Flurbiprofen and Fludrocortisone in Severe Autonomic Neuropathy

Perkins, C. M.; Lee, M.R.

doi:10.1016/s0140-6736(78)92392-9

Cited by 6 publications

(1 citation statement)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previously, we did not find any improvement after indomethacin in the postural hypotension in three fully diagnosed cases of the Shy Drager syndrome. However, in one study in which the diagnosis was proven, benefit did occur during the use of fludrocortisone and flurbiprofen in combination (Perkins & Lee, 1978). In this study, the greater than normal excretion of urinary PGFM before indomethacin treatment suggests that prostaglandins of various series might be involved in the pathogenesis of postural hypotension.…”

Section: And In Patients Withmentioning

confidence: 55%

The pressor actions of noradrenaline and angiotension II in chronic autonomic failure treated with indomethacin.

Davies¹,

Bannister²,

Hensby³

et al. 1980

Brit J Clinical Pharma

View full text Add to dashboard Cite

1 Indomethacin treatment of postural hypotension in four patients with chronic autonomic failure increased their pressor supersensitivity to intravenous noradrenaline without causing fluid retention. 2 All patients were supersensitive to angiotensin II in spite of normal levels of plasma renin activity in the supine position and therefore (by inference) of angiotensin II. This suggests that in autonomic failure, the degree ofangiotensin receptor occupancy by endogenous angiotensin II is not important in determining pressor sensitivity to exogenous angiotensin II. Indomethacin increased the pressor supersensitivity to angiotensin II in all patients 3 Indomethacin treatment decreased supine plasma renin activity to 50% of the level present before indomethacin treatment. 4 Indomethacin increased the lying but not the standing blood pressure. The failure to raise the standing pressure may be the result of the additional postural stress overcoming any vasoconstriction resulting from the increased sensitivity of vascular receptors to noradrenaline. The decrease in plasma renin activity could also contribute to the failure of indomethacin to prevent a fall in blood pressure on standing. 5 In our patients the excretion of the main urinary metabolite (PGFM) of prostaglandin F2X was higher than recorded previously in normal controls. During treatment with indomethacin, plasma indomethacin levels were in the range at which inhibition of prostaglandin synthesis occurs and the excretion of PGFM was decreased. 6 Indomethacin was not effective in the treatment of postural hypotension in these patients with autonomic failure.

show abstract

Section: And In Patients Withmentioning

confidence: 55%