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Mark Kidd

Publications and source records attributed to Mark Kidd.

At least 37 records · Page 2Linked to original sources
PubMed2004

From the lumen to the laparoscope.

Throughout the ages, the issues that have defined the management of disease processes have been particularly exemplified in the gastrointestinal tract. The use of gas lamps and candles with reflectors by Bozzini, Segalas, Cruise, and Fisher (19th century) allowed for some ingress into both the upper and lower gastrointestinal tract. Von Mikulicz, Leiter, Nitze, Kelling, and Jacobaeus contributed to the development of rigid instruments that could be used endoscopically or laparoscopically. Endoscopic efforts were amplified and extended by Rosenheim, Sternberg, Wolf, and, finally, Schindler, who not only introduced novel lens systems but also for the most part overcame the problems of flexibility and illumination. Bernheim, Ruddock, Veress, and Palmer made significant technical and clinical contributions to abdominal cavity exploration. The subsequent application of Hopkins and Kapany's work on optics, and the development by Hirschowitz and Curtiss of the flexible fiber optic endoscope, enabled the design of instruments that would allow the appropriate illumination and vision of both the farthest reaches of the bowel as well as the interior of the abdomen. Thus, the same endoscopic instruments coupled with a surgical interest in diagnostic laparotomy allowed for the evolution of minimally invasive surgery along a similar timescale. The cycle whereby diagnostic laparotomy in the early part of the century was supplanted by endoscopy and laparoscopy has now attained full circle whereby laparoscopy has evolved from a diagnostic procedure into one with major therapeutic applications and is perceived as the state-of-the-art technique for a wide variety of operations, including appendectomy, cholecystectomy, hernia repair, fundoplication, splenectomy, colectomy, and gastrointestinal anastomoses.

Cholangiopancreatography, Endoscopic Retrograde↗
PubMed2004

The relationship of a Helicobacter heilmannii infection to the mucosal changes in abattoir and laboratory pig stomach.

PURPOSE: A pig ulcer model in which ulceration is reproducibly induced in the pars oesophagea (a tongue of the oesophageal squamous epithelium that extends into the pig stomach) by bile duct ligation (BDL) was used in this study to determine whether Helicobacter heilmannii (Hh) is a predisposing factor in the ulceration of this region. The infection with Hh and its relationship to ulceration and mucus integrity was examined. METHODS: We microscopically investigated the occurrence of spontaneous pars oesophageal ulceration in 33 pigs from a local abattoir and 5 pigs nurtured in pens in our surgical laboratory (JSM). Further groups of 5 and 6 JSM pigs underwent a sham operation and a BDL, respectively. Giemsa staining was used to detect Hh and purified mucin was characterized by gel filtration. RESULTS: Ten of 33 and 2 of 5 of the stomachs of abattoir and JSM pigs, respectively, were positive for Hh by Giemsa stain. Three of the 33 abattoir pigs showed ulceration in the pars oesophagea and none of these was Hh-positive. All six of the bile duct-ligated pigs showed ulceration in the pars but only 2 of these were Giemsa-positive. Only 8 of 33 of the abattoir pigs had > or =50% large polymeric mucin that was eluted in the void/excluded volume of a Sepharose 2B column. CONCLUSIONS: There was no consistent correlation between an infection of the pig stomachs by Hh, an ulceration of the pars oesophagea, and mucin degradation. There was a significant difference between the percentage of polymeric mucin from the abattoir pigs and that of the JSM group (P < 0.003), the JSM group vs sham-operated pigs (P < 0.011), and JSM vs BDL pigs (P < 0.0005), but there appeared to be no association between the infectivity with Hh and mucin degradation.

Animals↗
PubMed2004

GERD 2004: issues from the past and a consensus for the future.

