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Biomedical subjects

B L Nguyen

Publications and source records attributed to B L Nguyen.

At least 19 recordsLinked to original sources

Assessment of right ventricular function by strain rate imaging in chronic obstructive pulmonary disease.

The purpose of the current study was to compare right ventricular (RV) myocardial wall velocities (tissue Doppler imaging) and strain rate imaging (SRI) parameters with conventional echocardiographic indices evaluating RV function in chronic obstructive pulmonary disease (COPD) patients. In total, 39 patients with COPD and 22 healthy subjects were included in the current study. Seventeen patients had pulmonary artery pressure <35 mmHg (group I) and 22 patients had pulmonary artery pressure >35 mmHg (group II). Tissue Doppler imaging, strain and strain rate (SR) values were obtained from RV free wall (FW) and interventricular septum. Respiratory function tests were performed (forced expiratory volume in one second/vital capacity (FEV(1)/VC) and carbon monoxide diffusion lung capacity per unit of alveolar volume (D(L,CO)/V(A))). Strain/SR values were reduced in all segments of group II patients compared with group I patients and controls with lowest values at basal FW site. A significant relationship was shown between peak systolic SR at basal FW site and radionuclide RV ejection fraction. A significant relationship was shown between peak systolic SR at basal FW site and D(L,CO)/V(A) and FEV(1)/VC. In conclusion, in chronic obstructive pulmonary disease patients, strain rate imaging parameters can determine right ventricular dysfunction that is complementary to conventional echocardiographic indices and is correlated with pulmonary hypertension and respiratory function tests.

Case-Control Studies↗

Impact of intracoronary aspiration thrombectomy during primary angioplasty on left ventricular remodelling in patients with anterior ST elevation myocardial infarction.

OBJECTIVE: To evaluate prospectively the impact on left ventricular (LV) remodelling of an intracoronary aspiration thrombectomy device as adjunctive therapy in primary percutaneous coronary intervention (PCI) in patients with anterior ST elevation myocardial infarction (STEMI). METHODS: 76 consecutive patients with anterior STEMI (65.3 (11.2) years, 48 men) were randomly assigned to intracoronary thrombectomy and stent placement (n = 38) or to conventional stenting (n = 38) of the infarct related artery. Each patient underwent transthoracic echocardiography immediately after PCI and at six months. At the time of echocardiographic control, major adverse cardiovascular events (MACE) in terms of death, new onset of myocardial infarction, and hospitalisation for heart failure were also evaluated. RESULTS: After a successful primary PCI, patients in the thrombectomy group achieved a higher rate of post-procedure myocardial blush grade 3 (36.8% v 13.1%, p = 0.03) and effective ST segment resolution at 90 minutes (81.6% v 55.3%, p = 0.02). Six months after the index intervention, 19 patients (26.8%) developed LV dilatation, defined as an increase in end diastolic volume (EDV) >or= 20%: 15 in the conventional group and four in the thrombectomy group (p = 0.006). Accordingly, at six months patients treated conventionally had significantly higher end systolic volumes (82 (7.7) ml v 75.3 (4.9) ml, p < 0.0001) and EDV (152.5 (18.1) ml v 138.1 (10.7) ml, p < 0.0001) than patients treated with thrombectomy. No differences in cumulative MACE were observed (10.5% in the conventional group v 8.6% in the thrombectomy group, not significant). CONCLUSION: Compared with conventional stenting, adjunctive aspiration thrombectomy in successful primary PCI seems to be associated with a significantly lower incidence of LV remodelling at six months in patients with anterior STEMI.

Adult↗

Effect of extent of resection on intestinal muscle adaptation.

