[Protocol diagnosis and empirical treatment of acute bronchitis]. / Protocolo diagnóstico y tratamiento empírico de la bronquitis aguda.

Acute bronchitis is an inflammatory disease of the highest caliber area that appears most frequently in cold months, affecting up to 5 % of the adult population. Clinically characterized by cough, may be associated with purulent sputum, and in some cases self-limiting existing bronchial hyperreactivity. Systemic antibiotics for treatment is not recommended.

The effect of verbal instructions on blood pressure measurement.

AIM: To determine whether orally delivered instructions can modify the intensity and direction of blood pressure and heart rate fluctuation. METHODS: The blood pressure of 120 subjects, 60 hypertensive and 60 normotensive, was measured before and after oral instructions. The normotensive subjects were selected from a sample of university students and the hypertensive patients were selected at a routine medical screening. Each sample of 60 subjects was randomly divided into four groups of 15. Each subject was left seated alone in a room for 5 min. The researcher then measured the subjects' blood pressure and heart rate. Following this, each group of normotensives and hypertensives was told that their blood pressure would diminish, or that it would not change or that it would increase. The control group was given no instructions. After 5 min the blood pressure and heart were measured again. RESULTS: In the normotensive and hypertensive groups who were told that their blood pressure would increase, systolic blood pressure increased by 4.3 and 2.5 mmHg, respectively. In the groups who were told that their blood pressure would decrease, systolic pressure fell by 7.8 and 7.4 mmHg, respectively. Those who were told that no change would occur showed a systolic pressure decrease of 3.5 and 1.8 mmHg, respectively. In the control groups systolic blood pressure decreased by 5.6 and 4.2 mmHg, respectively. CONCLUSIONS: These results show that oral instructions are a source of variation in the assessment of blood pressure and emphasize the need for 24-h blood pressure monitoring to eliminate this type of variation.

Gastrointestinal aluminium absorption: is it modulated by the iron-absorptive mechanism?

Gastrointestinal aluminium (A1) absorption has been proved but its mechanism is still unknown. This study investigates the pattern of A1 absorption in patients with different degrees of iron stores. We studied 29 haemodialysis patients forming three groups according to their serum ferritin values. Over seven days all patients received the same dose of aluminium hydroxide after which patients with 'low-normal' and normal serum ferritin increased their serum A1 proportionally with the increased aluminium hydroxide intake. By contrast patients with high serum ferritin did not show any change in their serum A1 values. Our results therefore suggest that a 'common pathway' of metal absorption could be implicated in A1 absorption. Serum ferritin might be a valuable predictor of different behaviour.

Assessing the benefit of changing aluminium hydroxide schedule on anaemia and serum phosphorus control.

Convincing evidence exists concerning aluminium hydroxide (A1 (OH)3) absorption and risk of toxicity. Over recent years our aim has been to reduce exposure to this risk. In this study we evaluated the effect of changing our A1 (OH)3 prescription policy, reducing its intake by stopping the breakfast dose, separating the iron intake from the binder's influence, and tailoring the A1 (OH)3 dose according to the protein intake patterns. The change was done gradually, initially in a pilot group and then in the whole unit. The results from the pilot group, who completed two years follow-up and from the whole unit, when more patients adhered to the new scheme, were similar. After the A1 (OH)3 reduction serum phosphorus did not change, haemoglobin increased and the blood transfusion requirements decreased. These results support our preliminary findings that A1 (OH)3 might interfere with erythropoiesis and stress the necessity of reassessing the prescription of binders thoroughly aiming to give adequate individual doses according to the different protein intake patterns.

Response of aldosterone and blood pressure to angiotensin II infusion in anephric man. Effect of sodium deprivation.

Angiotensin II, infused intravenously, increased plasma aldosterone concentration in two of six anephric subjects taking their usual dietary quantities of sodium. After 3 days of dietary sodium restriction and weight-reducing hemodialysis, the aldosterone response to infused angiotensin II in the two previously reactive subjects was enhanced, while the four previously unreactive subjects also showed a rise in plasma aldosterone. Before and after sodium depletion the anephric subjects were less responsive than normal subjects. Even when sodium-depleted, the anephrics showed no further rise in plasma aldosterone when arterial plasma angiotensin II was increased by infusion to concentrations greater than 50-199pg/ml, in contrast to sodium-depleted normals who show progressive aldosterone responses with plasma angiotensin II concentrations up to at least 370pg/ml. Before the infusion of angiotensin II, arterial plasma renin, angiotensin II, and aldosterone were detectable in the anephrics, but were unchanged by dietary sodium restriction or weight-reducting hemodialysis. Sodium depletion caused significant falls in weight, plasma sodium, and blood pressure, but no changes in plasma potassium or cortisol. Increases in blood pressure in relation to increments of arterial plasma angiotensin II were unaffected by sodium depletion, as might be expected in the absence of a rise in endogenous angiotensin II.

Mechanism of renal hypertension.

Renal hypertension of the two-kidney type is divided into three stages. In the first, hypertension results from the vasoconstrictor effect of angiotensin II. This persists to some extent in the second phase but there is in addition a slow-developing pressor effect, also resulting from angiotensin II and probably attributable to sodium. In the first two phases removal of the abnormal kidney corrects the hypertension. This fails in the third phase because changes in the opposite kidney maintain hypertension. Renin and angiotensin are probably not involved at this stage.