In the early 1900's, gastroesophageal reflux disease (GERD) was an almost unknown entity with less than 200 cases reported worldwide. Currently the disease is regarded as almost endemic with as much as 25% of the population in some countries exhibiting signs or symptoms of reflux. Early therapies directed at chemical neutralization (milk drip, antacids) were of modest effect and required constant administration for efficacy. The introduction of histamine 2 receptor antagonists in the 1970's dramatically improved the management of GERD, but was limited by problems of tachyphylaxis and adverse events. The advent of the PPI class of drugs revolutionized medical care of GERD, given their efficacy and safety profile. As a consequence, the surgical approach with its pronounced dependence on individual operator skill and its high morbidity and even mortality has fallen into disregard. Thus, modest surgical outcome results as compared to the efficacy of PPIs has led to the widespread recognition that pharmacological therapy for GERD represents the platinum standard of care and the current consensus is that the PPI class of drugs provide the safest and most effective form of therapy for GERD. Furthermore, it is apparent based on acid suppression, symptom relief and healing rates, that all PPIs are on a milligram for milligram basis similarly efficacious for the management of GERD. While a consensus exists in regard to the current management of GERD with PPIs there is little agreement as to the management of the associated mucosal metaplastic process. At this time there is inadequate understanding of the biological basis of the mucosal transformation and minimal information about the mechanistic regulation of this event and its perpetuation. A future consensus thus requires the identification of the appropriate tools to detect Barrett's early, identify the specific molecular markers associated with neoplastic transformation and establish a definitive therapeutic algorithm.

Barrett Esophagus↗
PubMed2004

Siegfried Oberndorfer: origins and perspectives of carcinoid tumors.

Carcinoid tumors are rare, indolent neoplasms that, although clinically well defined, are regarded as exotic and are consequently often unrecognized. Although little is known of the lives of the men who defined the tumor, described its distinct histology and cell type, and delineated the clinical hallmarks of the disease even less is known of the pathobiology of the lesion. In the nineteenth century, T. Langhans (1839-1915), O. Lubarsch (1860-1933), and W. B. Ransom (1860-1909) described unusual tumors in the small bowel but each failed to adequately investigate these novel entities. This responsibility fell to Siegfried Oberndorfer (1876-1944), who became the first to adequately characterize the nature of the tumors and refer to them as "benign carcinomas." During his tenure at the Pathological Institute of the University of Munich, Oberndorfer noted in 1907 that the lesions were distinct clinical entities and named them "karzinoide" ("carcinoma-like"), emphasizing in particular their benign features. In 1929 he amended his classification to include the possibility that these small bowel tumors could be malignant and also metastasize. Although the enterochromaffin cell, the carcinoid cell of origin, had been identified as early as 1897 by N. Kulchitsky (1856-1925), it was not until 1953 that F. Lembeck (1922-) established that such cells synthesized and secreted serotonin--a potent bioactive amine. Thereafter the protean clinical effects of serotonin, including "flushing," were recognized as was the associated relationship of carcinoid heart disease (Biörck in 1952) and fibrosis (Moertel in 1961). As the centennial of the observations of Oberndorfer approaches, it should be noted that the legacy of one of Germany's most distinguished pathologists, teachers, and scientists (whose career fell victim to the machinations of the Third Reich) has been largely unrecognized. Similarly, the biology and mechanistic analysis of these lesions remain to a large extent unexplored. The present article describes the contributions of the clinical and scientific pioneers in the elucidation of carcinoid disease and traces the evolution of the discovery and understanding of carcinoid tumor biology. It also serves to memorialize the extraordinary accomplishments of Oberndorfer, whose vision exceeded his times.

Carcinoid Tumor↗
PubMed2004

Gastric and duodenal mucosal protein fractional synthesis and growth factor expression in patients with H. pylori-associated gastritis before and after eradication of the organism.

