ABSTRACT
Several scoring systems for clinical prediction of the severity of acute pancreatitis (AP) have been proposed. Yet, there is still a need for an easy-to-measure biomarker. Osteopontin (OPN) may be released to the circulation early during tissue injury, but the significance of OPN in AP has not yet been established. We aimed to evaluate plasma levels of OPN in relation to the severity of AP. In 39 individuals with confirmed AP, plasma was collected on the day of admission and consecutively for three days thereafter. Sex- and age-matched healthy blood donors (n = 39) served as controls. Plasma OPN was measured by a commercial enzyme-linked immunosorbent assay. At admission, patients with AP displayed higher OPN, 156.4 ng/mL (IQR 111.8-196.2) compared to controls, 37.4 ng/mL (IQR 11.7-65.7) (p < 0.0001). However, OPN levels on admission could not discriminate between mild and moderate-to-severe disease (132.6 ng/mL vs. 163.4 ng/mL). Nevertheless, the changes in OPN within 24 h of admission and Day 2/3 were higher among patients with moderate/severe AP (33.7%) compared to mild AP (-8.1%) (p = 0.01). This indicates that OPN is a relevant biomarker reflecting tissue injury in AP. The increase in OPN over time suggests that serial OPN measurements could contribute to the early detection of at-risk patients. Prospective studies assessing OPN in relation to outcome in AP are warranted.
ABSTRACT
INTRODUCTION: Herniation of cerebellar vermis through the foramen magnum, internal hydrocephaly and spina bifida cystica are the major signs of Chiari type II malformation. Spina bifida cystica (1 in 2000 neonates) is very often the first clinical manifestation of the disease. AIM: To discuss the pathomorphology, clinical picture and possible treatment of this underestimated malformation. PATIENTS AND METHODS: Lumbosacral spina bifida aperta and flaccid paraplegia of the lower limbs were found in a female newborn. Later on, pneumonia and evidence of markedly expressed internal hydrocephaly were found. At 48 days of age, surgical correction of the meningocele was undertaken. There was a sudden heart and respiratory arrest at the end of surgery but in spite of the cardiopulmonary resuscitation the infant died 24 hours later. RESULTS: Postmortem pathological examination revealed expressed internal hydrocephaly, small posterior fossa, herniation of vermis and atrophic medulla oblongata; presence of these signs verified the Chiari type II malformation. It is very difficult to diagnose this malformation antemortem without magnetic resonance imaging. Brainstem dysfunction is the most common cause of death in children under 2 years of age with Chiari type II malformation. Its clinical manifestation can be episodic and poorly expressed. CONCLUSIONS: A thorough understanding of this entity (clinical and pathomorphological manifestations) and magnetic resonance imaging are mandatory for the malformation to be diagnosed. Early recognition of symptoms of brainstem compression and a subsequent surgical decompression can decrease the high mortality rate among children with Chiari type II malformation.
