[Conducting a surgical intervention without permission...].
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Biomedical subjects
Publications and source records attributed to R Detry.
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We describe the case of a 51-yr-old man with systemic sarcoidosis, complicated by the occurrence of a lymphoproliferative disease following a 36-month (duration) immunosuppressive treatment with methotrexate (MTX) and methylprednisolone. Four years after the onset of sarcoidosis, the patient presented a large necrotizing anal fistula. Pathological examination of this lesion showed a diffuse polymorphic infiltrate containing large Epstein-Barr virus (EBV)-positive lymphoid cells associated with areas of necrosis, all features similar to classical B-cell lymphoproliferative disorders occurring in immunosuppressed solid-organ recipients. MTX has been recently implicated in the development of lymphoproliferative disease in connective tissue diseases. This case supports the hypothesis that immunosuppression therapy may contribute to an increased risk for the development of EBV-associated lymphoproliferative disorders in patients suffering from sarcoidosis.
Adiponectin (ApN) is thought to play a major role in the pathogenesis of the Metabolic Syndrome. Production of ApN and regulation of its related gene (apM1) have not yet been studied in human visceral adipose tissue. ApN was mainly associated with adipocyte membranes and abundantly secreted in medium from isolated adipocytes. apM1 gene expression, restricted to the adipocyte fraction of adipose tissue, decreased spontaneously when adipose explants were cultured in basal medium for 24 h while the expression of other adipose genes barely changed (PPARgamma, GAPDH) or increased (PAI-1). Unexpectedly, the fall of apM1 mRNA was prevented by the addition of actinomycin D, an inhibitor of transcription, or cycloheximide, an inhibitor of protein synthesis, and by reducing the amount of adipose tissue cultured per dish, thereby suggesting that a newly synthesized factor released by adipose tissue destabilizes apM1 mRNA. apM1 gene expression was also negatively regulated by glucocorticoids and positively by insulin and IGF-1. This regulation could contribute to the decreased apM1/ApN levels in insulin-resistant patients with obesity and the Metabolic Syndrome.
To fully understand the present state of surgery in Belgium, it is necessary to know the structure of the Belgian State, the type of education, the statutory health insurance system, and the professional bodies representing surgeons. One of the most important problems is the excessive number of physicians, which recently led to the establishment of limits on the number of candidates receiving medical certification. Surgical training modalities are described and the results of a retrospective study concerning the quality of training are detailed. The continuing medical education and peer-review system (accreditation) is presented.
Plasma levels of type 1 plasminogen activator inhibitor (PAI-1), a risk factor for cardiovascular disease, are elevated in obese subjects, especially those with omental fat accumulation. We investigated the hormonal control of PAI-1 gene expression and secretion in cultured human adipose tissue. We more particularly focused on the effects of glucocorticoids, insulin, cAMP, and catecholamines in explants from the omental region. The addition of dexamethasone to the culture medium increased PAI-1 secretion in a time-dependent manner for up to 24 h. The stimulation by the glucocorticoid was preceded by a 2-fold rise in PAI-1 messenger ribonucleic acid levels between 4-8 h of culture. The effectiveness of the glucocorticoid was concentration dependent, with a half-maximal effect within a physiological range. This stimulation was also observed in sc fat, but dexamethasone-stimulated as well as basal PAI-1 secretion rates were always higher in omental fat. Unlike dexamethasone, 24-h insulin did not modify PAI-1 secretion while accelerating glucose consumption. In contrast, 24-h cAMP inhibited PAI-1 gene expression and protein production under basal conditions and in the presence of dexamethasone. This inhibition was already detectable after 1 h and was maximal after 4 h at the level of gene expression. It occurred in both omental and sc adipose tissues. Importantly, epinephrine dose dependently inhibited PAI-1 parameters, an effect that was reproduced by isoproterenol. Dexamethasone- and cAMP-induced changes in PAI-1 messenger ribonucleic acid abundance were similar in explants and isolated fat cells. In isolated stromal-vascular cells, only dexamethasone was effective. In conclusion, we provide evidence for a reciprocal regulation of PAI-1 by dexamethasone (positive effector) and cAMP/catecholamines (negative effectors) in cultured human adipose tissue. The stimulation by glucocorticoids could contribute to enhanced production of PAI-1 by adipose tissue and high plasma levels of PAI-1 associated with central obesity and thereby be a link between this disorder and cardiovascular disease. Impaired inhibition by catecholamines could also contribute, as in vivo adipose tissue responses to these hormones are usually blunted in obese individuals.
Subacute ischaemic proctitis is a rare condition. We describe the case of a 60-year-old male patient who developed, after aortic aneurysm repair, a transient ischaemic colitis that totally healed without sequelae. He eventually developed symptoms of severe proctitis. Investigations identified a stenosis of the mid rectum, while the upper rectum was inflammatory. On angiogram, there was a poor blood flow through the Riolan's arcade and a stenosis of the proximal aorto-graft anastomosis. Diagnosis of subacute ischaemic proctitis due to poor blood supply through the internal iliac arteries was made. Anti-inflammatory drugs and dilations were inefficient. A subtotal proctectomy with low colorectal anastomosis was required. On pathological specimen, the lesions were strongly suggestive of an ischaemic process. The patient had an excellent recovery and was asymptomatic 8 months after the operation.