Our purpose was to study the effect of Helicobacter pylori (HP) on mucosal protein fractional synthesis (MPFS) and growth factor expression. 14C-leucine incorporation, and TGF-alpha, beta-FGF, and EGF-receptor levels were assessed in gastric and duodenal mucosa in 20 patients with HP-associated gastritis and repeated after treatment of the gastritis, with or without eradication of the organism. At entry, MPFS in the fundus, antrum, and duodenum was 43.1, 38.2, and 28.3%/day, respectively. Following HP eradication, fundal and antral rates fell to 28.1 and 21.4%/day (P < 0.05), whereas the duodenum was unchanged. MPFS in the patient subset not eradicated remained similar to entry values (35.9, 31.6, and 25.4%/day). Expression of TGF-alpha, beta-FGF, and EGF receptors was unchanged. Eradication of HP results in reduction of gastric, but not duodenal, MPFS and has no effect on the growth factors measured. Increased MPFS associated with HP gastritis may relate to the potential for neoplastic transformation.

Adult↗
PubMed2004

A 50-year analysis of 562 gastric carcinoids: small tumor or larger problem?

OBJECTIVES: Interest in gastric carcinoid tumors has amplified considerably given the biological establishment of their relationship to gastrin and advances in the elucidation of the pathobiology of such lesions. The recognized propensity of acid-suppressing agents such as the proton pump inhibitor class of drugs to increase plasma gastrin levels has been proposed as a causal relationship in the apparent increase in the identification of such lesions although the increased prevalence of endoscopy and the enhanced awareness of pathologists have also been considered as contributory factors. We sought to examine if there has been an increase in gastric carcinoid incidence time correlative with these parameters. METHODS: Carcinoid tumor cases from the End Results Group (1950-1969) and the Third National Cancer Survey (TNCS) (1969-1971) databases were combined with the most recent release of the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) registry (1973-1999); these three datasets revealed 13715 carcinoid cases, of which 562 were gastric in origin. Age-adjusted analyses as well as population-based gender and race correction ratios were completed in conjunction with United States decennial census data. To allow a finer granularity in incidence trends, the SEER database was divided into early (1973-1991) and late (1991-1999) subsets. RESULTS Since 1950, the percentage of gastric carcinoids among all gastric malignancies has increased from 0.3% to 1.77%. Since 1969, the proportion of gastric carcinoids among all enteric carcinoid lesions has increased from 2.4% to 8.7%. Age-adjusted incidence rates among male, female, black, and white population subsets have all increased since the TNCS time period, with the greatest increase (800%) noted in white females. The male:female ratio has fallen from 0.90 to 0.54. The occurrence of synchronous or metachronous noncarcinoid tumors with gastric carcinoid tumors has decreased by 26% during the course of SEER data collection. The 5-yr survival rate for gastric carcinoids overall has risen from 51% to 63% during the same time period. CONCLUSIONS: Gastric carcinoids have increased in incidence over the last 50 yr. Differential increases in predominance across gender and race subdivisions may reflect genetic-based propensities (or protection) for gastric carcinoid tumors among certain ethnic populations. Increased endoscopic surveillance and associated sophisticated pathological evaluation of gastric biopsies undoubtedly are responsible for some of the observed increase in the incidence of gastric carcinoid tumors. These data allow no specific role to be assigned to the effects of acid-suppressive medications. Nevertheless the role of such agents cannot be discounted at this time since the time frame of the increased incidence is somewhat comparable to the introduction of these agents as is the known biological effect of gastrin on ECL cell proliferation.

Aged↗
PubMed2004

Determinants and consequences of different levels of CagA phosphorylation for clinical isolates of Helicobacter pylori.

