Timing of invasive procedures during chest tube therapy in spontaneous pneumothorax is undefined. Evaluation of 115 patients with primary and secondary spontaneous pneumothorax treated with tube thoracostomy revealed nearly maximal healing rates after 48 hours without a relevant increase if drainage was maintained for up to 10 days. In secondary spontaneous pneumothorax, a significantly lower healing rate was observed after 48 hours compared with primary spontaneous pneumothorax (60% vs 82%). Therapeutic success was not predictable by single clinical variables available at admission (eg, age, gender, and smoking habits) nor by their combinations. Recurrence rates were 30% in both primary and secondary spontaneous pneumothorax. Hospital stay averaged 6 days in primary and 15 days in secondary spontaneous pneumothorax. Considering their efficacy and the low incidence of complications, the early use of invasive procedures such as surgical pleurectomy, after 48 hours of persistent gas leaking, seems justified. Shorter in-patient care and lower recurrence rates may result.

No abstract

A B S T R A C r To determine the quantitative relationship of urinary hydroxyproline peptide excretion to collagen breakdown, known quantities of radioactive hydroxyproline peptides were administered to unlabeled animals and excertion of radioactivity in respiratory carbon dioxide, urine, and feces was measured. The major routes of excretion of collagen peptide metabolites were respiratory carbon dioxide (75%) and urine, as hydroxyproline-containing peptides (25%).Since the predominant urine hydroxyproline peptide linkage is prolyl-hydroxyproline, L-prOlyl-L-hydroxyproline-3H was administered to unlabeled animals. Greater than 80% of the administered dipeptide was excreted in urine, suggesting that this peptide linkage is not hydrolyzed to a significant extent in vivo.These data suggest that urinary hydroxyproline excretion is a "fairly" sensitive indicator of collagen breakdown and can be used at the clinical level to quantitate changes in collagen breakdown. creted in urine, about 97% in the form of peptides and 3% as the free imino acid (3). The dietary intake of gelatin has resulted in a marked increase of urinary excretion of bound hydroxyproline (3,4). The amino acid composition of urinary hydroxyproline peptides before (5, 6) and after (6) gelatin feeding in normal subjects suggests that urinary hydroxyproline peptides are endproducts of collagen degradation. The predominant urinary hydroxyproline peptides, prolyl-hydroxyproline and glycyl-prolyl-hydroxyproline, contain amino acid sequences known to occur frequently in the collagen molecule (7). To further implicate collagen breakdown as the source of urinary hydroxyproline peptides are the observations that excretion increases or decreases in a number of clinical conditions where an increase or decrease in collagen breakdown would be expected (8)(9)(10)(11). INTRODUCTIONUrinary hydroxyproline peptide excretion would be most useful in the analysis of diseases of connective tissues at the clinical level if it represents a quantitatively significant and fairly constant fraction of the hydroxyproline released by collagen degradation. Since urinary hydroxyproline excretion is almost entirely in the form of peptides, its quantitative importance would appear to depend on what proportion of the peptides released by the degradation of collagen is excreted in urine, what proportion is further degraded to carbon dioxide, and whether this is a fairly constant relationship.The present investigation approaches the question of the quantitative significance of urinary hydroxyproline peptide excretion by techniques similar to those used in the study of plasma proteins (12, 13). Known quantities of radioactive hydroxyproline peptides were administered to unlabeled animals and the distribution of excretion in urine, respiratory carbon dioxide, and feces was measured. This approach permits an estimation of the quantitative significance of each of these pathways from the distribution of excretion of radioactivity. The Journal of Clinical Investigation Volume 48 1969 1These s...

No abstract

A patient with a phaeochromocytoma and severe left ventricular heart failure caused by a catecholamine-induced cardiomyopathy is described. The clinical signs of congestive heart failure resolved rapidly on treatment with captopril and myocardial performance became normal within two weeks of medical treatment with captopril for one week and with captopril in combination with phenoxybenzamine for another week. (Br Heart J 1992;68:527-8) figure).During the next two days the patient's blood pressure fluctuated considerably. On the third day extubation could be performed and treatment with vasopressors was stopped. The patient became again hypertensive; systolic blood pressure peaked at over 230 mm Hg. Medical treatment with diuretics and nifedipine was unsuccessful. Captopril, however, controlled blood pressure and improved the clinical signs of left ventricular failure within eight hours.A tenfold increase in the catecholamine concentration in a 24 hour urinary sample confirmed the suspected phaeochromocytoma. A computer tomogram of the abdomen showed a mass of 5-5 x 3 5 cm in diameter in the region of the left adrenal gland. This mass was the only area to show increased uptake of '35I-meta-iodobenzyl-guanidine. The appearance of the endomyocardial biopsy specimen was consistent with a catecholamine-induced cardiomyopathy. One week later treatment with captopril was started and the patient was also given increasing doses of the ac antagonist, phenoxybenzamine (up to 60 mg a day). A week later, a radionuclide angiocardiography showed a complete normal myocardial performance and the calculated ejection fraction was 65%.The phaeochromocytoma was removed one week later without complication. One week after operation the serum and urinary concentrations of catecholamines were within the normal ranges. Discussion