Thirty three patients were placed under early oral feeding after elective colorectal surgery. There were 15 male and 18 female patients, mean age: 52 years. Nasogastric tube was removed as soon as they were widely awake, or on the morning following the afternoon operations. Oral feeding was resumed 4 hours later, and the first meal consisted in a slight solid meal. There was no postoperative mortality or significant morbidity. Liquid and solid oral intakes were resumed 18 and 24 hours respectively after the operation. Tolerance was perfect in 22 patients (66%), good (slight complaints) in 16%, and was considered as fair or bad in the last six cases. Intestinal transit was observed after a median period of 2 days. Tube insertion rate was 12%. No adverse effect on the anastomoses was noted. Data from the literature confirm that early feeding is tolerable and safe after open colorectal surgery. More patients should be included in this protocol to take benefit of the physiological effects of early oral feeding.
Familial adenomatous polyposis (FAP) is characterised by hundreds of colorectal adenomas. Endocrine neoplasms have occasionally been reported, as have gastric polyps, which are usually hamartomatous in the fundus of the stomach and adenomatous in the antrum. A 57 year old man with colorectal, gastric, and periampullary adenomatous polyposis, in association with three bilateral adrenocortical adenomas, is presented. Mutation screening showed a 5960delA germline mutation in the adenomatous polyposis coli (APC) gene predicted to lead to a premature stop codon. This mutation was found in three of the four children of the patient. Western blot analysis of a lymphoblastoid cell line derived from the patient failed to detect any truncated APC polypeptide. This rare 3' mutation is responsible for an unusually complex and late onset phenotype of FAP.
BACKGROUND: The ultimate goal of surgery for hematological disorders is the complete removal of both the spleen and accessory spleens in order to avoid recurrence of the disease. Whereas splenectomy by open surgery provides excellent results, the validity of laparoscopic splenectomy in this regard remains unknown. OBJECTIVE: The purpose of this study was to evaluate the detection of accessory spleens during laparoscopic splenectomy for hematologic diseases. METHODS: We therefore evaluated the pre-, intra-, and postoperative detection of accessory spleens in a consecutive series of 18 patients treated by elective laparoscopic splenectomy for hematological diseases by using computed tomography (CT) and denatured red blood cell scintigraphy (DRBCS). RESULTS: Preoperative CT, DRBCS, and laparoscopic exploration detected 25%, 25%, and 75% of accessory spleens, respectively. At time of laparoscopy, 16 accessory spleens were detected in seven of the 18 patients (41%). In two patients (11%), laparoscopic exploration failed to detect accessory spleens, whereas preoperative CT (one case) and DRBCS (one case) did reveal them. Postoperatively, during a mean follow-up of 28 months (median, 24; range, 12-44 months), nine patients (50%) showed persistence of splenic tissue by DRBCS, and three of them had signs of disease recurrence. CONCLUSIONS: This prospective clinical study suggests that elective laparoscopic surgery for hematological diseases does not allow complete detection of accessory spleens. Moreover, after such a laparoscopic approach, residual splenic tissue is detectable in half of the patients during the follow-up.
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The direct role of hormones on leptin synthesis has not yet been studied in cultured adipose cells or tissue from lean and obese subjects. Moreover, this hormonal regulation has never been addressed in human visceral fat, although this site plays a determinant role in obesity-linked disorders. In this study, we investigated the hormonal control of ob expression and leptin production in cultured visceral adipose tissue from lean and obese subjects. We more particularly focused on the interactions between glucocorticoids and insulin. We also briefly tackled the role of cAMP, which is still unknown in man. Visceral (and subcutaneous) adipose tissues from eight obese (body mass index, 41 +/- 2 kg/m2) and nine nonobese (24 +/- 1 kg/m2) subjects were sampled during elective abdominal surgery, and explants were cultured for up to 48 h in MEM. The addition of dexamethasone to the medium increased ob gene expression and leptin secretion in a time-dependent manner. Forty-eight hours after dexamethasone (50 nmol/L) addition, the cumulative integrated ob messenger ribonucleic acid (mRNA) and leptin responses were, respectively, approximately 5- and 4-fold higher in obese than in lean subjects. These responses closely correlated with the body mass index. The stimulatory effect of the glucocorticoid was also concentration dependent (EC50 = approximately 10 nmol/L). Although the maximal response was higher in obese than in lean subjects, the EC50 values were roughly similar in both groups. Unlike dexamethasone, insulin had no direct stimulatory effect on ob gene expression and leptin secretion. Singularly, insulin even inhibited the dexamethasone-induced rise in ob mRNA and leptin release. This inhibition was observed in both lean and obese subjects, whereas the expected stimulation of insulin on glucose metabolism and the accumulation of mRNA species for the insulin-sensitive transporter GLUT4 and glyceraldehyde-3-phosphate dehydrogenase occurred in lean patients only. This inhibitory effect was already detectable at 10 nmol/L insulin and was also observed in subcutaneous fat. Although a lowering of intracellular cAMP concentrations is involved in some of the effects of insulin on adipose tissue, this cannot account for the present finding, because the addition of cAMP to the medium also decreased ob mRNA and leptin secretion (regardless of whether dexamethasone was present). In conclusion, glucocorticoids, at physiological concentrations, stimulated leptin secretion by enhancing the pretranslational machinery in human visceral fat. This effect was more pronounced in obese subjects due to a greater responsiveness of the ob gene and could contribute to the metabolic abnormalities associated with central obesity by para/endocrine actions of hyperleptinemia on adipocytes and liver. Unlike dexamethasone, insulin had no direct stimulatory effect on ob gene expression and leptin secretion, and even prevented the positive response to dexamethasone by a cAMP-independent mechanism that remained functional despite insulin resistance.