BACKGROUND & AIMS: The Helicobacter pylori cag pathogenicity island encodes a secretory system that translocates CagA into epithelial cells, where it becomes tyrosine phosphorylated and induces cytoskeletal rearrangements. Strains with more CagA tyrosine phosphorylation motifs are most closely associated with gastric cancer. Here we assess whether clinical strains can deliver CagA, whether strains with different numbers of CagA phosphorylation motifs have CagA phosphorylated to different degrees, and whether this induces different amounts of epithelial cytoskeletal change. METHODS: Forty-four H. pylori strains from South African patients, all cagA gene positive, were cocultured with the gastric adenocarcinoma cell line AGS. CagA expression and phosphorylation were determined by Western blot and interleukin-8 secretion by enzyme-linked immunosorbent assay. The cagA 3' variable regions of 22 strains were sequenced and shown to possess 3-6 phosphorylation motifs. These strains were used to quantify CagA phosphorylation and cytoskeletal rearrangements. RESULTS: cagA genotype and typing of cag pathogenicity island genes were poorly predictive of phenotype. Thirty-four of 44 strains expressed CagA protein that could be delivered to and phosphorylated within AGS cells. Only these 34 strains induced interleukin-8 secretion from AGS cells. Among those strains, the number of CagA tyrosine phosphorylation motifs determined the degree of CagA phosphorylation and the level of biologic activity in terms of degree and extent of AGS cell elongation. CONCLUSIONS: H. pylori strains that deliver CagA with more phosphorylation motifs induce higher levels of CagA phosphorylation in epithelial cells, induce more cytoskeletal changes, and are more likely to be associated with gastric cancer.

Amino Acid Sequence↗
PubMed2004

Carcinoid tumors and fibrosis: an association with no explanation.

Carcinoid tumors are slow-growing neuroendocrine neoplasms most commonly associated with the gut and broncho-pulmonary system. In many instances, they are identified at surgery for unexplained bowel obstruction or during exploration of the small bowel in search of a primary tumor once distant metastases have been detected. Carcinoid tumors of the small bowel often present with pronounced fibrosis in the peri-tumoral tissues, distant in the heart or lungs, and locally in the peritoneal cavity. Despite medical and therapeutic advances that have alleviated symptoms and prolonged life, a substantial subset of patients develops mesenteric and small bowel carcinoid fibrosis and/or carcinoid heart disease. Fibrosis, and increasingly cardiac heart disease, are important components of intestinal carcinoid disease and are of considerable clinical concern, as both of these conditions reflect a connective tissue disorder whose etiology, biology, and therapy are unknown. In the past, individuals with carcinoid disease died of metastasis and uncontrollable symptomatology. Currently, there exists no clinical method to determine the development of fibrosis and little is understood about the biological basis of fibrosis. The elucidation of the biology and management of fibrosis is thus an issue of paramount clinical and scientific importance in determining appropriate diagnostic and therapeutic strategy. Therefore, the unraveling of the molecular events indicative of fibrosis in these cells and the identification of appropriate therapeutic targets is of considerable patient-care relevance. We have surveyed the world literature over the past 40 yr to evaluate both the incidence of carcinoid processes and track the evolving understanding of this process. In addition, we have provided more current mechanistic information in regard to the biological basis of fibrosis associated with small bowel carcinoid tumors.

Carcinoid Heart Disease↗
PubMed2004

GERD 2003: issues from the past and a consensus for the future.

Gastroesophageal reflux disease (GERD) has evolved from a scarcely reported, little understood disease process just a century ago to a now highly prevalent disease with up to 25% of the population complaining of symptoms of reflux. Throughout history attempts have been made to delineate the esophagus and related pathologies, but it has not been until relatively recently that enough has been understood about its screening, diagnosis and treatment to make a substantial impact on sufferers. Although the use of antacids and thereafter histamine 2 receptor antagonists dramatically improved the management of GERD, it was the advent of the proton pump inhibitor (PPI) class of drugs that revolutionized medical care. Although the relationship of hiatus hernia to reflux was well accepted, the modest results of open fundoplication fell into further disregard given the efficacy of PPIs. The PPIs are currently the most effective form of therapy and are equivalent on a milligram for milligram basis. While currently no novel drugs or devices are of proven efficacy for GERD, the development of an acid-suppressive agent of equal efficiency to a PPI but with a more rapid onset of action and a greater duration of effectiveness would be of particular clinical utility for the future.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2003

Investigation of the biological relevance of Helicobacter pylori cagE locus diversity, presence of CagA tyrosine phosphorylation motifs and vacuolating cytotoxin genotype on IL-8 induction in gastric epithelial cells.

