Heat probe treatment for antral vascular ectasia.

Antral vascular ectasia ("watermelon stomach") has recently been defined and characterized. This condition may be a source of significant bleeding from the stomach. Although steroids have been useful in some patients, antrectomy has been advocated as definitive therapy. We have treated 12 patients who were bleeding from this lesion with the Olympus HeatProbe Unit and have eliminated further hemorrhage. All presented with gastrointestinal bleeding, iron-deficiency anemia, and compatible antral biopsies. Using the large probe, vascular streaks were treated until the endoscopic appearance returned to normal (average four treatment sessions). No further bleeding was evident from the antral vascular ectasia over an average follow-up period of 20.9 months. Eight of 10 patients who had required transfusion prior to therapy no longer needed transfusion, but two received blood for other conditions. We conclude that antral vascular ectasia can be successfully treated with the HeatProbe Unit and this should be the initial modality of therapy for this condition.

Endoscopic therapy for gastrointestinal bleeding.

The use of endoscopic techniques to control gastrointestinal bleeding is an exciting addition to the therapeutic armamentarium. Alternatives include lasers, bipolar probes, heater probes, and sclerosing agents. The lack of statistically significant data should be viewed cautiously, because it is difficult to devise controlled trials for gastrointestinal bleeding that incorporate enough patients to avoid a type II statistical error. However, a healthy degree of skepticism is necessary to prevent the use of highly remunerative techniques of questionable benefit to the patient.

Endoscopic management of upper gastrointestinal polyps and periampullary lesions in familial adenomatous polyposis and Gardner's syndrome.

Upper gastrointestinal polyps and carcinoma, especially of the periampullary area, may occur in patients with familial adenomatous polyposis. Upper gastrointestinal polyps were present in about 43% of patients in the polyposis registry of the Cleveland Clinic who underwent screening esophagogastroduodenoscopy. Approximately one-third of these polyps were neoplastic. Three distribution patterns were recognized: 1. fundic, 2. duodenal, and 3. fundic plus duodenal. Despite the occurrence of a few gastric cancers in patients with familial adenomatous polyposis, the risk of carcinoma of the major duodenal papilla and periampullary area is more significant. It is necessary to examine the duodenal papilla with a side-viewing instrument and to obtain biopsy specimens from this structure in these patients. The major duodenal papilla was abnormal in about one-half of our patients in whom this structure was specifically examined with a side-viewing endoscope. The preliminary results of a trial of endoscopic treatment of upper gastrointestinal polyps and lesions of the major duodenal papilla in patients with familial adenomatous polyposis are described.

Gastric antral vascular ectasia. A histologic and morphometric study of "the watermelon stomach".

Gastric antral vascular ectasia (GAVE) is an uncommon but important cause of gastrointestinal blood loss and iron deficiency anemia that is characterized by a distinctive endoscopic appearance consisting of parallel erythematous folds traversing the gastric antrum. In order to clarify the histologic features of this lesion, nine antral biopsy specimens from seven patients with the clinical and endoscopic diagnosis of GAVE were reviewed and compared with specimens from normal controls and patients with other common antral lesions. Specimens obtained using standard endoscopic biopsy forceps were evaluated for mucosal vascularity, presence of intravascular fibrin thrombi, and the following histologic changes: mucosal inflammation, fibromuscular hyperplasia of lamina propria, epithelial regeneration, and mucosal architectural distortion. Mucosal vascularity was determined by counting the absolute number of vascular lumina per slide, measuring the mean cross-sectional area of each vessel lumen, and determining the percentage of each specimen occupied by vessels. Histologic changes were graded as absent to minimal, moderate, or marked. Significant differences (p less than 0.05) between GAVE and control groups were mean vessel cross-sectional area, percentage of area occupied by vessels, presence of intravascular fibrin thrombi, and fibromuscular hyperplasia. GAVE appears to demonstrate sufficiently distinctive histopathologic features to allow its recognition in antral biopsy specimens obtained by endoscopy.

Endoscopic sclerotherapy for bleeding esophageal varices secondary to extrahepatic portal vein obstruction.

Portal hypertension and variceal bleeding secondary to extrahepatic portal vein obstruction continue to present a therapeutic challenge. We performed endoscopic injection sclerotherapy in eight patients with extrahepatic portal vein obstruction and bleeding esophageal varices. In contrast to other reported series, all but one of our patients were adults at the time sclerotherapy was initiated. Six had episodes of continued bleeding after a variety of surgical procedures. After sclerotherapy, five had no further bleeding with a mean follow-up of 26 months. Three patients had episodes of bleeding prior to variceal obliteration; two of these patients underwent surgical intervention after emergency sclerosis to stabilize their condition. Transfusion requirements were less after sclerosis (p = 0.035), although the follow-up has been relatively short (mean, 24 months) compared to the duration of bleeding. Our results suggest that endoscopic sclerotherapy is an effective therapeutic alternative, and perhaps the initial treatment of choice, in patients with extrahepatic portal vein obstruction and bleeding esophageal varices.

A serologic follow-up of the 1942 epidemic of post-vaccination hepatitis in the United States Army.

An epidemic of icteric hepatitis in 1942 affected approximately 50,000 U.S. Army personnel. This outbreak was linked to specific lots of yellow-fever vaccine stabilized with human serum. To identify the responsible virus and the consequences of the epidemic, during 1985 we interviewed and serologically screened 597 veterans who had been in the army in 1942. These subjects were selected from three groups. Group I consisted of patients who had received the implicated vaccine and had jaundice; Group II had received the implicated vaccine but remained well; Group III had received a new, serum-free vaccine, with no subsequent jaundice. Ninety-seven percent of Group I, 76 percent of Group II, and 13 percent of Group III were positive for antibodies to hepatitis B virus. Only one subject had hepatitis B surface antigen, for a carrier rate of 0.26 percent among recipients of the implicated vaccine. The prevalence of hepatitis A antibody was similar in all three groups, and no subject had antibody to hepatitis delta virus. We conclude that hepatitis B caused the outbreak, that about 330,000 persons may have been infected, that the hepatitis B virus carrier state was a rare consequence, and that the outbreak induced hepatitis B antibodies that appear to persist for life.

Cerebrospinal fluid pleocytosis after seizures.

Cerebrospinal fluid (CSF) pleocytosis after seizure activity has been anecdotally reported for many years, but it has not been well documented. We reviewed the records of all adult patients admitted to Grady Memorial Hospital from November 1979 through October 1980 with the diagnosis of seizure. Of 102 patients whose CSF was examined, 35 (34%) had pleocytosis; in 31 (30%) there was no explanation for the pleocytosis despite laboratory and radiologic tests to rule out established causes. For those patients without an identifiable cause of pleocytosis the mean number of white cells was 72/cu mm with a median of 10 and a range from 3 to 464. A predominance of polymorphonuclear leukocytes (PMNs) was found in 57% of the initial CSF examinations. Eighty-six percent of patients with seizures due to ethanol withdrawal had a PMN predominance in their CSF, and 88% of patients with seizures due to a recent or remote cerebrovascular accident had a mononuclear cell predominance. The pleocytosis was usually transient; normalization of the CSF was associated with the rapid recovery of the patient. We conclude that an abnormal CSF leukocyte count may be entirely attributable to seizure activity, although the mechanism is unknown. Before assigning this cause, however, a thorough search is imperative to rule out treatable disorders that may cause CSF pleocytosis.