A case of acquired zinc deficiency in a mature breast-fed infant.

We describe a 5-month-old Japanese infant with zinc deficiency, who was exclusively breast-fed and showed improvement after zinc supplement was administered. His serum zinc level and the zinc content of breast milk from his mother were extremely low, although the mother's serum zinc level was within normal limits. Zinc deficiency would not be latently uncommon in a mature breast-fed infant.

Reducing cell membrane n-6 fatty acids attenuate mucosal damage in food-sensitive enteropathy in mice.

Mucosal damage is commonly observed in food-sensitive enteropathy in infants, and the generation of leukotrienes is involved in the pathogenesis of this enteropathy. Because supplementing n-3 fatty acids is known to modify the production of leukotrienes, we investigated whether a change of dietary fatty acid composition affects leukotriene synthesis and food hypersensitivity reactions in the intestine by using a mouse model of food-sensitive enteropathy. The model was prepared by feeding ovalbumin to BALB/c mice after intraperitoneal injection of cyclophosphamide. Diets were prepared from soybean oil (control), perilla oil, lard, corn oil, and 0.125 volume of corn oil (low fat diet) and given to mice for 4 wk. Villous heights, crypt depths, leukotriene B4 and C4 production in the intestine were measured. Crypt hyperplasia and villous atrophy were severer in the corn oil-fed group than those of control group, whereas mucosal damage in the perilla oil and low fat diet groups was minimal. In the corn oil-fed group, red blood cell membrane levels of n-3 fatty acids were lower than the control, and the synthesis of leukotrienes was highest among all groups. In the perilla oil and low fat diet groups, n-6 fatty acids were lower than those of control group and leukotriene production was significantly suppressed. These results indicate that reducing cell membrane levels of n-6 fatty acids by feeding less n-6 fatty acids or supplementing n-3 fatty acids, is important to suppress leukotriene biosynthesis for prevention from mucosal damage in food-sensitive enteropathy.

The regulation of intestinal hypersensitivity reactions to ovalbumin by omega-3 fatty acid enriched diet: studies of IEL and LPL in mucosal damage.

In order to clarify the mechanisms of food-sensitive enteropathy, a food hypersensitive model was generated by feeding ovalbumin to female BALB/c mice after intraperitoneal injection of cyclophosphamide and morphological and immunological changes in the gut mucosa were investigated. Villus atrophy, crypt hyperplasia and increased numbers of intra-epithelial lymphocytes (IEL) were confirmed in this model, as seen in food-sensitive enteropathy in humans. Subpopulations of IEL and lamina propria lymphocytes were enumerated by immunohistochemical observation. CD8-positive cells were increased both in epithelium and lamina propria, whereas CD4-positive cells were decreased in lamina propria. We document here that orally administered food antigen actually induces food-sensitive enteropathy and mucosal damage is generated by lymphocytes that infiltrate the intestinal mucosa. We also investigated the effect of feeding an omega-3 fatty acid-enriched diet in this model and found that it was efficient in attenuating mucosal damage.

Prostaglandin E1, E2, and F2 alpha in human milk and plasma.

Concentrations of prostaglandin E1, E2, and F2 alpha (PGE1, PGE2, and PGF2 alpha) were determined in milk and plasma from mothers of 9 preterm and 11 term infants. The concentration of PGE1 in milk was similar to that in plasma, and the concentrations of PGE2 and PGF2 alpha were approximately 1.2-2 times higher than those in plasma. However, no significant differences in the levels of PGE1, PGE2, and PGF2 alpha were observed between the foremilk and hindmilk, among the colostrum, transitional milk, and mature milk, and between preterm and term milk. Further studies have to be performed to confirm that the stable levels of PGE1, PGE2, and PGF2 alpha in human milk found in this study play an important role in the gastrointestinal function of infants.

Prostaglandin and fatty acid metabolism in patients with extrahepatic biliary atresia.

The relationship between essential fatty acid (EFA) deficiency and disturbance of prostaglandin (PG) biosynthesis was studied in children after radical operation for extrahepatic biliary atresia (EBA). In addition, to investigate the method for treatment of postoperative EFA deficiency and disturbance of PG biosynthesis, the serum fatty acid and plasma PG levels were determined before and after supplementation of an EFA-rich powder (38 g of linoleic acid per 100 g of powder) through Suruga II enterostomy. Before administration of the EFA-rich powder, linoleic acid, arachidonic acid, PGE1, and PGF2 alpha levels were significantly lower in both good bile excretion and poor bile excretion groups than in the control group. After administration, linoleic acid and PGE1 levels significantly increased in the good bile excretion group as compared with the preadministration values. These results suggest that the supplementation of EFA-rich powder is an effective treatment for linoleic acid deficiency and disturbance of PGE1 biosynthesis in postoperative EBA patients.

Primary hyperparathyroidism. Case report and management.

A 13-year-old girl presenting with abdominal pain, polyuria, polydipsia, and radiologically confirmed renal calculi was diagnosed as having primary hyperparathyroidism. Laboratory data revealed markedly elevated serum calcium, low phosphorus, and elevated parathyroid hormone. Other parathyroid function tests also confirmed the diagnosis of primary hyperparathyroidism. Ultrasound examination showed a small echogenic nodule in the parathyroid gland. Following a single gland resection, the extremely high serum calcium level promptly decreased to normal range, and it has remained normal.