Isolates of Helicobacter pylori from dyspeptic patients in England and South Africa were tested for ability to induce interleukin-8 (IL-8) in gastric cells. All isolates were cagA-positive, which was used as a marker for the presence of the cag pathogenicity island. The aims were to determine if activities were related to diversity within cagE (HP0544), a locus encoding a key component in the Type IV secretion system, and if disease severity might be linked to a combination of strain features. We found that isolates were heterogeneous in ability to induce IL-8 activity with the 23 positive isolates (59%) showing activities ranging from 260 to 3200 pg ml(-1). The cagE locus was detected in most isolates and RFLP analysis of a 1.52-kb internal fragment showed interstrain diversity with 12 combined (MboI/NlaIII) types. Most cagE genotypes were not associated with IL-8 induction, however two genotypes were found only in IL-8-inducing strains and one genotype was associated with lack of IL-8 induction. IL-8 activity was not associated with either the number or composition of cagA tyrosine phosphorylation motifs and vacA m-type. Although we found a weak association between cagE type and the ability to induce IL-8, our results imply that gastric cell factors or bacterial factors other than vacA, cagA and cagE are involved in the induction of IL-8 and the development of severe gastric disease.

Antigens, Bacterial↗
PubMed2003

Traces of human migrations in Helicobacter pylori populations.

Helicobacter pylori, a chronic gastric pathogen of human beings, can be divided into seven populations and subpopulations with distinct geographical distributions. These modern populations derive their gene pools from ancestral populations that arose in Africa, Central Asia, and East Asia. Subsequent spread can be attributed to human migratory fluxes such as the prehistoric colonization of Polynesia and the Americas, the neolithic introduction of farming to Europe, the Bantu expansion within Africa, and the slave trade.

Africa↗
PubMed2003

A 5-decade analysis of 13,715 carcinoid tumors.

BACKGROUND: Carcinoid tumors represent an unusual and complex disease spectrum with protean clinical manifestations. This compilation of several large United States-based databases comprising patients from 1950 to 1999 examines 13,715 carcinoid tumors and provides epidemiologic information regarding the natural history and evolution of the detection and diagnosis of this entity. METHODS: The authors evaluated 10,878 carcinoid tumors that were identified by the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute (NCI) from 1973 to 1999 in addition to 2837 carcinoid tumors that were registered previously by two earlier NCI programs. To the authors' knowledge, this represents the largest current epidemiology series addressing carcinoid tumors to date. RESULTS: Specific trends in incidence for carcinoid tumors of certain sites were identified. Among the most recently collected subset of data, sites that demonstrated the greatest incidence of carcinoids were the gastrointestinal tract (67.5%) and the bronchopulmonary system (25.3%). Within the gastrointestinal tract, most carcinoid tumors occurred in the small intestine (41.8%), rectum (27.4%), and stomach (8.7%). For all sites, age-adjusted incidence rates were highest in black males (4.48 per 100,000 population per year). Associated noncarcinoid tumors were frequent in conjunction with small intestinal (29.0%), gastric (20.5%), colonic (20.0%), and appendiceal (18.2%) carcinoids. The highest percentages of nonlocalized lesions were noted for cecal (81.5-83.2%) and pancreatic (71.9-81.3%) carcinoids, whereas the highest percentage of localized disease was found among rectal (81.7%), gastric (67.5%), and bronchopulmonary (65.4%) carcinoids. The best 5-year survival rates were recorded for patients with rectal (88.3%), bronchopulmonary (73.5%), and appendiceal (71.0%) carcinoids; these tumors exhibited invasive growth or metastatic spread in 3.9%, 27.5%, and 38.8% of patients, respectively. CONCLUSIONS: Carcinoids appear to have increased in overall incidence over the past 30 years; for some sites, this trend has been evident for nearly half a century. Recent marked increases in gastric and rectal carcinoids and a concomitant decrease in appendiceal carcinoid incidence may be due in part to varying rules of registration among the compiled databases examined in this report or to improvements in diagnostic technology; increased awareness of and about carcinoid tumors also may play a significant role. In 12.9% of all patients with carcinoid, distant metastases already were evident at the time of diagnosis; the overall 5-year survival rate for all carcinoid tumors, regardless of site, was 67.2%. These findings bring into question the widely promulgated relative benignity of carcinoid disease. Certain carcinoid tumors, such as those of the rectum, appear to be over-represented among the black and Asian populations within the United States, suggesting the role of genetics in the development of this intriguing disease.

