Pylorus-Resecting Pancreaticoduodenectomy Offers Long-Term Outcomes Similar to Those of Pylorus-Preserving Pancreaticoduodenectomy: Results of a Prospective Study

Background

We showed in a previous study that pylorus-resecting pancreaticoduodenectomy (PrPD), which divides the stomach adjacent to the pylorus ring, preserves more than 95 % of the stomach and significantly reduced the incidence of delayed gastric emptying (DGE) compared with pylorus-preserving pancreaticoduodenectomy (PpPD). However, long-term outcomes of PrPD and the adverse effect of early postoperative DGE on long-term outcomes remain unclear.

Methods

A total of 130 patients enrolled in a previous study were followed for 24 months after surgery. Primary endpoint was whether PrPD is a better surgical procedure than PpPD regarding long-term outcomes.

Results

Weight loss > grade 2 (Common Terminology Criteria for Adverse Events, Version 4.03) at 24 months after surgery was significantly better in group PrPD (16.2 %) than in group PpPD (42.2 %) (p = 0.011). Nutritional status and late postoperative complications were similar for the two groups. The incidence of weight loss > grade 2 at 24 months was 63.6 % in DGE patients with DGE and 25.3 % in non-DGE patients (p = 0.010). T _max (time to peak ¹³CO₂ content in ¹³C-acetate breath test) at 24 months in DGE patients was significantly delayed compared with that in non-DGE patients (27.9 ± 22.7 vs. 16.5 ± 10.1 min, p = 0.023). Serum albumin level at 24 months was higher in non-DGE patients than in those with DGE (3.7 ± 0.6 vs. 4.1 ± 0.4 g/dl, p = 0.013).

Conclusions

PrPD offers long-term outcomes similar to those of PpPD. DGE may be associated with weight loss and poor nutritional status in patients with long-term outcomes.     

Lasers and lights for the treatment of striae distensae

Striae distensae (SD) or “stretch marks” are a common and well-recognized dermatologic entity affecting patients of all ages, genders, and ethnicities. The treatment of SD has long been plagued by disappointing outcomes and remains a frustrating entity for both physicians and patients. While striae may become less conspicuous over time, they rarely resolve without intervention. Inspired by the success of lasers for the treatment of scars and rhytides, these devices have been applied to the treatment of SD in the hopes of achieving similar efficacy.     

Changes in orientation of the major interlobar fissure in chronic liver diseases

The orientation of the major interlobar fissure, as an indicator of right lobar atrophy, was evaluated using axial MR imaging in 64 patients with histologically proven chronic liver diseases. The "interlobar fissure angle" was determined by a line drawn through the middle hepatic vein and inferior vena cava and a horizontal line at the level of hepatic hilus. The angle was significantly smaller in cirrhosis than in either chronic persistent or active hepatitis. A much smaller angle was observed in cirrhosis associated with colonic interposition. The increasing incidence of small "interlobar fissure angle" (less than 30 degrees) was observed to parallel the histological stages from chronic persistent hepatitis to liver cirrhosis. All the cirrhotic patients with colonic interposition and an angle of less than 30 degrees. This simple method is considered useful in the diagnosis of right lobar atrophy and disease severity in chronic liver disease.     

The effect of cardiac sympathetic nerve stimulation on the right ventricle in canine heart

The change in coronary hemodynamics during right or left cardiac sympathetic nerve stimulation was studied in anesthetized open chest dogs. No difference in the increasing rate of mean coronary blood flow between right coronary artery (RCA) and left anterior descending coronary artery (LAD) was observed. However the increasing rate of right ventricular systolic pressure X heart rate (RVSP X HR) was greater than that of left ventricle (LV). With phentolamine injection, cardiac sympathetic nerve stimulation showed similar changes as the controls. Beta-stimulation by isoproterenol infusion did not cause different effects on the increasing rate of coronary blood flow between RCA and LAD. These results showed that cardiac sympathetic nerve stimulation increased the double product of the right ventricle (RV) more than that of the LV and the increase was not affected by phentolamine. Moreover, cardiac sympathetic nerve stimulation, either the right or the left, caused the greater effects on the RV compared to the LV mainly through beta-adrenoceptors, and that the response of the RV to increase in oxygen demand was possibly, in part, different from that of the LV.     

A non-thrombocytopenic bleeding disorder due to an IgG4-kappa anti-GPIIb/IIIa autoantibody

Autoantibodies in chronic immune thrombo-cytopenic purpura occasionally interfere with platelet function. We describe a patient with a normal platelet count who had clinically significant mucosal bleeding, a prolonged bleeding time and abnormal platelet aggregation. The patient had high titres of an IgG4 kappa autoantibody, directed to a cation-dependent epitope on platelet glycoprotein IIb/IIIa, which blocked the binding of fibrinogen and fibronectin to this complex. Corticosteroid treatment resulted in clinical improvement and a marked drop in autoantibody concentration. The lack of thrombocytopenia in this patient, despite high autoantibody levels, is best explained by the poor recognition of IgG4 antibodies by phagocytic cells.     

Inhibition of autoantibody binding to platelet glycoprotein IIb/IIIa by anti-idiotypic antibodies in intravenous gammaglobulin

Intravenous immunoglobulin (IVIgG) causes an acute rise in the platelet count in the majority of patients with chronic immune thrombocytopenic purpura (ITP) but the mechanism(s) of action is still unknown. We evaluated the ability of three different IVIgG preparations to inhibit the in vitro binding of autoantibody to platelet glycoprotein (GP) IIb/IIIa. ITP plasma, known to contain anti-GPIIb/IIIa antibodies, was incubated overnight with either IVIgG or bovine serum albumin (BSA) followed by measurement of the autoantibody titer. Binding of autoantibody from eight ITP patients was inhibited by IVIgG in proportion to the IVIgG concentration. Using 3.2% IVIgG, compatible with therapeutic concentrations expected in vivo, mean inhibition of autoantibody binding ranged from 20.2% to 41.3%. No inhibition by IVIgG of alloantibody binding to the same or different molecules was detected (five patients with anti-GPIIb/IIIa and two with anti-HLA alloantibodies). F(ab')2 fragments of IVIgG also inhibited the binding of both plasma autoantibodies and purified anti-GPIIb/IIIA autoantibodies prepared by elution from antigen affinity columns. A portion of the anti-idiotypic antibodies could be adsorbed from IVIgG using insolubilized, purified anti-GPIIb/IIIa autoantibody. These results show that IVIgG preparations from normal donors contain anti-idiotypic antibodies directed against idiotypes located on GPIIb/IIIa autoantibodies but do not have anti-idiotypes to platelet alloantibodies against the same or different molecules. The importance of these anti-idiotypic antibodies in the therapeutic response to IVIgG remains to be established.