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PubMed1982

Induced vasodilation as treatment for Raynaud's disease.

We examined the efficacy of induced vasodilation as a treatment of idiopathic Raynaud's disease. Eight persons with Raynaud's disease and seven normal persons each received 27 simultaneous pairings of hand immersion in warm water (43 degrees C) for 10 minutes with exposure of the whole body to cold (0 degrees C). A second group of seven normal persons and nine persons with Raynaud's disease received no treatments. All subjects had cold test exposures (0 degrees C) at the start and end of the study. Subjects with Raynaud's disease who received treatments showed significant increases in digital temperatures (2.2 degrees C) during the cold test compared with the values of untreated subjects with Raynaud's disease (p less than 0.05); normal subjects who had received treatments showed no difference from those who had not. Digital temperatures of subjects with Raynaud's disease after treatment increased to levels approaching those of normal subjects, although they showed lower digital temperatures during initial exposure to cold (p less than 0.01). This therapy offers a practical alternative to traditional treatments.

Adult↗
PubMed1982

Topical glyceryl trinitrate as adjunctive treatment in Raynaud's disease.

The effects of topical glyceryl trinitrate in Raynaud's disease were compared with those of placebo in a double-blind, crossover trial in 17 patients with bilateral Raynaud's disease and an associated collagen disease, who were receiving oral sympatholytic agents at the maximum levels they could tolerate. 1% glyceryl trinitrate ointment or a placebo of lanolin was applied to one hand only for 6 weeks, then patients changed to the other preparation for 6 weeks. The results were evaluated every 2 weeks. The frequency of attacks, severity of attacks, and size of ulcers in the treated hand were significantly lower when the patients were using glyceryl trinitrate ointment than when they were using placebo. The treatment of Raynaud's disease may be improved by using topical glyceryl trinitrate ointment as an adjunct to a basic regimen of oral sympatholytic agents. Glyceryl trinitrate ointment may obviate the need for more aggressive treatment, such as intraarterial reserpine, in selected patients.

Administration, Topical↗
PubMed1999

The cutaneous vasoconstrictor response to venous stasis is normal in subjects with primary Raynaud's disease.

In control subjects and in subjects with primary Raynaud's disease, sudden sound or a mild cool stimulus evokes the pattern of alerting response that includes cutaneous vasoconstriction but vasodilatation in forearm muscle. In control subjects, response habituates on repetition of these stimuli both within experimental sessions and over successive days. However, in subjects with primary Raynaud's disease, the cutaneous vasoconstriction and the muscle vasodilatation persist. We have now tested whether a similar disparity exists for the cutaneous vasoconstriction evoked by venous stasis, a response considered to be a veno-arteriolar reflex mediated by sympathetic fibers, but not requiring transmission through the spinal cord. In 10 subjects with primary Raynaud's disease and in 10 matched controls, a sphygmomanometer cuff on the left arm was inflated to 40 mm Hg for 2 minutes, five times on each of three experimental sessions on days 1, 3, and 5. Cutaneous red cell flux (RCF) was recorded from the pulp and dorsum of the left index finger by using a laser Doppler meter; digital vascular conductance (DCVC) was computed as RCF divided by arterial pressure. The first venous stasis, in session 1, evoked a decrease in pulp and dorsum DCVC in the control and primary Raynaud's subjects. There were no differences between the groups in the magnitudes or durations of these responses. Within session 1, the magnitude of the decrease in DCVC diminished on repetition of venous stasis in the dorsum in controls and in the pulp in primary Raynaud's subjects. We propose these effects reflected the similar reductions in baseline DCVC over time; there was no change in the duration of the responses. Repetition of venous stasis had similar effects in both groups of subjects within sessions 2 and 3. Further, judging from the mean of the responses evoked in each Session the decreases evoked in pulp and dorsum DCVC by venous stasis were fully consistent in magnitude and duration over the three sessions in both groups. These results indicate that the direct constrictor influence of sympathetic fibers upon cutaneous blood vessels is similar in magnitude and similarly reproducible in controls and subjects with primary Raynaud's disease. This reinforces our view that the lack of habituation of the cutaneous vasoconstrictor component of the alerting response in subjects with primary Raynaud's disease reflects impairment of the central neural process of habituation, rather than a peripheral phenomenon, and that this lack of habituation predisposes these subjects to vasospasm.

Adult↗
PubMed1980

Cold hypersensitivity after sympathectomy for Raynaud's disease.

Two patients with socially handicapping Raynaud's disease underwent bilateral upper thoracic sympathectomy. One to two days after the operation, both developed local hypersensitivity to cold in the form of a rebound. The cold hypersensitivity persisted in one of the patients, although complete degeneration of vasoconstrictor fibres was proven by absence of the sympathetic veno-arteriolar reflex after sympathectomy. Pre-operative sympathetic blockade could not predict the outcome of sympathectomy.

Adult↗
PubMed1987

Beta-blockers: a new therapeutic approach to Raynaud's disease.