Carcinoid Tumor↗
PubMed2003

Carcinoid tumors of the stomach.

Interest in gastric carcinoid tumors has in recent time amplified considerably as the understanding of both their biological background and clinical significance has developed. The increase in identification associated with the widespread availability of upper gastrointestinal endoscopy has facilitated diagnosis. In addition concern related to the consequences of long-standing hypergastrinemia generated by the use of potent acid-suppressive medications has augmented both clinical and scientific focus on gastric neuro endocrine issues. The elucidation of the regulatory mechanisms of the progenitor cell (ECL cell) of the gastric carcinoid tumor, the refinement of a pathological grading system for ECL cell proliferation, and the availability of specific immunohistologic identification techniques have further amplified the characterization of this lesion. Although the putative malignant potential of gastric carcinoids may ultimately be of only modest concern in a background of hypergastrinemia its relationship to gastric adenocarcinoma is still enigmatic and worthy of further consideration. This review will describe the molecular interrelationship between low-acid states, gastrin, and ECL cell proliferation and will discuss the pathological classification of the distinct types of gastric carcinoid tumors. In addition, the clinical rationale of current diagnostic and therapeutic strategies will be examined, providing a logical basis for the formulation of appropriate management strategies for patient care.

Adenocarcinoma↗
PubMed2003

Historical perspectives on the treatment of gastroesophageal reflux disease.

The current vogue in the historical evolution of the management of the problem of reflux is represented by augmentation procedures for the lower esophageal sphincter. Rather than employ a transperitoneal approach, these are directed at the sphincter by the transesophageal route and include stitching, collagen injection and radio-frequency-induced fibrosis. It is however probable that these techniques will suffer all the drawbacks of any mechanical intervention but somewhat decrease the morbidity of open, albeit minimally invasive surgery. Similarly, a specific pharmacotherapeutic probe targeting the lower esophageal sphincter, while long fantasized, remains to be identified.

Gastroesophageal Reflux↗
PubMed2003

Gastric stem cells: an update.

Cells of the gastric mucosa undergo constant renewal, the rate depending on the health of the tissue (inflammation, ulceration, carcinogenesis). While much attention has been focused on the mechanism of mucosal damage and the pathogenesis of ulceration, there has recently been the recognition that elucidation of the nature of the gastric stem cell lineages as well as the regulators of phenotype expression of this system may yield considerable biological information as well as open the door to the identification of areas of therapeutic relevance. Chimeric and X-inactivation studies in mice and humans demonstrate that each region of the gastric mucosa is morphologically diverse (antrum is different to the fundus), with its own repertoire of cell types and glandular structures. The current evidence suggests that a single stem cell in every gastric gland indirectly gives rise to a clone of all differentiated cells, by production of committed progenitor cells. It is also this multipotential cell that produces new crypts by crypt fission, repairs entire crypts when damaged, and gives rise to the ulcer-associated cell lineage and gastric carcinomas. It is likely that this stem cell occupies a niche in the isthmus composed of mesenchymal cells and extracellular matrix factors, which regulates the function of the cell via mesenchymal-epithelial cross talk. The molecular events (IGF-signaling) that regulate the development of the gastric gland in the mice have begun to be understood. Ultimately, the identification of these pathways will play an important role in identifying new molecular targets for the treatment of gastric disease.

Cell Division↗
PubMed2002

Surgery of chronic pancreatitis: chronicle of confusion and despair.

