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Biomedical subjects

F Y Chang

Publications and source records attributed to F Y Chang.

At least 289 records · Page 16Linked to original sources
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Hereditary hemorrhagic telangiectasia: demonstration of portosystemic venous shunts using power Doppler sonography and sonographically guided percutaneous transhepatic portovenography.

Hereditary hemorrhagic telangiectasia is a rare autosomal dominant inherited disease associated with vascular abnormalities, which may occur in any organ. Cases of hereditary hemorrhagic telangiectasia accompanied by intrahepatic portosystemic venous shunts, however, have rarely been described. We report a case of hereditary hemorrhagic telangiectasia in which intrahepatic portosystemic shunts were detected using power Doppler sonography and portovenography with percutaneous transhepatic contrast agent injection. On gray-scale sonography, the common hepatic artery was dilated, and dilated tubular structures mimicking dilated biliary tracts were found. Power Doppler sonography demonstrated the continuity of tortuous vascular channels connecting a branch of the right portal vein to a branch of the right hepatic vein. The dilated vascular channels and tributaries of the right hepatic vein showed a monophasic waveform pattern on spectral analysis. Portovenography showed a tangle of vascular structures connecting with a branch of the right hepatic vein.

Aged↗
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Complement pathway activity in serum from patients with classical dengue fever.

Complement activity in 125 cases of classical dengue fever was examined through the measurement of haemolytic activity. During the first 3 d of fever, the classical complement pathway activity (CCPA) was not altered in 109 cases. After 4 d of fever, 9 of 16 patients in the viraemic period had CCPA decreased by 45% (995 +/- 119 units/ml) and serum complement component C4 decreased by 40% (10.4 +/- 0.9 mg/dl). The alternative complement pathway activity was not affected in any case tested throughout both viraemic and convalescent stages. Both CCPA and C4 persistently decreased in 3 of these 9 patients at the convalescent stage. A decrease in serum C3 was also observed in these 3 patients only, and circulating immune complexes (CIC) levels were particularly high in these 3 patients. These results indicate that there is little evidence of complement activation on days 1-3 of viraemia but that complement activation may occur subsequently. It is concluded that both CIC and other unknown factors not related to CIC may contribute to complement activation in some cases (9/125) of classical dengue fever.

Adult↗
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Serum pepsinogen I levels in patients with non-ulcer dyspepsia.

In order to understand whether the serum pepsinogen I (PGI) levels of non-ulcer dyspepsia (NUD) patients differed from those of healthy controls and which kinds of factors might influence these levels of the former, serum PGI levels were determined by radio-immunoassay in 120 healthy controls and 361 NUD patients. The mean serum PGI level was significantly lower in NUD patients than in the controls (75.8 +/- 38.2 ng/mL versus 95.9 +/- 39.3 ng/mL; P less than 0.0001); in NUD patients, it was significantly higher in males than in females (79.6 +/- 40.4 ng/mL versus 63.2 +/- 26.4 ng/mL; P less than 0.001). However, corrected serum PGI levels according to the lean body mass disclosed no sex difference. Nevertheless, there was a weak correlation between the ages of patients and serum PGI levels (r = 0.403). The serum PGI levels in blood groups A, B, AB and O did not differ significantly. Smoking might be a decisive factor, for the mean serum PGI level was significantly higher among the smokers than among the non-smokers (86.7 +/- 44.6 ng/mL versus 70.6 +/- 33.7 ng/mL; P less than 0.001). It is concluded that the mean serum PGI level of NUD patients, while affected by sex, age, smoker status and the body size, is lower than that of the healthy controls. Without endoscopy, assay of serum PGI level has no place in the diagnosis of dyspepsia because of the wide overlapping of serum PGI levels between NUD patients and patients with other common gastric lesions.

Age Factors↗
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Medical treatment of duodenal ulcer: acid inhibition or Helicobacter pylori eradication?

To ascertain whether acid inhibition or Helicobacter pylori (HP) colonization is the decisive factor in the healing of duodenal ulcer, we treated 54 patients with famotidine and carried out long-term follow-up. Helicobacter pylori colonization was found in 70.4% of patients before treatment. There were no differences in the pre-treatment characteristics between patients with HP positive or HP negative ulcers. The 4-week and 8-week healing rates after famotidine treatment were 72.5% and 82.4% respectively. No difference in HP colonization was found between patients with ulcer healed and those with ulcer not healed (78.4% vs 64.3% at 4th week and 77.3% vs 71.4% at 8th week, P greater than 0.05). In patients with ulcer healed at 4th week, the intragastric pH was raised significantly and the antral acute inflammation was less severe than those with ulcer not healed. Ulcer recurrence was found in 76.9% of patients within 1 year, but there was no difference in ulcer recurrence between the patients with positive or negative HP colonization at the time of ulcer healing. Our results suggest that duodenal ulcer healing and recurrence are closely related to acid inhibition rather than to HP colonization.

Duodenal Ulcer↗
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Oesophageal perforation following endoscopic variceal ligation and balloon tamponade.