The response of intestinal muscle to resection has received less attention than mucosal adaptation but may be important in relation to altered motility and improved intestinal absorption. Our aim was to determine the effect of extent of resection on intestinal muscle adaptation. Distal resections of 25% (n = 5), 50% (n = 5), and 75% (n = 5) of the intestine were performed. Transverse intestinal sections were taken at resection and 12 weeks later to evaluate changes in mucosa and circular and longitudinal muscle thickness. Muscle cell number and size and muscle length were also measured. Mucosal thickness increased (P < 0.05) after all resections, (1007 +/- 253 microns vs 1259 +/- 181 microns, 25%; 1019 +/- 191 microns vs 1366 +/- 293 microns, 50%; and 927 +/- 88 microns vs 1432 +/- 213 microns, 75%). Longitudinal muscle thickness (169 +/- 35 microns vs 254 +/- 45 microns, 50%; 207 +/- 71 microns vs 353 +/- 103 microns, 75%) and length (180 +/- 10 cm vs 203 +/- 16 cm, 50%; 90 +/- 16 cm vs 110 +/- 21 cm, 75%) increased (P < 0.05) following 50% and 75% resections but not after a 25% resection. Circular muscle length increased after 75% resection alone (4.4 +/- 0.2 cm vs 5.8 +/- 0.4 cm, P < 0.05). There was no significant change in circular muscle thickness after any resection. Muscle cell size and number per unit area were unchanged in all groups. We concluded that: (1) Intestinal muscle adapts after intestinal resection and this response is related to the extent of resection; in contrast, mucosal adaptation was evident following even the least extensive resection. (2) Increased thickness and length of the longitudinal muscle layer are the most prominent changes. (3) This increased muscle thickness results from hyperplasia rather than hypertrophy.

Adaptation, Physiological↗

Transformation of estrone and estradiol in hormone-dependent and hormone-independent human breast cancer cells. Effects of the antiestrogen ICI 164,384, danazol, and promegestone (R-5020).

Using different hormone-dependent (MCF-7, T-47D) and hormone-independent (MDA-MB-231, Hs-578S, MDA-MB-436) human breast cancer cells, the interconversion estrone (E1)<-->estradiol (E2) was explored. The data show very clearly that in the hormone-dependent cells the tendency is to form E2 after incubation with E1, whereas after incubation with E2 most of this estrogen remains unchanged. In the hormone-independent cells, in contrast most of E1 remains E1, while E2 is converted into E1. The tendency of the reductive<-->oxidative direction is supported by the analysis of estrogens in the culture medium. To explore the possible action of different drugs on the 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activity, it was observed that the potent antiestrogen ICI 164,384 inhibits the conversion of E1 to E2, while a lesser effect is observed with Danazol and only weak inhibition is obtained with the progestagen Promegestone (R-5020). It is concluded that the orientation of 17 beta-HSD activity for the interconversion E1<-->E2 in hormone-dependent and -independent cells is related to the hormonal status of the cells.

17-Hydroxysteroid Dehydrogenases↗

Regional variation in canine intestinal muscle mass and function.

Our aim was to investigate the contribution of variations in intestinal muscle morphology or function to regional differences in motor properties in vivo. We quantitated intestinal muscle thickness and surface area along the canine gut and compared the in vitro contractile properties of the jejunum and ileum. The thickness and cross-sectional surface area of both circular and longitudinal muscle demonstrated a parabolic distribution along the intestine, with the greatest values occurring in the proximal and distal regions. The terminal ileum had the greatest circular (885 +/- 194 microns) and longitudinal muscle (367 +/- 135 microns) thickness. Circular muscle was 2.5-3 times thicker than longitudinal muscle at all points. Passive tension was similar in muscle strips from the mid-jejunum, mid-ileum, and terminal ileum (2.8 +/- 0.8, 2.5 +/- 0.4, and 2.3 +/- 0.8 vs 2.5 +/- 0.5, 1.9 +/- 0.5, and 2.8 +/- 1.0, longitudinal and circular, respectively). Active and total tension, however, were significantly greater in longitudinal than circular muscle in mid-jejunum (active; 8.5 +/- 1.4 vs 5.6 +/- 1.2, P < 0.05 and total 11.3 +/- 1.7 vs 8.1 +/- 1.2) and in mid-ileum (active 9.5 +/- 1.6 vs 5.8 +/- 1.2 and total 12.0 +/- 1.6 vs 7.7 +/- 1.2). Values for each layer were similar in both sites. In contrast, in the terminal ileum, longitudinal and circular muscle strips demonstrated similar active (10.1 +/- 1.7 vs 9.0 +/- 2.7, NS) and total tension (12.4 +/- 2.0 vs 11.9 +/- 3.4, NS). Dose-response curves to carbachol (10(-8)-10(-2) M) were similar in all these regions. We conclude (1) there are regional variations in muscle mass but contractile properties are similar in jejunum and ileum; and (2) the unique motor properties of the terminal ileum may be related more to differences in muscle morphology and neural input than intrinsic function.