The evolution of surgery for pancreatitic disease has been arduous owing to the technical difficulties of addressing the organ and the lack of understanding the mechanisms of the disease processes involving it. In particular, the tardy advance of surgery in the management of chronic pancreatitis exemplifies these problems. Because no specific target has been identified, mechanical intervention has for the most part reflected intuitive or creative attempts to address perceived pathologic issues such as sphincter disease, calculi, and fibrotic masses. The past and present remain a confusion of etiologies and diagnoses. Treatment remains for the most part a dramatically disappointing scenario, and both patients and their physicians are frustrated. Although the remarkable technologic progress exhibited by the odyssey of operative strategy from simple drainage, to ductal drainage, to the complex refinements of extensive resection is a testimonial to surgical skill and determination, it has been nullified to a large extent by the inability to address the initiating factors of the disease or alter those that engender progress of the pathology. It is not unreasonable to recognize that we are facing an enigmatic disease process generically classified as "chronic pancreatitis" for want of any more specific terminology. In the light of our current knowledge and experience, intervention should probably be modest in the extreme and limited to centers and individuals with expertise or who are involved in specific studies to determine the precise criteria and techniques necessary for optimum intervention. It is important that when charting such a course future surgeons involved in the management of chronic pancreatitis have an understanding of the historical evolution of the subject. As Theodor Billroth, the greatest of the surgical innovators remarked: "An awareness of the past is necessary to comprehend the present, and without it no consideration of the future is possible."

Chronic Disease↗
PubMed2002

Perspectives and reflections on integrated digestive surgery.

The history of the integration of surgery is both extensive and complex involving internecine machinations that have, over time, variously encompassed the alchemical, religious, technological and biological phases of societal development. Thus, the discipline has evolved from a mystic rite through a guild phase to its current eristic status as a therapeutic modality considered by some as an art form as opposed to a quasi-scientific endeavour of often unpredictable beneficial effect. This brief prolepsis provides an exposition of the evolution of surgeons and surgical thought proceeding from Galen in 3rd century Rome through Paré of Renaissance France, Billroth of fin de siècle Vienna, to Kocher and Whipple of Bern and New York respectively. It is apparent that in surgery, ontogeny may not readily recapitulate phylogeny and thus the need for a contemporary revaluation of integration within a novel educational nexus that encompasses the burgeoning matrix of biotechnological, ethical and fiduciary revolution is a critical requirement. Such an exercise must embody contemporary scientific and educational advance with evolving societal goals that include ethical variances, fiduciary issues and alterations in individual perceptions of life quality at both the medical and personal level. An incorporation of the basic tenets of digestive surgery as well as a delineation of its potential direction is both a vital and necessary exercise to ensure the attainment of appropriate future goals of medical, ethical, societal, scientific and educational validity. Current medical and surgical training programmes and the sub-specialization system are archaic, cumbersome, cost ineffective and, for the most part, represent endless computations and permutations of intellectually antiquated and stultifying processes designed more than a hundred years ago. As such, the maieutic skills as well as the clinical vista available for the delivery of visceral disease care bear little relation to the needs and desires of contemporary society, whether medical or lay. Indeed, the century old notion of surgery and medicine as mutually exclusive disciplines that embraced diagnosis and therapy as divergent events needs to be cast aside to facilitate the development of a new model of disease management (organ specific). Specifically, training programmes require to be shortened (educational node) and their focus dramatically reconfigured (focus module) to ensure the establishment of a unified group of specialists (cluster convergent) each interfaced in delivery of a particular skill (component specific) to the resolution of a disease affecting a specific organ system. In this fashion, a time sensitive training programme producing educationally pre-focused physicians can be implemented to deliver time effective care in a cost contained environment with maximization of expertise and comprehensive interdisciplinary integration of knowledge, experience and skill (cluster care module). As such, digestive surgery itself should cease to be regarded as an end in itself or separate entity, but rather as representative of one facet in the delivery of a multifaceted integrated health care modality focused on the digestive tract.

Digestive System Surgical Procedures↗