It has been reported [10–12] that the incidence of AP in children has shown an upward trend in recent years. The incidence rate in children in the United Kingdom was about 0.78/100 000 [13], while in the United States, this figure was 3–13/100 000 [3]. In this study, the clinical characteristics of AP in children in southwest China were analyzed and summarized. As far as we know, this is the first report in English on the clinical features of AP in children from China.
The etiology of AP in children is significantly different from that in adults. In previous studies, Poddar et al. [14] studied 320 children with AP from India and found that trauma (21%) and biliary tract disease (10%) were the most common causes of AP in children. Park et al. [15] found that the biliary tract (36.2%) and drugs (25.6%) were the leading causes of AP in 215 children in the United States. In another study of 115 children in the United States [16], idiopathic (31%) and drug associated (23%) were the main causes. We found that biliary (31.5%), idiopathic (28.5%) and traumatic (16.2%) were the main causes, which was consistent with most studies. In adults, biliary obstruction leading to AP is almost always due to a stone or tumor; however, in children, 30% of cases are caused by biliary silt rather than complete calculus [3, 6]. No study has reported on this difference. In addition, metabolic problems such as hyperlipidemia in children were significantly rarer than in adults. Only 2–7% of children with AP have metabolic causative factors [10, 11]. In this study, 12 cases (9.2%) were caused by hyperlipidemia. In the control group of adults, high fat levels accounted for 33.8%, and the difference was significant. The most exciting finding in our study was that viral infectious pancreatitis was more common in young children and the rate was significantly different from that in adults. We consider that is was related to the incomplete development of the immune system in young children. The mechanism of AP related to virus infection is not clear at present, although some research has shown that the virus directly invades pancreatic cells [3]. In recent years, with the extensive use of drugs, drug-induced pancreatitis has shown a significant increasing trend, although, overall, it is still constitutes less than 10% of cases [17].
Our study showed that the severity of AP in children was similar in all age groups, which is consistent with a previous report [3], but the disease was less severe than in adults. Possible reasons are: (1) Children were admitted to the hospital earlier than adults because of reduced tolerance, in order to get treatment as soon as possible; (2) In terms of etiological composition, hyperlipidemia and alcoholic pancreatitis account for few cases in children, and some studies have shown that hyperlipidemia and alcohol can easily lead to SAP [18]; (3) In terms of complications, pancreatic necrosis is positively correlated with the severity and prognosis of the disease. Necrotizing pancreatitis is rare in children. According to the literature [19], necrotizing pancreatitis occurs in less than 1% of children with AP. Among the five large sample pediatric cases reported in the United States [20], only 3 of 1014 children with AP had pancreatic necrosis, which was significantly less severe than that of adults. (4) Pediatric biliary AP often results from the formation of silt, so the rate of operation is less than in adults, and there are fewer complications due to biliary diseases.
For AP with specific causes, such as bile duct stones, anatomical abnormalities, bile duct dilatation, etc., it has been suggested that surgery should be performed as soon as possible after the condition is controlled and stable, to prevent recurrence [11, 21]. In the literature [22], the mortality rate of pediatric AP is less than 5%, which is significantly lower than that of adult AP, possibly because: (1) Alcoholic pancreatitis is rare in pediatric cases, and alcoholic pancreatitis is a known cause of high mortality, with a mortality rate as high as 30.6% [23]. (2) With age, adults may lose some critical protective mechanism, which children retain [6]. (3) Adult cases may be associated with severe underlying diseases, while AP in children is rarely associated with multiple problems with organ function. (4) The severity of the disease in children is significantly lower than that in adults, which has also been confirmed in this study.
Some single-center studies have estimated that 10–35% of children with AP develop ARP [24, 25]. These studies showed that mutations of PRSS1, SPINK1, CFTR, and CTRC13 were firmly related to the progression of ARP. During the first attack of AP in children, age, male sex, pancreatic necrosis, and higher Body Mass Index (BMI) have been associated with the progression of ARP. Anatomic abnormalities of the biliary tract, hyperlipidemia, and genetic factors should be evaluated in cases of recurrence [11, 16, 26]. In our study, among the 19 children (14.6%) with ARP, includes a 2-year-old toddler with congenital bile duct dilatation. We found that female sex, hyperlipidemia, and primary AP with pancreatic necrosis were significantly correlated with ARP, and the severity of primary AP was positively correlated with ARP. The relationship between ARP and sex is controversial and perhaps related to the predominance of hyperlipidemia and biliary tract disease in women [27, 28].
Differences in our findings from those of from previous studies may have resulted from differences in race, region, and environment. Hyperlipidemia is an apparent cause of AP and ARP in adults [29], but there has been no analysis of a large sample of ARP cases in children. It has been reported in the literature that hypertriglyceridemia occurring secondary to AP may be related to various genetic mutations [30]. From this point of view, our findings coincide with previous research results.
The disadvantage of this study is that it was a single-center study in China. Thus, the findings of this study cannot be generalized. For the 19 patients with ARP, the etiology of recurrence needs to be examined by endoscopic retrograde cholangiopancreatography and genetic analysis, and there is a lack of corresponding genetic and clinical data in this study. In future, multi-center studies with a larger sample and more rational perspective are needed to analyze pediatric pancreatitis in order to facilitate better treatment.