胃肠外营养支持治疗慢性阻塞性肺病29例

用胃肠外营养支持治疗29例慢性阻塞性肺病患者并设对照组，临床结果表明胃肠外营养支持治疗能改善慢性阻塞性肺病患者的营养状况，增加体重和提高白蛋白；能弥补慢性阻塞性肺病病人的微量元素缺乏；能增强慢性阻塞性肺病病人的细胞免疫和体液免疫功能，以上结果与对照组比较有极显著性差异（P＜0.001）。     

输注脂肪乳剂对肝功能变化的动态观察

报道葡萄糖加10％脂肪乳剂双能源完全胃肠外营养(TPN)支持病例118例,TPN时间1～2周者78例,2～4周者32例,4～8周者6例,8周以上者2例。TPN支持期间通过检测血清胆红素、ALT、AKP对肝功能进行动态观察。本组118例TPN支持前后肝功能无异常改变。结果表明,在双能源TPN支持时,脂肪供能占总热能的25％～30％是一个安全的剂量。     

胃肠外营养对Wistar大鼠胃癌细胞动力学影响的研究

通过测定TPN后不同时间内,肿瘤细胞周期中各时相细胞百分率的变化,对15例Wistar大鼠胃癌进行了前瞻性、随机化研究。结果发现TPN支持后24小时,肿瘤细胞周期中的5％、增殖细胞百分率增加而GO/G~_1％下降,而持续TPN达48小时这些改变消失。由此提出:(1)TPN加速肿瘤细胞更新,促进肿瘤生长;(2)辅助性TPN可能提高肿瘤对周期特异性化疗药物的敏感性;(3)TPN对肿瘤细胞动力学的影响有时间性,要使周期特异性药物产生最佳抑瘤效应,须在TPN后一段特定时间内给药。     

降低葡萄糖含量预防全肠外营养所致淤胆的作用

作者将39例使用低热量、低葡萄糖 TPN 患者的 AKP,I-GT,TBil,ALT,白蛋白、氮平衡与30例使用高热量、高葡萄糖 TPN 患者的相应值进行了比较。结果发现,使用低热量、低葡萄糖 TPN 可延缓和减轻临床长期使用 TPN 患者的 AKP,I-GT,TBil,ALT 异常的发生。作者提出,在临床长期使用 TPN 时,应注意非蛋白质热量,葡萄糖、脂肪的给量,以热量30kcal·kg~(-1)/d(125.4kJ·kg(-1)/d),葡萄糖≤5g·kg(-1)/d,脂肪≤2g·kg(-1)/d,糖脂比6∶4,热氮比150kcal∶1(627kJ∶1)为佳;AKP,I-GT,TBil,ALT 联合应用可作为 TAN 所致淤胆的观察指标。     

Suppressor of cytokine signaling-2: a growth hormone-inducible inhibitor of intestinal epithelial cell proliferation

BACKGROUND & AIMS: Growth hormone (GH) and insulin-like growth factor-I (IGF-I) increase intestinal growth. GH is thought to act indirectly via IGF-I. In several models, including rats given total parenteral nutrition (TPN), IGF-I more potently stimulates mucosal growth than GH, even when GH induces similar circulating IGF-I levels. These studies test the hypothesis that GH induces a suppressor of cytokine signaling (SOCS), which inhibits intestinal epithelial cell (IEC) proliferation. METHODS: Rats on TPN received vehicle, GH, or IGF-I. Jejunal SOCS (SOCS-1, -2, -3, and cytokine-inducible SH2-domain-containing protein [CIS]) and IGF-I messenger RNA (mRNA) were quantified. Caco-2, IEC-6 cells, and SOCS-2 null and wild-type (WT) mice were used to examine the expression and functional role of SOCS-2. RESULTS: As reported previously, IGF-I, but not GH, prevented mucosal atrophy during TPN, although GH elevated plasma IGF-I and increased body weight. GH, but not IGF-I, induced jejunal SOCS-2 mRNA. SOCS-2 mRNA levels in GH and IGF-I-treated rats inversely correlated with mucosal weight. SOCS-2 is expressed in Caco-2 cells, and elevated SOCS-2 expression in postconfluent cells is associated with reduced proliferative rates. SOCS-2 overexpression in Caco-2 cells inhibited cell proliferation and promoted differentiation. In IEC-6 cells, GH induced SOCS-2 and reduced basal or IGF-I-induced proliferation. GH also reduced proliferative activity in isolated crypts from WT but not SOCS-2 null mice, and SOCS-2 null crypts showed enhanced proliferative responses to GH and IGF-I. SOCS-2 null mice have increased intestinal weight and length. CONCLUSIONS: SOCS-2 is a GH-inducible, novel inhibitor of intestinal epithelial cell proliferation and intestinal growth.     

Total parenteral nutrition therapy and liver injury: a histopathologic study with clinical correlation

Total parenteral nutrition (TPN) therapy is a well-recognized cause of liver injury. The histologic changes attributed to TPN in the literature vary widely. In this study, we describe the histopathologic changes associated with TPN therapy and relate these changes to various clinical parameters. We conducted a retrospective study of 89 patients who underwent biopsy or liver transplantation while on TPN. We report that (1) ductopenia, a previously unreported finding, is seen in a significant number of patients on TPN. It is more frequently seen in patients with low stage of fibrosis and may have an inverse relationship with the length of therapy; (2) Perivenular fibrosis is a feature frequently seen in patients with high-stage portal fibrosis. In fact, we find the combination of portal and perivenular fibrosis to be a characteristic of TPN injury; (3) Infants are more susceptible to TPN-related hepatocellular injury, are more likely to develop fibrosis, and progress to high-stage fibrosis more rapidly than older children and adults; (4) Cholestasis, although more common in infants, is the most common pathologic finding in all age groups; (5) Steatosis is more commonly seen in older children and adults than in infants; (6) Progression to fibrosis in infants may be dependent on the length of therapy and the underlying disease for which TPN is administered; and (7) Clinical markers of liver injury (eg, elevated liver enzymes) do not predict the degree of hepatocellular injury or fibrosis, and therefore, serial biopsies may be indicated for patients on TPN therapy.     

Sclerosing encapsulating peritonitis as a potential complication of cytoreductive surgery and HIPEC: Clinical features and results of treatment in 4 patients

Sclerosing encapsulating peritonitis (SEP) is a rare entity characterized by encapsulation of the small bowel and/or the colon by a fibrous tissue that forms a shell. Intraperitoneal chemotherapy (IPC) has been reported to be a potential causative factor of secondary SEP. However, few studies have reported on secondary SEP related to cytoreductive surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPEC). Here, we review results from four clinical cases of SEP associated with CRS and HIPEC. In all four patients, additional surgery was necessary to alleviate recurrent episodes of small bowel obstruction. These obstructions can occur as early as several weeks after CRS plus HIPEC or as late as 3 years after treatment. Of utmost importance is the prevention of fistulization which can result in enteric contamination of the peritoneal space. To date, no solution to SEP has been identified except additional surgery but it is evident that these reoperative experiences are difficult for both surgeon and patient. The etiopathogenesis of SEP in this setting remains unknown but it is clear that it is related to chronic inflammation of the peritoneum. Large studies are needed to identify the incidence and potential common causes of SEP after CRS and HIPEC.