Zinc homeostasis is achieved after intake variation by changes in the expression levels of zinc transporters. The aim of this study was to evaluate dietary intake (by 24-h recall), absorption, plasma zinc (by absorption spectrophotometry) and the expression levels (by quantitative PCR), of the transporters ZIP1 (zinc importer) and ZnT1 (zinc exporter) in peripheral white blood cells from 24 adolescent girls before and after drinking zinc-fortified milk for 27 day. Zinc intake increased (p < 0.001) from 10.5 ± 3.9 mg/day to 17.6 ± 4.4 mg/day, and its estimated absorption from 3.1 ± 1.2 to 5.3 ± 1.3 mg/day. Mean plasma zinc concentration remained unchanged (p > 0.05) near 150 µg/dL, but increased by 31 µg/dL (p < 0.05) for 6/24 adolescents (group A) and decreased by 25 µg/dL (p < 0.05) for other 6/24 adolescents (group B). Expression of ZIP1 in blood leukocytes was reduced 1.4-fold (p < 0.006) in group A, while for the expression of ZnT1 there was no difference after intervention (p = 0.39). An increase of dietary zinc after 27-days consumption of fortified-milk did not increase (p > 0.05) the plasma level of adolescent girls but for 6/24 participants from group A in spite of the formerly appropriation, which cellular zinc uptake decreased as assessed by reduction of the expression of ZIP1.

Severe hypertriglyceridemia is a rare cause of acute pancreatitis especially in non-alcoholic, non- gallstones, non-obese, non-diabetic patients and has a few options for its management. Hypertriglyceridemia-induced pancreatitis causes 1 to 14 percent of all cases of acute pancreatitis. The risk of developing acute pancreatitis is approximately 5 percent with serum triglycerides &gt;1000 mg/dL and 10 to 20 percent with triglycerides &gt;2000 mg/dL. This is the case of a 63-year-old female who came to the Emergency Department with acute onset of abdominal pain, located at the mid-epigastric region, radiating to back, 10/10 in a scale of severity, no alleviating or aggravating factor, accompanied by nausea, 5 episodes of bilious emesis. Past medical history includes recurrent acute pancreatitis induced by hypertriglyceridemia (3 episodes last year), arterial hypertension, and dyslipidemia treated with Fenofibrate and Atorvastatin. Denies toxic habits. Physical examination showed abdominal tenderness with positive bowel sounds. Laboratories report cholesterol: 44mg/dl, triglycerides: 5,831mg/dl, LDL: -735 mg/dl, and HDL: 13 mg/dl. The patient condition warranted admission to the intensive care unit with the diagnosis of severe hypertriglyceridemia induced pancreatitis. Initially managed with insulin drip, bowel rest, and conservative management, which did not result in any improvement in her symptoms. A successful method of treatment relies on plasmapheresis for the lowering of triglyceride levels. This was first reported in 1978 by Betteridge and can result in a rapid decrease in triglyceride levels over a short period of time compared to the other treatment options. In this case, vascular surgery was consulted for apheresis catheter placement, with triglyceride improvement from 5,831mg/dl to 973 mg/dl after initial and single apheresis intervention, as the patient's symptoms resolved. Triglyceride levels decreased to 113 mg/dl after a week of therapy with plasmapheresis. The patient continues evaluation at the outpatient clinic and currently has been without recurrence of pancreatitis for the last year. Finally, the use of insulin infusion in conjunction with plasmapheresis has been demonstrated to be a viable option for rapid improvement in symptoms associated with acute pancreatitis associated with elevated triglycerides. Plasmapheresis rapidly removes triglycerides from the circulation removing the inciting factor, decreasing inflammation, and damage to the pancreas. The patient's triglyceride level decreased to 973 mg/dl the next day from 5,831mg/dl initially and the patient's symptoms resolved. Plasmapheresis is not an established guideline for the management of hypertriglyceridemia -induced pancreatitis. Plasmapheresis lowers the lipid levels drastically within hours compared to conservative therapy that usually takes several days to achieve the same reduction in triglycerides levels. Presentation: No date and time listed

We report on a case of West Indian (Caribbean) punctate keratopathy (WIPK) in a pediatric patient living in Puerto Rico, USA. A 9-year-old Hispanic girl presented for a routine ophthalmic follow-up. The patient had a history of juvenile idiopathic arthritis and chronic bilateral anterior uveitis. At the presentation, her visual acuity was 20/30 in the right eye and 20/20 in the left eye. An examination of the right eye was remarkable for one round, white subepithelial corneal opacity of approximately 0.1 mm in height by 0.1 mm in width, located slightly lateral to the center of the cornea, which was consistent with WIPK. This case highlights the importance of recognizing WIPK in children who have a history of living on any one or more of the Caribbean islands.