 Impact Factor
Article: Raynaud's phenomenon.[show abstract] [hide abstract]
ABSTRACT: Vascular acrosyndromes constitute a common reason for physician visits. They are associated with connective tissue disease; for example, 90% of patients with scleroderma experience Raynaud's phenomenon. The rheumatologist must strive to establish the diagnosis, to identify a potential underlying cause, and to prescribe effective treatment when the symptoms are incapacitating. Raynaud's phenomenon is the acrosyndrome most commonly encountered by rheumatologists. The diagnosis of Raynaud's phenomenon rests on clinical grounds. Nailfold capillaroscopy and immunological tests are useful chiefly for determining the cause. Calcium-channel antagonists are the treatment of reference for Raynaud's phenomenon. Drugs introduced over the last few years for severe refractory forms include prostacyclin and its derivatives, endothelin receptor antagonists, and phosphodiesterase inhibitors. These drugs were developed as a result of new knowledge on the pathogenesis of Raynaud's phenomenon. Acrocyanosis, which is extremely common, and erythromelalgia are the other main vascular acrosyndromes.Joint, bone, spine: revue du rhumatisme 02/2007; 74(1):e1-8. · 2.25 Impact Factor
Article: 7-oxo-DHEA and Raynaud's phenomenon.[show abstract] [hide abstract]
ABSTRACT: Patients with Raynaud's phenomenon have abnormal digital vasoconstriction in response to cold. The pathogenesis remains unknown but may involve a local neurovascular defect leading to vasoconstriction. Diagnosis of primary Raynaud's phenomenon is based on typical symptomatology coupled with normal physical examination, normal laboratory studies and lack of observable pathology by nail fold capillaroscopy. Secondary Raynaud's phenomenon is known to occur associated with several connective tissue diseases, vascular injury due to repeated vibrational trauma, and other causes which produce demonstrable vascular and microcirculatory damage. Treatment of Raynaud's symptoms is conservative and aimed at prevention of attacks. Patients are advised to remain warm and, if possible, to live in warm climates. We suggest that an ergogenic (thermogenic) steroid, 7-oxo-DHEA (3-acetoxyandrost-5-ene-7,17-dione), which is available without prescription as the trademarked 7-keto DHEA, may be very helpful in prevention of primary Raynaud's attacks by increasing the basal metabolic rate and inhibiting vasospasm.Medical Hypotheses 04/2003; 60(3):391-7. · 1.39 Impact Factor