An outbreak of Salmonella reactive arthritis in Northern Ireland.

During a five month period in the summer of 1987, seven cases of reactive arthritis were seen at Musgrave Park Hospital, Belfast. Of the seven patients, five were male and two female. Their ages ranged from 13 to 44 (mean: 26 +/- 4) years. Five patients gave a preceding short history of diarrhoea which was usually mild. All patients presented with acute inflammatory oligoarthritis which predominantly affected the lower limbs. The knees were involved in 100%, the ankles in 70% with enthesopathy in 30% of cases. The diagnosis was confirmed in all cases by positive serology for Salmonella enteritidis. In three patients, stool cultures grew a particular strain of Salmonella enteritidis (phage type 4). Six patients were HLA-B27 positive. It is not possible to estimate the prevalence of reactive arthritis in this outbreak because there were different sources of infection and the total number of gastroenteritis cases was unknown. However, gut infections with Salmonella enteritidis are becoming increasingly common in this community and throughout the Western world. Over the past two years, in our area, there has been an almost thirty-fold increase in the number of recorded cases of infections due to this organism. By far the commonest source of infection appears to be poultry and egg products.

The effect of acute and chronic captopril therapy on baroreflex function in man.

1. The effect of captopril 12.5 mg three times daily for 14 days on baroreflex sensitivity was investigated in six normotensive salt-replete male subjects. 2. Baroreflex sensitivity [delta R-R interval ms/mmHg systolic blood pressure (SBP)] was assessed following decreases and increases in SBP with glyceryl trinitrate and phenylephrine respectively and during Valsalva's manoeuvre. 3. Captopril had no effect on supine intra-arterial SBP or R-R interval on days 1 and 15 compared with placebo. However decreases (P less than 0.05) which occurred in plasma angiotensin II on day 1 (12.3 +/- 0.8 to 7.6 +/- 1.5 pg ml-1) and on day 15 (14.5 +/- 1.5 to 6.3 +/- 0.5 pg ml-1) and increases (P less than 0.02) in plasma renin activity on day 1 (1.2 +/- 0.7 to 4.8 +/- 0.8 ng A I ml-1 h-1) and on day 15 (1.1 +/- 0.2 to 5.4 +/- 0.9 ng A I ml-1 h-1) compared with placebo, indicated angiotensin-converting enzyme inhibition. 4. Baroreflex sensitivity was unchanged by captopril on day 1 and day 15 compared with placebo following the use of glyceryl trinitrate and phenylephrine to deactivate and activate respectively the baroreceptors, and during the strain and release phases of Valsalva's manoeuvre.

Renal and cardiovascular effects of caffeine: a dose-response study.

The effects of increasing oral doses of caffeine (45, 90, 180 and 360 mg) on effective renal plasma flow (ERPF), plasma renin activity (PRA), serum electrolytes, plasma noradrenaline, blood pressure and heart rate were studied in eight healthy male volunteers. Urine volume was increased by 360 mg of caffeine only. At caffeine doses greater than 90 mg urinary sodium excretion was significantly increased. There were no changes in ERPF. Serum potassium was significantly reduced by 360 mg of caffeine. Caffeine increased systolic pressure in a dose related manner. Diastolic pressure was also increased, but not in relation to dose. A 360 mg dose of caffeine produced a late increase in heart rate. These changes were not associated with any alterations in PRA or in plasma noradrenaline.

The effect of chronic captopril therapy on platelet angiotensin II receptor density and vascular responsiveness to angiotensin II infusion.

The density of angiotensin II (Ang II) receptors on the platelet and the vascular responsiveness to infused angiotensin II before and after two weeks of captopril therapy were examined in ten healthy male volunteers. There was a significant increase in blood flow to the forearm, but no significant changes in either the density of angiotensin II receptors or the pressor response to infused angiotensin II following captopril therapy. The study demonstrates that long term reduction of angiotensin II formation by captopril in man does not increase the responsiveness of the receptors to infused angiotensin, nor results in an "up regulation" of the angiotensin receptors. It also provides further evidence that some of the long term vasodilator effects of captopril may be mediated by mechanisms other than inhibition of angiotensin I (Ang I) converting enzyme.

The effect of chronic captopril therapy on adrenergic receptors, plasma noradrenaline and the vascular responses to infused noradrenaline.

Adrenergic receptors (alpha 2, beta 2), plasma noradrenaline, heart rate and the pressor responsiveness to infused noradrenaline were examined in ten healthy male volunteers before and after 2 weeks of placebo or captopril therapy in a double blind cross-over study. No significant differences in these measurements were observed between the captopril and placebo treated groups. The study shows that in sodium replete normotensive subjects, long-term angiotensin converting enzyme inhibition does not lead to changes in adrenoceptor density. There is also no alteration in plasma noradrenaline levels nor in the pressor responsiveness to infused noradrenaline. These data suggest that the known interaction between the renin-angiotensin system and the sympathetic nervous system observed in animals is probably of little significance in man.

Comparison of the acute vascular effects of frusemide and bumetanide.

The acute peripheral vascular and diuretic effects of intravenous frusemide 10 mg and 20 mg were compared with those of bumetanide 250 micrograms and 500 micrograms in a group of 10 salt depleted volunteers. Significant reductions in forearm blood flow (FBF) were observed after frusemide 10 mg (-0.77 ml 100 ml-1 min-1 P less than 0.05) and 20 mg (-0.75 ml 100 ml-1 min-1 P less than 0.01 at 15 min). No changes were observed after bumetanide. The reductions in blood flow produced by frusemide were significantly different from those of bumetanide (P less than 0.05) at 15 min. Increases in venous capacitance (VC) and mean arterial blood pressure (MAP) were observed after frusemide but these differences were not statistically different from placebo or bumetanide. No increases were seen after bumetanide. Plasma aldosterone concentrations were unchanged after either drug but plasma renin activity (PRA) was increased after frusemide 10 mg (4.42 +/- 1.01----8.50 +/- 1.90 ng A I ml-1 h-1 P less than 0.01) and 20 mg (4.01 +/- 0.72----7.81 +/- 2.27 ng A I ml-1 h-1 P less than 0.05). No increases were observed after bumetanide and significant differences between bumetanide and frusemide were observed (P less than 0.01). This study demonstrates that the acute peripheral arterial effects of frusemide are not observed after comparable diuretic doses of bumetanide. The differences appear to be related to the ability of the drugs to stimulate acute renin release from the kidney.