Respiratory failure in acute pancreatitis: the role of free fatty acids

Hypertriglyceridemia has been noted in patients with acute pancreatitis and respiratory failure. Utilizing an isolated, perfused, canine pulmonary lobe, the effect of triglyceride infusion on pulmonary function was evaluated. When heparin was used to anticoagulate the perfusion circuit, the addition of triglyceride to the autologous blood perfusate resulted in massive weight gain (226 gm), intrapulmonary shunting (36%), and a marked drop in pulmonary compliance (congruent to 50%). Heparin activates lipoprotein lipase, and therefore some triglyceride in the perfusate was lipolyzed with a resultant increase in serum free fatty acids (FFAs) to 253 mumole/dl. When anticoagulation of the perfusion circuit was accomplished by defibrinogenation with Arvin, the addition of triglyceride to the autologous blood perfusate caused minimal weight gain (28 gm), no intrapulmonary shunting, and only a slight decrease in pulmonary compliance (22%). Arvin has no effect on lipoprotein lipase, and the FFA level in the perfusate remained normal (less than 70 mumole/dl). Thus it appears that FFA release secondary to the action of pulmonary lipoprotein lipase on blood triglyceride is the important pathogenic step in the induction of respiratory failure in this model.     

Colitis cystica profunda

Colitis cystica profunda is a benign disease of the colon. Its importance lies in differentiating it from mucus-producing adenocarcinoma. It has rarely been described in the surgical literature. A review of records of patients seen at the Mayo Clinic produced 66 clinical cases of localized colitis cystica profunda, and in 21 patients the diagnosis was confirmed histologically. Follow-up, which was available in all patients, ranged from 2 months to 29 years, with a mean follow-up of more than 8 years. The data suggest that local excision is the preferred initial therapy.     

Breast-feeding protects against respiratory syncytial virus infections

Eight out of 115 infants admitted to hospital with respiratory syncytial (RS) virus infection had been breast-fed compared with 46 out of 167 controls; this difference was statistically significant. Twenty-one specimens of human colostrum were examined, and all contained RS virus neutralising activity. Specific IgA and IgG were detected in 18 specimens, whereas IgM was detected in none. The titre of IgA antibody was usually higher and correlated more closely to the titre of neutralising activity than that of IgG. Infants inhale milk feeds and regurgitate them through the nose, and the IgA collecting in the respiratory tract might protect against severe respiratory infection. Alternatively, if severe RS virus illness is a sign of hypersensitivity to the virus breast-feeding might protect the infant from an early sensitising infection.     

Granulomas and cholestatic--hepatocellular injury associated with phenylbutazone. Report of two cases

A combined cholestatic-hepatocellular injury and noncaseating granulomas occurred in two patients 1 and 4 weeks after phenylbutazone therapy. Both patients were jaundiced, one had a macular rash, and both had peripheral blood eosinophilia. Symptoms and signs subsided, and abnormal findings from tests of hepatic function rapidly returned to normal following withdrawal of the drug. Sections of liver biopsy specimens 6 months later showed no granulomas or other pathologic changes. Previously reported cases are reviewed.     

Repeated neonatal deaths in families with special reference to causes of death

It is recognized that one infant death in a family indicates an increased risk of death of a subsequent sibling. This study examines which cause of death of a sibling is related to the mortality of the younger sibling and when. Longitudinal vital events data from the maternal and child health and family planning (MCH-FP) project and the comparison areas in Matlab, Bangladesh, were used. Primary causes of 868 neonatal deaths and 624 post-neonatal deaths resulting from 18,865 singleton live births in 1989-92 and those (967 as neonates and 708 as post-neonates) of their immediate elder siblings were categorised into infectious and non-infectious diseases. Multinomial logistic regression was used to estimate the risk of younger siblings dying in each age period from infectious and non-infectious diseases given the age and cause of deaths of older siblings and controlling for other biosocial correlates of infant mortality. A neonatal death of non-infectious causes in a family was twice as likely to be followed by another one occurring at the same age from similar causes compared with a surviving infant followed by a neonatal death from non-infectious causes. The MCH-FP project, though successful in reducing the risk of neonatal and post-neonatal mortality from infectious diseases, did not reduce the risk of dying from non-infectious diseases.     

Protein kinase C regulation of ATP-induced phosphoinositide hydrolysis in bovine aorta endothelial cells

This study investigated the mechanism of protein kinase C-mediated inhibition of ATP-induced phospholipase C activation in cultured bovine aorta endothelial cells (BAEC). In BAEC labeled with 3H-inositol, phorbol myristate acetate (PMA) prevented ATP-induced inositol bisphosphate and inositol trisphosphate formation. In membranes prepared from these PMA-treated cells, Ca(2+)-, sodium fluoride-, GTP gamma S-, and ATP plus GTP gamma S-stimulated inositol bisphosphate, but not inositol trisphosphate, formation was inhibited. Inositol trisphosphate phosphatase activity was not altered in membranes from PMA-treated BAEC. These results suggest that 1) protein kinase C inhibits ATP-induced phospholipase C activation in BAEC through interference with the coupling of phospholipase C with a G-protein and through an effect on phospholipase C itself, and 2) different mechanisms are responsible for the inhibition by protein kinase C of the phospholipase C-mediated hydrolysis of phosphatidylinositol bisphosphate and phosphatidyl-inositol phosphate.