[The role of local excision in the treatment of rectal tumors].
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Biomedical subjects
Publications and source records attributed to W Montorsi.
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In 1989 there were 151,000 new cases of colorectal carcinoma in the United States. Approximately 50% of these patients will be at risk of developing liver metastases together with other sites of recurrence. However, the liver will be the main site of relapse in only 14,000 patients with colorectal cancer. Approximately 25% of patients with colorectal carcinoma have technically resectable hepatic metastases at the time of operation for primary lesion, and an additional 8-25% will develop metachronous hepatic metastases after primary resection. Recent reported experiences with surgical treatment of metastatic colorectal cancer in the liver seem to indicate that hepatic resection has become more acceptable, safe and effective therapy, and offers today when technically possible, the best prospect of survival in a conspicuous number of patients. For these reasons, although a prospective randomized trial has not been done comparing resection with nonresection, resection seems to give the best hope for cure and actually is the treatment of choice for selected patients. In fact in these patients is reported a significant prolongation of survival compared with those patients with unresectable liver metastases treated only with adjuvant therapy in the form of chemotherapy or radiation therapy. Median survival of resected patients with hepatic metastases has been reported to range from 6-12 months, and for patients with single metastases is reported to range from 4.5-6.2 months to 11 and 21 months. The benefits of surgical therapy have been emphasized by different experience, with a 5-year overall survival rate ranging from 20-40%. In a recent multicenter survey a 33% 5-year survival rate was demonstrated in 859 patients resected for hepatic metastases.
This study was performed to see whether or not protection of the endothelial cells contributes to the antithrombotic effects of heparin. New Zealand albino rabbits were subjected to jugular vein stasis by single caudal ligation for 2 h. Three treatments were given: saline (control group), heparin (0.2 mg/kg) 5 or 45 min before ligature of the vein. Groups of 6-8 animals were killed at 0, 5, 15, 30 and 120 min. The following parameters were determined: (1) involution and damage of the endothelial cells by scanning and transmission electron microscopy; (2) incidence and weight of thrombi in the lumens of the veins after 2 h stasis, and (3) effects of heparin on APTT and anti-Xa activity. In the control group, stasis caused a considerable involution of the endothelial cells in the first 30 min, followed by fibrin deposition and thrombus generation. Heparin strongly reduced the damage to the endothelial cells, with very evident protection of the cell membranes, and prevented thrombus generation: there were significant decreases in both incidence and weight of thrombi. These effects of heparin were evident both shortly after (maximal anticoagulant effect) and long after (no anticoagulant effect) pretreatment. We think that, under the experimental conditions we used, heparin prevented venous thrombosis at least partially by protection of the endothelial cells, through unknown mechanisms.
Horizontal gastroplasty has been performed on 100 pathologically obese patients over the last nine years. In our series, the mean age was 39.3 +/- 8.2 years and the mean body weight was 120.8 +/- 19.6 kg. One year after surgery the average weight loss was 29.7 kg which corresponds to a reduction of 24.6% of the preoperative weight (BMI:-24%). After three years, the body weight stabilised, reaching a total weight reduction of 30.5% (BMI:-28.7%), corresponding to 36.8 kg. The incidence of complications directly related to surgery was generally acceptable. The absence of specific malabsorption problems, the low incidence of severe complications and the satisfactory weight loss induced and maintained make, in our opinion, horizontal gastroplasty one of the most suitable and effective interventions in the long-term management of morbid obesity.
Jejuno-ileal bypass has been widely used for the surgical treatment of morbid obesity since 1954, but from 1978 onwards the operation has met with increasing disfavor, especially in the USA as a result of its unacceptably high complication rate. From 1982 onwards, 235 morbidly obese patients had a side-to-side jejuno-ileal bypass in our Department. Our data concerning weight loss and the overall incidence of complications show that jejuno-ileal bypass can still play a role in the surgical treatment of morbid obesity.
Gastric carbonic anhydrase (CA) is believed to play an important role related to cytoprotection, and duodenogastric reflux of bile salts (BS) is suspected of having a causal role in many pathologic conditions. Thus, we decided to investigate the effect of free and conjugated BS on human and rat gastric CA activity. Cholate exerted the most potent inhibitory activity on both human (I50 = 2.24 mM) and rat (I50 = 1.68 mM) gastric CA, followed by glycochenodeoxycholate and taurocholate (I50 = 6.90 mM and 13.67 mM on rat gastric CA). Human and rat whole bile produced 10-90% and 20-40% inhibition of gastric CA of the same species. Since the concentrations of free and conjugated BS tested in this study can be found in the postgastrectomized stomach, our data suggest that inhibition of gastric CA might be one mechanism contributing to the gastric mucosa damage caused by BS refluxing into the stomach after gastric surgery.
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Mast cells are known to participate in three phases of wound healing: the inflammatory reaction, angiogenesis and extracellular-matrix reabsorption. The inflammatory reaction is mediated by released histamine and arachidonic acid metabolites. Compound 48/80 and disodium-cromoglycate are both able to increase skin breaking strength shortly after wounding. Under light and electron microscopy we found that small, granule-poor, irregular mast cells (MLMC) accumulate in the wound. This suggests that the small MLMC (mucosal-like mast cells) migrate into the skin during wound healing, and that both CTMC (connective-tissue mast cells) and MLMC are involved in tissue repair. Moreover, there is some evidence that mast cells participate in angiogenesis, since heparin is able to stimulate endothelial-cell migration and proliferation in vitro, and protamine to inhibit these processes and also angiogenesis in vivo. When the effect of protamine on wound breaking strength was examined, we encountered a decrease which was not prevented by heparin administration. Further studies are needed to demonstrate that protamine is specifically involved in inhibiting heparin-mediated angiogenesis in wounded tissue. Finally, mast cells may play a role in the extracellular matrix remodelling, on the basis of in-vitro experiments (but there are still no in-vivo data).
The effects of the topical antiseptic agents mercurochrome and silver nitrate and of sodium hyaluronate on the process of wound healing were assessed by macroscopic examination, light microscopy histology, electron microscopy and scanning electron microscopy of wounds made by cutting or by abrasion of the skin of rats. It was found that wounds treated with hyaluronic acid underwent longer periods of inflammation (proportional to the presence of mastocytes) and greater amounts of collagen deposition than wounds that were either untreated controls or treated with silver nitrate or mercurochrome, but this did not impede the formation in the early stages of healing of bridges of fibrin between the edges of the wounds.
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Transient hypomagnesiaemia was noted postoperatively, particularly on the 1st day in patients submitted to intestinal procedures. Slight hypocalcaemia was also observed; this was often related to a low plasma Mg value. A hormonal mechanism is presumed to be the cause of this stress-linked fall in blood magnesium.
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