Animals↗

Estrone sulfate-sulfatase and 17 beta-hydroxysteroid dehydrogenase activities: a hypothesis for their role in the evolution of human breast cancer from hormone-dependence to hormone-independence.

The evaluation of estrogens (estrone, estradiol, and their sulfates) in the breast tissue of post-menopausal patients with breast cancer indicates high levels, particularly of estrone sulfate (E1S) which is 15-25 times higher than in the plasma. Breast cancer tissue contains the enzymes necessary for local synthesis of estradiol and it was demonstrated that, despite the presence of the sulfatase and its messenger in hormone-dependent and hormone-independent breast cancer cells, this enzyme operates particularly in hormone-dependent cells. Different progestins: Nomegestrol acetate, Promegestone, progesterone, as well as Danazol, can block the conversion of E1S to E2 very strongly in hormone-dependent breast cancer cells. The last step in the formation of estradiol is the conversion of E1 to this estrogen by the action of 17 beta-hydroxysteroid dehydrogenase. This activity is preferentially in the reductive direction (formation of E2) in hormone-dependent cells, but oxidative (E2-->E1) in hormone-independent cells. Using intact hormone-dependent cells it was observed that Nomegestrol acetate can block the conversion of E1 to E2. It is concluded, firstly, that in addition to ER mutants other factors are involved in the transformation of hormone-dependent breast cancer to hormone-independent, this concerns the enzymatic activity in the formation of E2; it is suggested that stimulatory or repressive factor(s) involved in the enzyme activity are implicated as the cancer evolves to hormone-independence; secondly, different drugs can block the conversion of E1S to E2. Clinical trials of these "anti-enzyme" substances in breast cancer patients could be the next step to investigate new therapeutic possibilities for this disease.

17-Hydroxysteroid Dehydrogenases↗

Somatostatin analogue inhibits intestinal regeneration.

Somatostatin analogue octreotide inhibits intestinal absorption and motility but its effect on epithelial cell migration and proliferation remains unclear. Our aim was to determine the effect of octreotide on parameters of intestinal regeneration, including epidermal growth factor (EGF)-induced changes. Thirty rabbits had full-thickness ileal defects patched with cecal serosa surface. Group 1 were controls. Groups 2 and 3 received 100 micrograms and 1000 micrograms, respectively, of subcutaneous octreotide daily. Group 4 received EGF at 1.5 micrograms/kg per hour via subcutaneous miniosmotic pump, and group 5 received both octreotide (1000 micrograms/d) and EGF (1.5 micrograms/kg per hour). Octreotide at 100 micrograms/d did not inhibit epithelial cell migration or proliferation at 7 days. Octreotide at 1000 micrograms/d inhibited normal but not EGF-stimulated cell migration. Octreotide decreased EGF-stimulated but not normal proliferation. Octreotide impairs epithelial cell migration in a dose-dependent manner. Octreotide inhibits EGF-stimulated proliferative activity but not EGF-stimulated migration. Prolonged administration of octreotide may adversely affect normal and adaptive intestinal regeneration by both direct and indirect effects.

Animals↗

Comparison of techniques for harvesting enterocytes for transplantation.

Selective enterocyte transplantation is a potential alternative to small intestinal transplantation for treatment of the short bowel syndrome. Our aim was to compare chelation and enzymatic methods of isolating enterocytes with respect to initial cell yield and characteristics and in vitro growth. Enterocytes were harvested from adjacent ileal segments in 35 rabbits using chelation with EDTA and warm trypsinization. Determinations were made of initial viability by trypan blue exclusion, cell yield, and proportion of intact crypts. Cells (5 x 10(6)) were seeded in growth media into culture vessels. Cell attachment was estimated by measuring cells liberated by Dispase at 24 hr. In vitro growth was assessed at 14 and 28 days. Although total cell yield (15.0 +/- 9.9 vs 12.5 +/- 8.3 x 10(6) cells/cm) and intact crypts were similar, the trypsin technique resulted in cells with higher initial viability (86 +/- 7 vs 71 +/- 18%, P < 0.05). Cell attachment (7 +/- 8 vs 8 +/- 4%) and enterocyte disaccharidase activity were similar using both techniques. While the number of epithelial cell growth foci was not significantly different at 14 days, there was significantly greater surface coverage on both plain (44 +/- 20% vs 1 +/- 0%, P < 0.05) and Matrigel-coated (80 +/- 14 vs 16 +/- 25%, P < .05) vessels at 28 days with trypsin-isolated cells. Trypsinization resulted in a cell population which had a higher percentage of viable cells but a similar proportion of intact crypts and differentiated cells compared to those resulting from the chelation technique. Trypsin-liberated cells had greater capacity for in vitro growth particularly on Matrigel-coated surfaces.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Action of danazol on the conversion of estrone sulfate to estradiol and on the sulfatase activity in the MCF-7, T-47D and MDA-MB-231 human mammary cancer cells.