Endoscopic variceal ligation (EVL) related complication is rarely reported. A case is presented of a 74 year old man with oesophageal variceal bleeding who developed oesophageal perforation following EVL and balloon tamponade. An oesophageal wall defect was induced by EVL and tissue repair was hindered by decompensated liver reserve and shock status; concomitant balloon tamponade precipitated oesophageal perforation. The case is reported to draw attention to oesophageal perforation after concurrent use of balloon tamponade and EVL.

Aged↗
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A single standard nocturnal dose of nizatidine enhances the healing of active duodenal ulcers among Chinese.

Chinese people have a lower maximal acid output and gastrin response to meals compared to Western people. The aim of the present study was to assess the efficacy of a half-single nocturnal dose of nizatidine (150 mg at bedtime [h.s.], n = 40) with a standard full dose given once nightly (300 mg h.s., n = 38) or twice daily (150 mg twice a day [b.i.d.], n = 43) in the treatment of Chinese patients with active duodenal ulcers. An endoscopy was performed upon entry and at 4 week intervals until the ulcer healed (up to 8 weeks). There is no statistical difference in healing rates after 4 weeks of treatment (52.5, 52 and 47% in nizatidine 150 mg h.s., 150 mg b.i.d. and nizatidine 300 mg h.s., respectively) whereas nizatidine 300 h.s. had a significantly higher healing rate compared to nizatidine 150 mg h.s. and b.i.d. after 8 weeks of treatment (89 vs 70 and 67%, P < 0.05) by uni- and multivariate analysis of clinical and endoscopic characteristics. Symptomatic response was not significantly different in these three treated groups. Our study suggested that a half-single nocturnal dose of nizatidine is not ideal for the treatment of duodenal ulcer in Chinese patients, whereas a single standard nocturnal dose appears more effective than a twice-daily regimen.

Adult↗
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Triple therapy for the eradication of Helicobacter pylori and reduction of duodenal ulcer relapse: comparison of 1 week and 2 week regimens and recrudescence rates over 12 months.

The aim of this study is to assess the relationship between Helicobacter pylori and the relapse of duodenal ulcer, and also to evaluate the differences in efficacy and side effects between 1 week and 2 week triple therapy. Sixty-two patients with active duodenal ulcer, which healed within 8 weeks of nizatidine treatment, were randomly allocated to one of two groups. Group 1 (n = 29) received no drugs, Group II (n = 33) received triple therapy for 1 week (IIa, n = 16) or 2 weeks (IIb, n = 17). Eleven patients whose ulcer did not heal after an 8 week nizatidine treatment period were randomly assigned into Group IIa (n = 5) and IIb (n = 6). Seven patients whose ulcer recurred after discontinuation of nizatidine were allocated to receive 2 weeks of triple therapy. All patients received endoscopy 6 weeks after entry, and again at 3, 6 and 12 months unless both ulcer recurrence and H. pylori infection were found. The frequency of ulcer relapse 6 weeks after the active duodenal ulcer had healed was 83% (24/29 in Group I, 13% in Group 11a and 14% in Group IIb. The cumulative rate of recurrence was significantly higher in Group I than in Group II (90 vs 30% at 12 months, P < 0.01). Ulcer relapse was associated with persistence of H. pylori infection (P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
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Influence of pregnancy and uterine weight on rat gastrointestinal transit.

Orogastric feeding of a charcoal meal to rats was employed to measure whether the various stages of pregnancy could influence gastrointestinal transit. The oestrous cycle of female Sprague-Dawley rats was checked daily. If pro-oestrus occurred, the first day of pregnancy was defined to be on the next day after the copulation. Gastrointestinal transit studies were conducted on day 7 (first trimester), day 14 (second) and day 21 (third), respectively. The rats were killed 15 min after the successful feeding of a calorie-free, charcoal-containing test meal via a transiently placed orogastric catheter. Gastrointestinal transit was defined as the per cent of charcoal transit divided by the total length of the small intestine. These results were compared with the data obtained from non-pregnant female rats. Mean percentages of transit for the first, second and third trimester, and for controls were 42.8 +/- 1.9, 45.3 +/- 4.1, 35.7 +/- 1.7 and 42.6 +/- 1.4%, respectively (mean +/- s.e.). Late pregnancy elicited a marked inhibition of transit (P < 0.01). A significant negative correlation between transit and uterine weight of all pregnant rats was seen (r = -0.50, P < 0.05). The present study indicates that inhibited gastrointestinal transit occurs in the late pregnant rat.

Animals↗
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Comparison of lansoprazole and omeprazole in the short-term management of duodenal ulcers in Taiwan.

