Loss of weight was limited after prophylactic gastrostomy placement and early tube feeding. Moreover, the complication rate was low. In 82% of the NED patients the PEG could eventually be removed.

fixed complete, heart block may be a phase in the natural history of the development of idiopathic heart block. In our study the results of 24 h ECG monitoring did not differ greatly between group 1 (symptomatic athletic patients) and group 2 (symptom-free normal athletes). Apart from the exceptional case 16 in group 1, we found only 2 patients with documented ventricular pauses longer than 2-5 s. Clinical appreciation of loss of consciousness and accompanying symptoms led us to label the syndrome in group 1 as cardiac syncope and/or Stokes-Adams attacks. Prolonged absence of pulse was witnessed clinically in 2 patients. The complete disappearance of syncope in patients given pacemakers further supports the diagnosis of cardiac syncope. Symptoms subsided completely in 8 unpaced patients; acceleration of basic heart rhythm after they stopped competitive sports is likely to be the reason for the relief of symptoms. This result accords with the findings of Meytes" and Rasmussen.13 The life-threatening condition required pacemaker implantation in 7 patients in group 1. The question of whether these patients will need pacemakers all their lives remains; it must be answered by a future generation of cardiac pacemakers with built-in Holter facilities. The normal 'athlete does not suffer from any discomfort correlated with bradycardia, pauses/or both. We believe that there is no reason for warnings against competitive sports. Recent case-reports and rumours tend to myth.17 In our group 2 athletes we found only minor abnormalities. Schnohr obtained information about 297 (96' 7%) of 307 male athletic champions born in Denmark between 1880 and 1910 and compared their mortality with that in the general Danish male population.18 The athletic champions had a significantly lower mortality than the general population under the age of 50 years; after 50 years of age the mortality was the same. The causes of death were the same as in the general population.

No abstract

Both angiotensin-converting enzyme (ACE) inhibitors like lisinopril and nonsteroidal anti-inflammatory drugs (NSAIDs) like indomethacin have been shown to lower urinary protein excretion in renal disease. If this effect is caused by different mechanisms of action, the combination of these agents could have an additive antiproteinuric effect. We studied the effects of lisinopril and indomethacin separately and in combination in 10 patients with the nephrotic syndrome. Proteinuria was lowered from 10.5 ± 1.8 g/24 h in the control period to 4.5 ± 1.1 g/24h on indomethacin, 4.3 ± 1.0 g/24h on lisinopril and to 2.4 ± 0.8 g/24h on the combination. Glomerular filtration rate (GFR) fell on either monotherapy, but particularly on the combination of drugs. The renal hemodynamic changes suggested a preglomerular vasoconstriction by indomethacin and a postglomerular vasodilation by lisinopril. Severe hyperkalemia occurred in 3 patients on the combination therapy. We conclude that the combination of indomethacin and lisinopril has an additive antiproteinuric effect. This, as well as the more pronounced fall in GFR on the combination, may suggest that both drugs lower proteinuria by decreasing intraglomerular capillary pressure but via different mechanisms. Combining these drugs may be useful in the symptomatic treatment of nephrotic syndrome, but renal function and serum potassium should be monitored carefully.