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The diagnosis of colorectal cancer must be considered in the presence of suggestive symptoms and must be endoscopy. Assessment of operability, including chest x-ray, is completed by CEA determination and x-rays of the colon, looking for a synchronous lesion. Complementary assessments must answer 3 questions: what operation needs to be performed, is any preoperative adjuvant treatment indicated, do any prognostic factors need to be identified before the operation. The treatment of cancer of the colon is now clearly defined; intraoperative hepatic ultrasonography and histological examination of the resection specimen provide all of the necessary data in the majority of the cases. In the presence of a cancer of the rectum, various therapeutic alternatives are available according to the site and stage of the tumour. The complementary assessment includes biopsy to confirm the malignant nature of the lesion, and measurement of the distance of the lower pole from the anal margin (digital rectal examination, endoscopy). A more precise preoperative staging by ultrasonography, computed axial tomography or magnetic resonance is required when the clinician considers that the invasive nature of the lesion justifies preoperative radiotherapy. This precise staging is fully justified in the presence of a small rectal tumour amenable to local resection. Although infiltration of the rectal wall is now very clearly defined, formal identification of metastatic lymphadenopathy still remains hazardous. Finally, the search for distant metastases by invasive and/or expensive techniques is indicated when looking for contraindications to surgery (high-risk patients, surgery for recurrence and metastases). In other cases, the presence of metastases does not contraindicate a palliative colonic resection and intraoperative exploration allows reliable identification of any liver metastasis.
The purpose of this study was to correlate the MRI features of the anal canal with histologic findings. T1- and T2-weighted MR images of nine anal canals were obtained after fixation in 10% formalin. In three specimens, imaging was repeated after removal of histologic layers with a dissecting microscope. Corresponding histologic slices were stained with hematoxylin-eosin, Masson trichrome, and periodic acid-Schiff. Four layers were visualized on T2-weighted images. An inner layer of high signal intensity and a second layer of low signal intensity corresponded to the mucosa as well as mucous secretions and to the submucosa. The high signal intensity layer vanished at the distal part of the anal canal in accordance with the lack of mucus-secreting epithelium below the level of the dentate line. A third layer of intermediate signal intensity corresponded to the internal sphincter. A fourth layer of low signal intensity corresponded to the longitudinal muscle and external sphincter. T2-weighted MRI is capable of showing the internal architecture of the wall of the anal canal. In particular, the internal sphincter can be differentiated from the external sphincter and longitudinal muscle.
OBJECTIVE: The aim of our study was to assess the value of sonography in the diagnosis of acute intestinal occlusion. MATERIAL AND METHODS: Sonographic findings were reviewed in 50 cases of intestinal occlusion (39 small bowel and 11 colonic occlusions). The final diagnosis was based on surgical findings (n = 40) or clinical course and further imaging findings (n = 10). RESULTS: Occlusion was correctly detected with sonography in 48 cases (96%). The location was correctly established with sonography in 43 cases (86%). The precise cause was suggested with sonography in 21 cases (42%). COMMENTARY: These results confirm the value of sonography for the diagnosis of intestinal occlusion and the identification of its level and its cause.
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For twenty years, opinions concerning local surgery of anal lesions in Crohn's disease have changed in practice and in the literature. We have reviewed 209 patients, usually in remission of disease, with at least 6 months' follow-up, who underwent local surgery for various anal lesions from 1974 to 1992. In this study, our indications and results are discussed and compared to the literature. Results of partial haemorrhoidectomy are successful. In anorectal stenosis, with rectal involvement, surgery improves the symptoms and can avoid or delay proctectomy. Results of surgery for simple fistulas appear to be identical in cases with or without Crohn's disease. In complex and suprasphincteric fistulas, seton management improves chronic suppuration, occasionally cures the lesion and reduces the number of tracts. After seton drainage, transanal rectal advancement flaps can be performed, but the results of this procedure have yet to be confirmed.