In the present studies the action of Danazol on the conversion of estrone sulfate (E1S) to estradiol (E2) as well as on the sulfatase activity in the MCF-7 and T-47D, hormone-dependent, and MDA-MB-231, hormone-independent, mammary cancer cell lines was explored. Using intact cells we observed that Danazol blocks very significantly the radioactivity uptake and the conversion of [3H]E1S to E2 in all the cells studied. In particular, a very strong effect (85% decrease of these parameters versus the control values) is observed in the T-47D cells. In another series of studies using cell homogenates it is observed that Danazol inhibits the sulfatase activity in all these cell lines. The effect of Danazol is dose-dependent and significant from a concentration of 1 microM. At concentrations of 8 microM E1S, 10(-5) M Danazol, the inhibition of sulfatase activity is 38% in MCF-7, 36% in MDA-MB-231, and 27% in T-47D cells. Analysis by Lineweaver-Burk plot shows that the inhibitory effect is competitive. As E1S is one of the main sources of E2 in human mammary tumors, the present data could open new possibilities for therapeutic applications in hormone-dependent breast cancer.

Breast Neoplasms↗

Effect of triptorelin (Decapeptyl) combined with heparin on estradiol levels in MCF-7 mammary cancer cells after incubation with estrone sulfate.

The effects of triptorelin (Decapeptyl) and heparin, alone or in combination, on the intracellular concentration of estradiol (E2) after incubation of estrone sulfate (E1S) with the MCF-7 mammary cancer cells was investigated. Although heparin (10 mg/l culture medium) or Decapeptyl (5 x 10(-7) or 5 x 10(-5) mol/l) did not affect the levels of radioactive E2 after incubation with [3H]E1S, the combination of Decapeptyl and heparin significantly decreased the radioactive uptake and the intracellular concentrations of [3H]E2. In the absence of Decapeptyl and heparin incubations with E1S, the resulting E2 concentration (in nmol/kg DNA +/- SD) was 558 +/- 44; after heparin (10 mg/l) plus Decapeptyl (5 x 10(-7) or 5 x 10(-5) mol/l) the values were 389 +/- 55 and 165 +/- 18, respectively. It is concluded that Decapeptyl with heparin can decrease very significantly the conversion of E1S to E2 in MCF-7 cells, an observation that suggests new possibilities for the control of E2 in hormone-dependent breast cancer.

Breast Neoplasms↗

Gas chromatographic-mass spectrometric determination of plasma selegiline using a deuterated internal standard.

A gas chromatographic-mass spectrometric method is described for the determination of plasma selegiline. Tetradeuteroselegiline was synthesized and served as the internal standard. Human plasma samples (1 ml) containing 1-6 ng of selegiline were acidified, washed with diethyl ether-hexane, then alkalinized and extracted with heptane-isoamyl alcohol. Analytical separations were performed on a dimethylsilicone capillary column. Detection was by selected ion monitoring of the electron impact generated m/z 96 and 100 alpha-cleavage fragments of drug and internal standard, respectively.

Deuterium↗

Effect of the progestagen R5020 (promegestone) and of progesterone on the uptake and on the transformation of estrone sulfate in the MCF-7 and T-47d human mammary cancer cells: correlation with progesterone receptor levels.

In the present study we have explored the actions of the progestagen R5020 (Promegestone: 17 alpha, 21-dimethyl-19-nor-pregna-4, 9-diene-3,20-dione) and progesterone on the uptake of [3H]estrone sulfate ([3H]E1S) and its conversion to estradiol (E2) by two hormone-dependent mammary cancer cell lines: MCF-7 and T-47D. R5020 or progesterone significantly decreased the uptake of [3H]E1 and its conversion to (E2). In the cells of the two lines, R5020 or progesterone (5 x 10(-6) M) decreased the E2 concentrations by 2-3 times in relation to the levels in untreated cells. E1S (1 x 10(-7) M) also increased expression of the progesterone receptor (PR) and both R5020 (5 x 10(-6) M) and progesterone (5 x 10(-6) M) blocked this stimulatory action of E1S in cells of both cell lines. As E2 is one of the main factors of cancerization in the breast and estrone sulfate is quantitatively the most important precursor of E2 in this tissue, the decrease of E2 by these progestagens could open new possibilities for the control of E2 in the breast cancer tissue.

