Biomedical subjects

S A Pfeil

Publications and source records attributed to S A Pfeil.

4 recordsLinked to original sources

PubMed1999

Wilson's disease: copper unfettered.

Wilson's disease is a rare autosomal recessive inherited disorder of copper metabolism. Hepatic excretion of copper is impaired due to mutation of the gene for a copper-transporting adenosine triphosphatase, ATP7B. Copper accumulation in liver, brain, and other tissues may cause a wide spectrum of hepatic, neuropsychiatric, and other clinical manifestations. The diagnosis may be supported by measurement of serum ceruloplasmin, urinary copper excretion, and hepatic copper content as well as by detection of Kayser-Fleischer rings. Several treatments are available to increase urinary excretion and decrease intestinal absorption of copper.

Animals↗

PubMed1994

The upper gastrointestinal endoscopy report.

In summary, the endoscopy report is the permanent documentation and communication of the endoscopic procedure. The computerized endoscopy report system has, of necessity, improved our standardization of terminology and report content. Computerization of the endoscopy report has opened the door to easier auditing and quality review, as well as easier tracking and recall for research and teaching purposes. Nonetheless, the components of the endoscopy report have not changed. As with all communication, our goal should be clear, accurate, and concise expression.

Communication↗

PubMed1993

Gastric mucosal calcinosis. Calcified aluminum phosphate deposits secondary to aluminum-containing antacids or sucralfate therapy in organ transplant patients.

We have noticed calcium deposits (gastric mucosal calcinosis, or GMC) in the superficial gastric mucosa of 28 organ transplant patients (OTPs) (11 liver, seven bone marrow, four kidney, three kidney/pancreas, two heart, and one each of liver and kidney transplant) who underwent endoscopic biopsies. The deposits were tinctorially similar to cytomegalovirus inclusions, ranged from 40 to 250 mu in diameter, and were present just beneath the surface epithelium at the tips of the foveolae. An x-ray microanalysis showed that these mucosal deposits contained the elements aluminum, phosphorus, calcium, and chlorine. Clinical chart review showed that all OTPs with GMC were taking aluminum-containing antacids or sucralfate. Review of biopsies from gastric ulcer patients found GMC in a significantly smaller percentage than in transplant patients (32.7% vs. 5.1%, p < 0.0002). In addition, all three ulcer patients with calcified deposits were chronic renal failure patients on long-term aluminum-containing antacid therapy. Gastric mucosal calcinosis appears to be caused by aluminum phosphate accumulation secondary to antacid or sucralfate therapy in organ transplant patients. The presence of GMC in OTPs and chronic renal failure patients rather than other gastric ulcer patients is most likely due to the longer duration of therapy with aluminum-containing compounds in the former two patient groups. The clinical relevance of GMC remains to be seen. In theory, however, accelerated bone demineralization via loss of phosphates and absorption of aluminum in the gastrointestinal tract may be a consequence of long-term aluminum-containing antacid or sucralfate therapy.

Aluminum↗

PubMedDate not supplied

Colonic lipomas: outcome of endoscopic removal.

Colonic lipomas are benign adipose tumors which are usually submucosal. With the increase in the number of endoscopic procedures being performed, these tumors are often detected incidentally at colonoscopy. Although the risks of removing these tumors have been recognized, numerous reports have documented safe removal by snare electrocautery. We have reviewed the clinical outcome and the endoscopic and histopathologic features of seven lipomas that were endoscopically removed over a 5-year period. Four patients recovered uneventfully, while three patients (42.8%) developed colonic perforation after the polypectomy. In the latter group, the lipomas were significantly larger than they were in the patients who did not develop colonic perforation (1.9 +/- 0.4 and 4.2 +/- 0.7 cm, respectively; p = 0.048). Furthermore, the polypectomy specimens from those patients who developed perforation all contained significant muscularis propria. Lipomatous polyps that are identified at endoscopy to be greater than or equal to 2 cm in diameter and to have a limited pedicle are at the greatest risk for endoscopic perforation.

Aged↗