Thirty-six patients with Raynaud's disease (RD) were treated with a low dosage of beta-blockers, atenolol (50 mg/day) or propranolol (20 mg/day). Previous data have suggested that the pathophysiology of RD may be mediated by presynaptic beta-adrenoceptors. In this research we report that chronic beta-blocker treatment, at low dosage, can prevent the cold-induced vasospasm. The majority of patients (28) responded to atenolol, and 8 patients refractory to atenolol responded to propranolol.

Adrenergic beta-Antagonists↗
PubMed1999

Anticentromere autoantibodies in patients without Raynaud's disease or systemic sclerosis.

Anticentromere autoantibodies (ACA) are associated with Raynaud's disease and systemic sclerosis (SSc). ACA usually bind at least one of three major centromere proteins (CENPs), particularly CENP-B. We identified 16 patients with ACA who do not have Raynaud's disease or SSc. The objective of this study was to determine whether these 16 ACA differ in antigenic specificity from the ACA found in patients with Raynaud's disease or SSc. Binding of these serum ACA was tested using competition experiments with recombinant CENP-B, and native centromere proteins from HEp-2 cells and HeLa nuclear extracts in ELISAs, immunoblots, and indirect immunofluorescence assays. The ACA from these 16 patients are strikingly different from those obtained from patients who have Raynaud's disease or SSc. Only 5 of the 16 index sera (31.25%) bound CENP-B from two or more different sources by at least two methods. Six of these 16 sera (37.5%) did not bind CENP-B on ELISA, and 8 of 16 (43.75%) did not bind CENP-B on immunoblots. Three sera did not bind CENP-B either by ELISA or immunoblots. Of the 13 sera that bound CENP-B, their patterns of binding to CENP-B strongly suggested that they bind different epitopes within the CENP-B antigen. Independently of their binding to CENP-B, these sera reacted mainly with minor CENP antigens detected by HeLa nuclear extracts. We have identified unusual ACA not associated with Raynaud's disease or SSc.

Adult↗
PubMed1996

Familial aggregation of primary Raynaud's disease.

OBJECTIVE: To determine the occurrence of familial aggregation of primary Raynaud's disease. METHODS: Twenty-three patients with primary Raynaud's disease and their first-degree relatives were assessed by questionnaire and, when possible, by physical examination. The same procedures were performed on the patients' spouses and the spouses' first-degree relatives, who served as the control group. RESULTS: The prevalence of Raynaud's disease was significantly higher in the families of the probands than in the control families when assessed by questionnaire (26.1% versus 5.5%; P < 10(-5)), and by physical examination (11.2% versus 2.8%; P = 0.015). CONCLUSION: These findings demonstrate that there is significant familial aggregation of primary Raynaud's disease.

Adult↗
PubMed1981

[Clinical and radiological observations in Raynaud's disease (author's transl)].

In Raynaud's phenomenon, there is functional abnormal blood flow in the vessels of the forearm. While blood flow is slow in the radial and ulnar arteries, it is good in the interosseous artery even accompanied by early filling of the deep veins--as seen on the flow of contrast material during angiography. This different behaviour of these three arteries makes a central nervous disorder an unlikely etiology, supported by the fact that drug therapy acting on the central nervous system are only of temporary help. The behaviour of the interosseous artery is easily diagnosed and presents an important clue for functional disturbance of blood flow in the radial and ulnar arteries. The findings were the same, regardless of the type of contrast material used (ionic, non-ionic or dimeric). X

Arm↗
PubMed1972

The pathogenesis of esophageal dysfunction in scleroderma and Raynaud's disease.

To determine the pathogenesis of esophageal dysfunction in scleroderma and Raynaud's disease, the lower esophageal sphincter (LES) was tested with: (a) methacholine acting directly at the cholinergic receptor on the muscle; (b) edrophonium, a cholinesterase inhibitor, enhancing the effect of released acetylcholine; and (c) gastrin I, acting through the release of acetylcholine. 10 patients with Raynaud's disease and 22 patients with scleroderma were compared with 20 normals and 20 patients with isolated LES incompetence. The mean basal LES pressure in normals was significantly greater than that recorded in both patients with scleroderma and Raynaud's disease. Six patients having scleroderma with normal peristalsis had an LES pressure significantly greater than that noted in 16 patients having scleroderma with abnormal peristalsis. In all groups, the per cent increase in LES pressure was similar when tested by direct muscle stimulation by methacholine. The response to agents that acted indirectly through intact cholinergic nerves differed in these groups. The LES response to gastrin I distinguished patients with normal peristalsis from those with abnormal peristalsis. The patients with normal peristalsis, either with scleroderma or with Raynaud's disease showed only a partial reduction in their response to gastrin I. The response to gastrin I was markedly reduced only in patients with abnormal peristalsis. These data indicate that in patients with scleroderma and Raynaud's disease, the LES response to direct muscle stimulation by methacholine was intact while the response to gastrin I and edrophonium was diminished.

Adult↗