Biotransformation↗

Basement membrane components enhance isolated enterocyte growth.

Isolated enterocyte transplantation may have a potential role in increasing intestinal surface area. However, enterocytes are notoriously difficult to grow. Basement membrane components (BMC) promote adherence, migration, and differentiation of enterocytes. Our aim was to determine if BMC enhance enterocyte growth. Twenty-nine rabbits had 5-cm ileal segments resected and serosal pouches (n = 22) created from the serosal surface of the colon. Harvesting of enterocytes by warm trypsinization resulted in 92 +/- 6% cell viability and yielded 5.0 +/- 2.4 10(6) enterocytes/cm intestine. Enterocytes (10(5) were cultured in vitro (n = 7) in 10 ml growth media in plain flasks and flasks coated with laminin alone or Matrigel (an extract of mouse basement membrane containing laminin plus Type IV collagen and heparan sulfate). The cells were subcultured at 2 weeks and examined after Geimsa staining at 4 weeks. Epithelial growth was confirmed by light microscopy and staining for cytokeratin and quantitated by image analysis (JAVA). Epithelial coverage of the flasks was greater with Matrigel (80 +/- 15%) than laminin (66 +/- 15%) which was greater than control (44 +/- 20%) (P less than 0.01). For in vivo studies 10(5) harvested cells were infused into the serosal pouches either in growth media (n = 9) or media + Matrigel (n = 13). Epithelial growth in the pouch was evaluated by qualitative scoring of cytokeratin staining. Cytokeratin staining was similar on control colon serosa (n = 5) and serosa after infusion of cells in media alone. However, Matrigel significantly enhanced the area, depth, and intensity of staining.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Recent data on estrogen sulfatases and sulfotransferases activities in human breast cancer.

Of the total number of breast cancers approx. 30-50% are hormone-dependent and estradiol is one of the main factors of cancerization. Consequently, the control of this hormone inside the cancer cell is of capital importance because it is well established that the inhibition of estradiol biosynthesis can have a positive effect on the evolution of the disease. The blockage of estradiol can be obtained by the action of anti-aromatases, anti-sulfatases, the control of the 17 beta-hydroxysteroid dehydrogenase activity or by the stimulation of the sulfotransferase which converted the estrogens in their sulfates. In breast cancer tissue estrone sulfate is quantitatively the most important source of estradiol. In the intact cell, estrone sulfatase activity is very intense in the hormone-dependent cell lines (e.g. MCF-7, T-47D) but very small activity is observed in the hormone-independent (e.g. MDA-MB-231, MDA-MB-436) cell lines. However, this activity became very strong after homogenization in the hormone-independent cells, suggesting the presence of repressive factor(s) for this enzyme or its sequestering in an inactive form, in the intact cells of these cell lines. In a series of previous studies it was found that in hormone-dependent cell lines different anti-estrogens: tamoxifen and derivatives, ICI 164,384, very significantly decrease the estradiol concentration originated from estrone sulfate, and recently it was observed that Decapeptyl (D-Trp6-gonadotropin-releasing hormone) in the presence of heparin can also decrease the conversion of estrone sulfate into estradiol. No significant effect was obtained in the presence of heparin or Decapeptyl alone. The estrone sulfatase activity can be inhibited by progesterone, the progestagen R-5020, and testosterone. In another series of recent studies the presence of very strong estrogen sulfotransferase activity has been shown in one breast cancer cell line, the MDA-MB-468. We can conclude that: (1) the control of estradiol concentration can be carried out in the breast cancer tissue itself; (2) estrone sulfate can play an important role in the bioavailability of estradiol in the breast cancer cell; and (3) as is the case for the aromatase, the control of: the estrogen sulfatase, estrogen sulfotransferase, and 17 beta-hydroxysteroid dehydrogenase can be new targets for therapeutic applications in breast cancer.

Breast Neoplasms↗

Selective versus routine antibiotic use in acute appendicitis.

