Jejunoileal bypass: change in the flora of the small intestine and its clinical impact.

Among the complications of jejunoileal bypass for morbid obesity are proctitis, bypass enteritis, liver disease, dermatitis, and arthritis, all of which are thought to be connected with the intestinal microflora. Quantitative cultures from the small bowel of patients before the establishment of the bypass and from patients with reoperations indicate colonization of both the functioning small bowel (bacterial counts, 10(5.0)-10(7.6)/ml) and of the bypassed loop (bacterial counts, 10(6.4)-10(9.7)/ml). Experiments in animals have shown that the presence of a bypassed loop, as compared with that of a resected bowel, is necessary for increased weight loss and for the development of liver disease. Clinical evidence for the impact of the intestinal microflora is based on the beneficial effect of antimicrobial agents, especially metronidazole, and on the demonstration of immunologic phenomena involving antigens of bacterial origin. Complications of jejunoileal bypass may serve to elucidate the pathogenesis of other diseases.

[Comparative endoscopic, light microscopy and scanning electron microscopy studies of the gastric mucosa in patients with chronic uremia]. / Vergleichende endoskopische, lichtmikroskopische und rasterelektronenmikroskopische Untersuchungen der Magenschleimhaut bei Patienten mit chronischer Urämie.

Ten patients suffering from chronic uremia were selected for comparison studies of gastric mucosa. With endoscopy erosive gastritis was seen in the corpus and antrum of five patients and in the fundus of two patients. Conventional microscopy (nine patients) revealed chronic gastritis I three times in the fundus and five times in the corpus. Gastritis II was localized once in the corpus and twice in the antrum. Gastritis III was present in the antrum of four patients. Under the scanning electron microscope lesions of gastric mucosa were present in all ten cases. Single cell necrosis (A), mucosal defects involving basal membrane (B), destruction of tunica propria (C), and muscularis mucosae with bleeding (D) were seen. Mucosal lesions A and B are early stages of gastric erosions. The most severe lesions were seen in the antrum mucosa with all three methods.

[Pancreatitis following kidney transplantation]. / Pankreatitis nach Nierentransplantation.

Follow-up of 249 recipients of cadaver renal allografts revealed 14 cases of pancreatitis. The minimum follow-up time was 2 1/2 years and the maximum 12 1/2 years. In 9 patients acute pancreatitis occurred within 4 months, 5 died from hemorrhagic-necrotizing disease. Later, 2 lethal cases of abscess-forming pancreatitis, 1 benign acute and 2 chronic forms were observed. The mortality in post-transplant pancreatitis is 7 out of 14, which corresponds to 7% of all fatalities after transplantation. Many different factors contribute to the development of pancreatitis, the most important being steroid medication.

Ruptured pancreatic pseudocysts: diagnosis by endoscopy. Report of 3 cases.

Report on 3 cases of spontaneous perforation of a pancreatic pseudocyst into the stomach; presenting symptom was in each case an acute upper GI-bleeding. The pseudocyst was endoscopically seen as a well delineated, hemorrhagic protrusion into the stomach. After full perforation the spontaneous ostium had the appearance of a surgical anastomosis. High amylase concentration in the aspirate ave further diagnostic evidence. All 3 patients survived, 2 of them without surgery.

Bacterial flora of the small bowel before and after bypass procedure for morbid obesity.

The contents of the proximal jejunum and distal ileum were cultured quantitatively in eight patients who were undergoing intestinal bypass procedure for obesity. Five jejunal specimens were sterile, and three contained low counts of a predominantly aerobic flora. Ileal contents yielded variable but usually higher counts than in the jejunum, and there were similar numbers of anaerobes and aerobes. In three patients in whom a bypass was established, contents of the functioning small bowel showed counts of 10(5.0)-10(7.6) colony-forming units/ml. These counts exceeded the counts in the normal terminal ileum, and the flora qualitatively resembled that of feces. Four specimens from excluded loops revealed colonization with fecal organisms, and the counts ranged between 10(6.4) and 10(9.7) colony-forming units/ml. In jejunoileal bypass both the functioning small bowel and the excluded loop become colonized with colonic flora, a phenomenon that may contribute to some of the side effects of this procedure.

Bypass enteropathy. Intestinal and systemic manifestations following small-bowel bypass.

Many manifestations following jejunoileal bypass are due to chronic inflammation of the excluded bowel rather than short bowel malabsorption. Diarrhea, abdominal distention, and gas-fluid levels were common diagnostic features of "bypass enteropathy." Exploration showed the bypassed bowel to be dilated, with serosal inflammation and pneumatosis cystoides intestinalis. The bypassed loops contained a fecal flora and the mucosa demonstrated nonspecific chronic inflammatory changes. Exudative protein losses were noted. Systemic complications of bypass enteropathy were similar to other inflammatory diseases of the bowel. Improvement following treatment with metronidazole or after dismantling of the bypass suggested that bacterial byproducts originating in the excluded bowel were causally related.

Pancreatitis after renal transplantation.

Pancreatitis is seldom seen as a severe complication of renal transplantation. In a review on 1321 renal transplants, 23 cases with 12 deaths are reported (Johnson and Nabseth, 1970). Single case reports may be added. In our departments pancreatitis has proved to be a fairly frequent complication. It developed in 10 (7 percent) of 147 patients with renal transplantation one week to seven and a half years after transplantation (patients with primary hyperparathyroidism excluded). Three of the eight acute cases had haemorrhagic pancreatitis, in two of them leading to death. Two patients had chronic calcifying pancreatitis. Pancreatitis was complicated in one case by abscess formation and in two by severe haemorrhage into a pseudo-cyst. In two patients the diagnosis was made at necropsy only and death was probably not related to the acute pancreatitis. The exact pathogenesis of pancreatitis after renal transplantation cannot be precisely assessed. Possible contributing factors are treatment with corticosteroids, azathioprin, and L-asparaginase, early hypercalcaemia after transplantation, surgery, infections of bacterial or viral origin, and unknown immunological processes.

Transduction and elimination of resistance determinants in methicillin-resistant Staphylococcus aureus.

Elimination and transduction of drug resistance was examined in methicillin-resistant strains of Staphylococcus aureus. Irreversible spontaneous loss and "curing" by aging of cultures and by treatment with ethidium bromide indicated that the determinants for penicillinase production and chloramphenicol resistance, and probably also for neomycin resistance, were located extrachromosomally. On the other hand, the determinants of resistance to erythromycin, streptomycin, tetracycline, and methicillin could not be eliminated by acridines, ethidium bromide, rifampin, sodium dodecyl sulfate, ultraviolet (UV) irradiation, growth at 43.5 C, aging of cultures, or combinations of these treatments. The stimulation of transduction frequency by UV irradiation of phage in the case of the stable markers, but not in the case of the unstable ones, supported further the hypothesis of chromosomal location of the markers of methicillin, erythromycin, tetracycline, and streptomycin resistance and extrachromosomal location of the determinants for penicillinase production and chloramphenicol resistance. Neomycin resistance could not be transduced. Joint elimination and co-transduction of the determinants for penicillinase production and resistance to chloramphenicol and neomycin were not observed, indicating the location of these markers on separate, mutually compatible plasmids. Co-transduction of chromosomal resistance determinants was usually less than 1%, which makes the location of these genes in a circumscribed area of the chromosome improbable.