Digestive Diseases and Sciences, Vol. 34, No. 6 (June 1989), pp. 959-966

LETTERS TO TIlE EDITOR

SUCRALFATE EFFECTS

To The Editor: Sucralfate has been shown in clinical trials to

accelerate both gastric and duodenal ulcer healing in man and prevent duodenal ulcer formation in experimental animals after pentagastrin/bethanecol stimulation. Although the mechanism of action is uncertain, sucralfate has been shown to increase prostaglandin synthesis in the gastric mucosa of experimental animals, but there are no studies on the effect of sucralfate on duodenal prostaglandin synthesis. We would like to report the results of preliminary studies on the effect of a single intra- gastric dose of sucralfate on duodenal and gastric prostaglandin synthesis.

Ten rats were given 200 mg sucralfate intragastri- cally with a metal feeding tube. This dose was chosen as we had previously shown it to be protec- tive against pentagastrin/bethanecol-induced duo- denal ulcers in the rat. Ten rats were given the vehicle, 0.9% saline as controls. Three hours fol-

lowing instillation of either sucralfate 200 mg or vehicle (0.9% saline), the animals were sacrificed with intraperitoneal ketamine. The stomachs were opened along the greater curvature, washed in ice water, placed on an ice block, and the fundal mucosa was freed from underlying muscle. The duodenum was opened and the mucosa scraped with a glass slide. Samples were quickly placed in 1 ml PBS 0.01 M, pH 7.4, minced with scissors, weighed, centrifuged in a fixed-speed Eppendorf bench centrifuge for 15 sec at 9000g, resuspended in 0.5 ml buffer, incubated for 1 min by vortex mixing at room temperature, and again centrifuged at 9000g for 15 min. The supernatant was aliquoted in five 50-txl amounts and frozen at -70 ~

PGE and 6-keto PGFI~ were determined by RIA using anti-PGE and anti-6-keto PGF1~ supplied by Seragen. The antisera for PGE cross-reacted 100% with PGE 1 + PGE2 and 1% with 6-keto PGFl~. The antisera for 6-keto PGFl~ cross-reacted 100% with 6-keto PGFI~ and less than 0.6% with PGE~ and

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control and sucralfate-treated rats.

Digestive Diseases and Sciences, Vol. 34, No. 6 (June 1989) 0163-2116/89/0600-0959506.00/0 �9 1989 Plenum Publishing Corporation

959

LETTERS TO THE EDITOR

PGE2. Statistical analysis was carried out by Stu- dent's t test. Results are given as mean + standard deviation.

PGE synthesis was significantly increased in the duodenal mucosa of sucralfate-treated rats (194 --- 55) when compared to controls (122 + 48, P < 0.0l) (Figure 1). PGE synthesis was significantly in- creased in the gastric mucosa of the sucralfate- treated rats (311 + 55) when compared to controls (174 -+ 53, P < 0.001).

The 6-keto PGFt~ synthesis in duodenal mucosa of sucralfate-treated rats was 30 - 13, compared to 24 + 12 for control rats, and the 6-keto PGFI~ synthesis in the gastric mucosa of sucralfate-treated rats was 312 -+ 66 as compared to 286 + 72 for control rats. Although there was a trend towards increased synthesis in the sucralfate-treated ani- mals, the results were not statistically significant (P > 0.05).

Although the role of mucosal prostaglandins in ulcer genesis and healing in man is not yet estab- lished, it does appear as though a number of ulcer drugs, in this instance sucralfate, are able to stim- ulate not only gastric mucosal prostaglandins but also such synthesis in the duodenum. Whether this also occurs in man is presently under investigation.

ALAN SANDB~RG, MD SIMMY BANK, MD

VICTORIA KRANZ Long Island Jewish Medical Center

Division o f Gastroenterology N e w Hyde Park, N e w York

NORMAL SERUM AMYLASE IN ACUTE PANCREATITIS

To the Editor: The diagnosis of acute pancreatitis is still one of

the most difficult in abdominal pathology. Accord- ing to our experience, the statement that hyperamy- lasemia occurs within 12-48 hr following the onset of pain (1, 2) is questionable (2-5).

As an example, we are presenting data on a 59-year-old male patient who was admitted for persistent epigastric pain lasting nearly 24 hr. The patient retained gas, had frequent episodes of colicky pain after fatty foods, lasting initially for 20 rain, but longer 6 months after admission. Exami- nation revealed diffuse abdominal tenderness with localization in the upper abdomen without rebound tenderness. Laboratory investigations were within

normal limits except for a slightly elevated bilirubin level of 28 ~mol/liter with direct component. His serum amylase was normal, but we observed a slightly elevated level of amylase in the urine (46 txkathiter), which led us to measure serum and urine amylase and isoenzyme levels. We also started therapy (NPO, intravenous fluids and electrolytes, glucose, and procaine HC1). As shown in Figure 1, hyperamylasemia was found only on the third and fifth days of hospitalization. However, a persistent hyperamylasuria, with its peak on the third day and lasting for 32 days, was present. The amylase isoenzyme levels were assessed for the first time on day 4. Nevertheless, the level of the pancreatic isoenzyme was elevated and decreased on the elev- enth day. With the conventional therapy listed above, the subjective complaints disappeared within 48 hr. Intravenous cholangiography revealed stones in the gallbladder, and the hypotonic duode- nography showed a double-contour appearance caused by compression of an enlarged head of the

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i 3 [i 7 [I il 1'3 1'5 1'7 i9 ~l 25 ~8 ~ day Fig 1. Serum amylase (S-AMS), urine amylase (U-AMS), serum pancreatic amylase isoenzyme (S-P-iso) in the patient K. J. with acute pancreatitis. The horizontal lines indicate the upper limits of the normal values.

960 Digestive Diseases and Sciences, Vol. 34, No. 6 (June 1989)