Lansoprazole is a novel H+/K+-ATPase inhibitor which exhibits a very potent and long-acting suppression of acid secretion. The object of this randomized, controlled trial was to compare duodenal ulcer healing rates after 4 weeks of treatment with a once-daily regimen of either 30 mg lansoprazole or 20 mg omeprazole. Of a total of 111 patients 57 received lansoprazole, whereas 54 received omeprazole. In intention-to-treat analysis at 4 weeks, 89.5% patients showed ulcer healing following treatment with lansoprazole compared with 83.3% of patients treated with omeprazole. Per protocol analysis indicated that 96.1% of patients treated with lansoprazole showed ulcer healing, compared with 93.6% of patients treated with omeprazole (NS). Age, smoking or ulcer size did not affect the ulcer healing rate. Both agents could effectively and quickly resolve ulcer symptoms. The Helicobacter pylori clearance was seen in 36 (73.5%) patients in the lansoprazole group and in 40 (80%) patients in the omeprazole group after four weeks of treatment (NS). In addition, both agents led to hypergastrinaemia, by approximately 1.6 fold. Adverse side effects included a few occurrences of reversible skin rash and constipation. It is concluded that lansoprazole elicits an adequate healing response and resolves symptoms of duodenal ulcer as well as omeprazole. Furthermore, lansoprazole is well tolerated with a few adverse side effects.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMedDate not supplied

Recurrence of H. pylori infection and dyspeptic symptoms after successful eradication in patients cured of duodenal ulcer disease.

BACKGROUND/AIMS: To evaluate the recurrence of Helicobacter pylori (H. pylori) infection and dyspeptic symptoms in patients previously cured of active duodenal ulcers followed by successful eradication with bismuth-based triple therapy. METHODOLOGY: Patients who remained H. pylori-negative by repeat endoscopy for 1 year were invited back and had their H. pylori status checked with a 13C-urea breath test. Those found positive for H. pylori underwent endoscopic confirmation by urease testing and histology. RESULTS: Thirty-four (69%) patients, 30 males/4 females, with a mean age of 56.4 years and a mean follow-up period of 4.8 years, were eligible for study. Five patients were considered recurrent with H. pylori infection, giving us a recurrence rate of 3% per patient per year. Sixty percent (3/5) of the patients with recurrence experienced typical ulcer symptoms, whereas none of the H. pylori-negative patients experienced typical ulcer symptoms if non-steroidal antiinflammatory drug (NSAID) use is excluded. CONCLUSIONS: Recurrence of H. pylori infection is low in Taiwan. Gender, age, smoking, alcohol consumption, and blood grouping do not appear to be significant risk factors for H. pylori recurrence. Reappearance of typical ulcer symptoms is suggestive of recurrence of H. pylori infection in patients cured of duodenal ulcer disease if the use of NSAID is excluded.

Adult↗
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Tuberculous peritonitis in a geriatric patient: a case report.

In geriatric patients with exudative ascites, malignant ascites is a common etiology. Tuberculous peritonitis is rarely seen and usually overlooked. We describe a 67-year-old man who suffered from exudative ascites for 1 month before admission. None of the noninvasive diagnostic methods utilized enabled us to make a correct diagnosis. Peritoneoscopic examination demonstrated multiple whitish miliary nodules and some larger nodules in the parietal and visceral peritoneum. Excisional biopsy confirmed the diagnosis of tuberculous peritonitis. This case reminds us that although malignant ascites is more prevalent in geriatric patients with exudative ascites, peritoneoscopy is indicated when noninvasive diagnostic methods allow no definite diagnosis.

Aged↗
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Effect of non-steroidal anti-inflammatory drugs on gastric and duodenal prostaglandin concentrations in patients with Helicobacter pylori infection.

BACKGROUND/AIMS: Both Helicobacter pylori and non-steroidal anti-inflammatory drugs are reported to affect gastroduodenal prostaglandin synthesis. However, their influence on gastric mucosal prostaglandins remains unclear. The aim of this study was to investigate the influence of nonsteroidal anti-inflammatory drugs on mucosal prostaglandin synthesis in patients with Helicobacter pylori infection. METHODOLOGY: We enrolled 87 Helicobacter pylori-infected patients in this study (gastric ulcer: 33, duodenal ulcer: 41, and non-ulcer dyspepsia: 13). Of them, 27 patients received non-steroidal anti-inflammatory drugs. Endoscopy was performed and biospy specimens from gastric body, antrum and duodenal bulb were assessed for Helicobacter pylori and prostaglandin concentration. RESULTS: A significantly lower mucosal prostaglandin E2 level at gastric body (142.2 +/- 28.1 ng/mg vs. 222.0 +/- 12.4 ng/mg, mean +/- SEM) and antrum (131.3 +/- 26.4 ng/mg vs. 226.0 +/- 19.0 ng/mg) was noted in Helicobacter pylori-infected gastric ulcer patients with non-steroidal anti-inflammatory drugs ingestion than in that of patients without non-steroidal anti-inflammatory drugs ingestion (p < 0.05). Using a multivariate analysis, we found that non-steroidal anti-inflammatory drug was an independent variable affecting gastric and duodenal mucosal prostaglandin E2 synthesis in patients with Helicobacter pylori-infected gastric ulcer. CONCLUSIONS: Non-steroidal anti-inflammatory drugs decrease gastroduodenal mucosal prostaglandin E2 synthesis in gastric ulcer patients with Helicobacter pylori infection.

Adolescent↗