OBJECTIVE. Our goal was to test the hypothesis that children who exhibit bed-wetting during childhood were less likely to be breastfed during infancy compared with normal controls. METHODS. A case-control study was conducted in a pediatric continence center and a general pediatric practice. Cases (n = 55) were recruited from the continence center and defined as children 5 to 13 years of age who experienced lifetime involuntary voiding of urine during nighttime sleep at least 2 times a week in the absence of defects of the central nervous system or urinary tract. Age- and gender-matched controls (n = 117) who did not exhibit bed-wetting were enrolled from a general pediatric practice. Infant feeding practices were measured as breastfeeding (yes/no) and, for those who were breastfeed, by the duration of breastfeeding and the time of formula supplementation. RESULTS. Among the case subjects, 45.5% were breastfed, whereas among the controls 81.2% were breastfed. The controls reported higher household incomes than the case subjects, and their mean family size (number of children) was slightly lower. After adjusting for race, income, and family size, the odds ratio was 0.283, indicating that case subjects were significantly less likely than controls to be breastfeed. Among all the study subjects who were breastfed, controls were breastfed for a significantly longer period than case subjects (an average of 3 months longer). Although breastfed controls were less likely to be supplemented with formula than breastfed case subjects, this difference was not statistically significant. CONCLUSIONS. Breastfeeding longer than 3 months may protect against bed-wetting during childhood. Breast milk supplemented with formula did not make a difference in the rate of enuresis.

Most studies testing vasoactive agents in portal-hypertensive rats have been performed in young animals. To assess age-related changes in hemodynamic responses to adrenergic stimuli, we examined (a) responsiveness to norepinephrine (0.14 to 12.0 micrograms.kg-1.min-1) in young (3-mo-old) and aged (9-mo-old) sham-operated and portal-hypertensive rats and (b) response to propranolol (2 and 10 mg.kg-1 body wt), nitroglycerin (3.6 mg.kg-1.min-1) or saline solution in aged portal-hypertensive rats. Aged rats exhibited significantly (p < 0.05) smaller responses to norepinephrine with regard to increases in mean arterial pressure and superior mesenteric arterial vascular resistance, irrespective of portal hypertension. Portal hypertension alone potentiated this reduced response in aged animals and was associated with cardiovascular hyporesponsiveness to norepinephrine in young rats. Portal pressure was significantly (p < 0.05) lower in aged sham-operated rats than in young sham-operated rats over a wide range of norepinephrine doses. Portal-hypertensive aged rats showed significantly (p < 0.05) lower heart rates. Furthermore, systemic and splanchnic cardiovascular responses to propranolol and nitroglycerin mediated by the sympathetic nervous system were decreased or negligible in aged rats, compromising the portal-hypotensive effects of these drugs. In summary, aged rats express diminished cardiovascular responsiveness to adrenergic stimuli. Therefore age should be considered an important factor in studies evaluating pharmacological agents for the treatment of portal hypertension.

Restenosis, the major limitation of balloon angioplasty, is the result of intimal hyperplasia after the procedure. Lovastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) inhibitor, may influence intimal hyperplasia by lowering serum cholesterol and by blocking deoxyribonucleic acid (DNA) synthesis. To determine whether lovastatin reduces intimal hyperplasia, a prospective, randomized blinded study was performed in 60 atherosclerotic New Zealand White male rabbits. Atherosclerosis was produced by air desiccation injury followed by a 28 day diet of 2% cholesterol and 6% peanut oil that was terminated before balloon angioplasty was performed. Angioplasty could not be performed in 14 rabbits with bilateral femoral artery occlusion, and in one rabbit the procedure was a technical failure.Forty-five rabbits underwent balloon angioplasty performed with use of a 2.5-mm balloon inflated to 10 atm for three 1 min dilations at 1 min intervals. Seven rabbits died during the procedure. Thirty-eight rabbits were randomized to either a lovastatin group (6 mg/kg body weight per day) or a control group. Angioplasty was performed on all patent vessels ( n = 54); the procedure was bilateral in 16 rabbits and unilateral in 22. Fifteen lovastatin-treated and 15 control rabbits survived 39 days after angioplasty and were then killed. Angiograms, obtained before and 10 min and 39 days after balloon angioplasty, were read with use of electronic calipers by two observers who had no knowledge of treatment data. After the rabbits were killed, vessels were pressure perfused using a standardized protocol to maintain in vivo dimensions for blinded quantitative histologic analysis.After balloon angioplasty, total cholesterol decreased 36 +/- 13% (mean +/- SEM) in the lovastatin group (p < 0.05) and 26 +/- 15% in the control group (p < 0.05, one-sided t test). The percent decrease in angiographic luminal diameter from 10 min to 39 days after angioplasty was less in the lovastatin group (n = 22) than in the control group (n = 23) (reader 1: 13 +/- 11% versus 47 +/- 8%, p < 0.05; reader 2: 17 +/- 8% versus 47 +/- 8%, p < 0.01). Intimal thickness was 0.16 +/- 0.02 mm in the lovastatin group and 0.30 +/- 0.04 mm in the control group (p < 0.01). Thus, lovastatin reduced intimal hyperplasia after balloon angioplasty of the femoral artery in the hypercholesterolemic atherosclerotic rabbit. Its effect in patients undergoing coronary angioplasty should be evaluated.