Whether prophylactic antibiotics should be employed routinely in all patients with presumed appendicitis rather than be administered selectively to those with suspected perforation remains a controversial issue. The outcome of 312 adult patients undergoing appendectomy during periods of selective (I, n = 153) and routine (II, n = 159) antibiotic use were compared. Although the rates of misdiagnosis were comparable (9% vs 13%), significantly more patients with appendicitis in Period II had perforated appendicitis (29 of 139 vs 44 of 139, P less than 0.05). Prophylactic antibiotics were given to 43 (28%) patients in Period I compared to 132 (83%) in Period II (P less than 0.001). This, increased frequency was true for both simple (21% vs 81%, P less than 0.001) and perforated (66% vs 86%, P less than 0.05) appendicitis. A single antibiotic, most frequently a cephalosporin, was used significantly more often in Period II (44% vs 82%, P less than 0.001). There was no significant difference in the methods of wound closure between the two periods. The incidence of infectious complications was similar in patients with simple appendicitis in both periods (8% vs 11%), but it was significantly greater during Period I in patients with perforated appendicitis (45% vs 20%, P less than 0.05). The overall infection rate was similar in both periods (16% vs 22%). Thus, high-risk patients with perforated appendicitis were more likely to receive antibiotics and had a lower infection rate with routine antibiotic use. Furthermore, there was no overall change in the infection rate during this period, despite the use of less toxic, single drug regimens and a greater percentage of perforated appendicitis.

Acute Disease↗

Estrone sulfatase activity and effect of antiestrogens on transformation of estrone sulfate in hormone-dependent vs. independent human breast cancer cell lines.

The effect of the anti-estrogens ICI 164,384 and tamoxifen on the estradiol (E2) concentration after incubation of estrone sulfate (E1-S) with different hormone-dependent (MCF-7 and T-47D) and hormone-independent (MDA-MD-231 and MDA-MB-436) mammary cancer cells, as well as the estrone sulfatase activity in these various cell lines, are presented. The anti-estrogen ICI 164,384 decreased very significantly the concentration of E2 after incubation of E1-S with MCF-7 (control, mean +/- SE: 100 +/- 24 pg/mg DNA; + ICI 164,384 [10(-6)M]: 7 +/- 2 pg/mg DNA). This effect was much more intense than with tamoxifen. A similar effect was observed with T-47D cells. However, no significant effect was observed in the hormone-independent cells. In the intact cell, estrone sulfatase activity was very intense in the hormone-dependent cells, but very small in the hormone-independent cells. However, this activity became very strong after homogenization in the hormone-independent cells. The data suggest that estrone sulfate can play an important role on the bioavailability of E2 in hormone-dependent breast cancer, and that understanding the control of estrone sulfatase activity can open new knowledge of the estrogen responses and new possibilities of therapeutic application in breast cancer.

Breast Neoplasms↗

Influence of the etiology of pancreatitis on the natural history of pancreatic pseudocysts.

We reviewed our experience with 90 patients with pancreatic pseudocysts to determine if the cause of pancreatitis influenced the patients' outcome. Acute pancreatitis (AP) occurred in 57 (63%) patients due to alcoholic (n = 15), postoperative (n = 14), biliary (n = 12), and other etiologies (n = 16). Thirty-three (37%) patients had chronic pancreatitis (CP) secondary to alcohol use (n = 27) or other causes (n = 6). Multiple pseudocysts were significantly more frequent in patients with acute alcoholic pancreatitis than in patients with chronic pancreatitis (47% versus 19%, p < 0.05). Spontaneous resolution occurred within 8 weeks in 10 (11%) patients with pseudocysts (AP = 9%, CP = 15%, p = NS). However, no patient with pseudocyst associated with biliary or postoperative pancreatitis underwent spontaneous resolution. Although pseudocysts associated with chronic pancreatitis were smaller in size (8.0 +/- 4.7 versus 5.7 +/- 3.8 cm, p < 0.05), a similar proportion of them required operation compared with AP pseudocysts (56% versus 58%). There were significantly more deaths in patients with postoperative pancreatitis compared with all other groups (29% versus 7%, p < 0.05). The outcome of pseudocysts was similar regardless of size (greater than 6 cm versus less than 6 cm) and presentation (acute versus delayed). Thus, the etiology of pancreatitis was a more important determinant of pseudocyst outcome than pseudocyst size or presentation.

Acute Disease↗