We have studied both the distribution and incidence of colorectal cancer using The Connecticut Tumor Registry, the oldest tumor registry in the United States. During the time period 1973 to 1985, left-sided colon cancers accounted for 63% of the cancers, right-sided cancers 33%, and cancers with unspecified sites 4%. Indeed, this pattern of distribution has remained constant for 25 years. For the period 1935 to 1985, we calculated the sex-specific, age-adjusted (normalized to the 1970 U.S. Census) incidence. Age-adjusted incidence of rectal cancer has remained stable for 50 years: for men, 22.8 cases/100,000/year, and for women, 13.9 cases/100,000/year. During these 50 years, the age-adjusted incidence of cecal carcinoma for men has increased from 3.6 to 16.7 cases/100,000/year, while for women, it has increased from 4.9 to 14.2 cases/100,000/year. Sigmoid carcinoma for men has increased from 8.8 to 18.7 cases/100,000/year, and for women, it has increased from 7.7 to 12.8 cases/100,000/year. The incidence of colon cancer at each site has been and continues to be increasing at a constant rate. Age-adjusted incidence for all colorectal cancers has increased from 35.2 to 70.2 cases/100,000/year for men and from 32.1 to 49.2 cases/100,000/year for women. Thus, distribution of colorectal cancers by site in Connecticut has remained stable for 25 years. More importantly, however, the age-adjusted incidence of colon cancer has continued to increase for 50 years, whereas that of rectal cancer has remained relatively stable.

We reviewed 100 consecutive cases of massive upper gastrointestinal hemorrhage (UGIH). The criteria for inclusion were a decrease in hematocrit greater than or equal to 6%, unstable vital signs, and greater than or equal to units of blood transfused (16 +/- 18 units, mean +/- SD). A multiple regression analysis of 96 variables was employed to determine the most accurate predictors of outcome. The overall mortality was 35%. Hospital status (whether the patient was an inpatient or outpatient when the UGIH began) showed a striking association with mortality (70% for inpatients vs. 22% for outpatients, p less than 0.001). Nonsurvivors also had a greater number of life-threatening diseases than survivors (1.4 +/- 1.1 vs. 0.3 +/- 0.5, p less than 0.001) and greater transfusion requirements (27 +/- 20 units vs. 10 +/- 13 units, p less than 0.001). Age, the presence of cirrhosis, and recent excessive alcohol intake were not important risk factors. At presentation, the most reliable predictor of a fatal outcome was the brevity of the interval between the onset of bleeding and the initiation of a medical work-up. The primary predictor when considering the entire hospitalization was the number of life-threatening diagnoses. Our data indicate that stratification for hospital status and for other potentially predictive risk factors should be incorporated in future trials of therapy for UGIH.

Leukopenia, thrombocytopenia, and hemolytic anemia occur commonly in advanced cirrhosis. Some investigators have reported that portacaval anastomosis (PCA) abolishes hypersplenism while others have not found PCA to be uniformly beneficial. We compared the frequency of hypersplenism before and after admission to a controlled investigation of the effects of PCA in 52 unoperated control subjects and 38 patients with patent PCA. The two groups were followed for an average period of 51/2 years. On admission to the study leukopenia was present in about 2% of patients, thrombocytopenia in 6%, and hemolytic anemia in 4%. Splenomegaly was present in 48% and hypersplenism in 11%. After randomization splenomegaly disappeared more frequently in the shunted group. In addition, fewer patients with PCA developed splenomegaly for the first time after inclusion into the study than did unoperated control subjects. Leukopenia, thrombocytopenia, and hemolytic anemia, when present at inclusion into the study, disappeared with equal frequency in the shunted and unshunted patients, and appeared with equal frequency in both groups after randomization in previously unaffected patients. In no instance was hypersplenism clinically significant nor was splenectomy considered or carried out in any of these 90 patients. In additional uncontrolled studies we observed that therapeutic PCA did not affect hypersplenism differently from prophylactic PCA. We conclude that PCA has neither clinically nor statistically significant effects on hypersplenism.

In order to determine the composition of “normal” ascitic fluid, the results of analysis of the first paracentesis on 347 consecutive cirrhotic patients with ascites at the West Haven Veterans Administration Hospital between 1955 and 1976 were examined. The ascites was considered “normal” in 259 patients. Bacterial peritonitis was present in 51, malignant ascites in 18, pancreatitic ascites in 15, and ascites of other types in 4 patients. Normal ascites is sterile, usually clear, and contains 281±25 leukocytes/mm3 (mean±Sem), 27±2% of which are polymorphonuclear. Inspontaneous bacterial peritonitis the fluid is usually cloudy, contains 6084±858 white blood cells/mm3, 77±4% of which were PMN and culture is positive for a single bacterial species, usually enteric in origin.Malignant andpancreatitis ascites are sterile, often cloudy, and contain an average of 696±273 and 1821±833 leukocytes/mm3, respectively, about half of which are polymorphonuclear. Amylase activity is increased in pancreatitic ascites, but not in other types of ascites. Stained smears of sediment for bacteria are often positive in bacterial peritonitis, but not in the other categories. Neither the specific gravity, protein concentration, nor glucose level is useful in the differential diagnosis of ascites. Based on the critical number of leukocytes alone, (500/mm3), one can accurately differentiate infected from uninfected fluid in over 90% of ascitic patients.