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Biomedical subjects

J C Sheu

Publications and source records attributed to J C Sheu.

At least 127 records · Page 7Linked to original sources
PubMed1990

Serum hepatitis B virus DNA in healthy HBsAg-negative Chinese adults evaluated by polymerase chain reaction.

Serum hepatitis B virus (HBV) DNA was assayed using polymerase chain reaction, in 107 HBsAg-negative normal Chinese subjects. The results showed that eight subjects (7.5%) had HBV DNA. In the subgroup with antibody to hepatitis B surface antigen (anti-HBs) and to hepatitis B core antigen (anti-HBc), 7.3% (5/68) were positive for HBV DNA; HBV DNA was not detected in six individuals with anti-HBs only and in nine with anti-HBc only. In four persons with anti-HBc and anti-HBe, one had HBV DNA. In 20 subjects negative for all hepatitis B serological markers, two (10%) were found to have HBV DNA. This study indicates that serological markers are not adequate to rule out HBV infection, and it further implies that present blood donor screening methods may need improving.

Adolescent↗
PubMed1990

Hepatitis C virus infection in an area hyperendemic for hepatitis B and chronic liver disease: the Taiwan experience.

To assess the contribution of hepatitis C virus (HCV) in liver disease in Taiwan, antibody to HCV (anti-HCV) was studied by radioimmunoassay in 392 patients with chronic liver disease and in 440 healthy adults and 444 subjects at risk. The anti-HCV prevalence was 0.95% in 420 volunteer blood donors, 90% in 100 hemophiliacs, and 81% in 58 parenteral drug abusers. Anti-HCV was present in 6 (7.7%) of 78 hepatitis B surface antigen (HBsAg)-positive and 28 (65%) of 43 HBsAg-negative patients with chronic hepatitis, 3 (10%) of 31 HBsAg-positive and 13 (43%) of 30 HBsAg-negative cirrhotics, and 7 (17%) of 42 HBsAg-positive and 15 (63%) of 24 HBsAg-negative patients with hepatocellular carcinoma (HCC). An outbreak of non-A, non-B hepatitis revealed 18% of 57 patients to be positive for anti-HCV, and in 29 patients with posttransfusion hepatitis prospectively followed, 7 (24%) developed anti-HCV. Thus, HCV infection appears to play a relatively minor role in HBsAg-positive liver disease in Taiwan but is strongly associated with HBsAg-negative chronic liver disease and HCC. The infection is extremely common in hemophiliacs and parenteral drug abusers.

Adult↗
PubMed1990

Intratumor injection of OK-432 for the treatment of small hepatocellular carcinoma.

Intratumor injection of OK-432, a biological response modifier, in the treatment of small HCC was studied in 7 inoperable patients. After evaluation with ultrasound (US), computed tomography (CT), angiography and US-guided biopsy, implantation of a steel coil in the tumor, intratumor injection was performed under US guidance. After completion of the treatment, liver biopsy and image studies were again done to evaluate the extent of tumor necrosis. One patient was alive and well without recurrence 19 months after treatment. Four had recurrent tumors at different site of the liver 4 months, 9 months, 9 months and 8 months later. Two died of progressive malignancy 3 months and 8 months later. In the 6 patients with elevated serum alpha-fetoprotein (AFP) levels, 4 had decreased AFP after treatment, and the 2 mortalities had steadily increased AFP. The most common side effects are fever and chills. Transient abdominal pain with elevated transaminase activities, cough with hemoptysis, and vomiting were seen in 1 case each. After treatment, the biopsy specimens showed total necrosis of HCC. Although the T4/T8 ratio of peripheral blood was increased as compared with that before treatment in 4 cases, peritumoral cytotoxic T lymphocyte and monocyte infiltration were seen in one specimen only, and another 7 examined specimens showed negative staining with monoclonal antibodies of T cells. We conclude that intratumor injection of OK-432 is an alternative treatment for small HCC in inoperable cases. The effectiveness may be due to the direct tumoricidal mechanism of OK-432.

Aged↗
PubMed1989

Biologic significance of the detection of HBsAg and HBcAg in liver and tumor from 204 HBsAg-positive patients with primary hepatocellular carcinoma.

Hepatitis B virus surface and core antigens (HBsAg, HBcAg) were examined in the resected primary hepatocellular carcinoma from 204 patients who had HBsAg in serum. Ninety patients had small (less than 5 cm) and 114 had large hepatocellular carcinoma (greater than 5 cm). HBsAg was detected in hepatocellular carcinoma in 65 cases (32%) and HBcAg in 30 cases (14.7%); hepatitis B virus antigens were more frequently detected in small (HBsAg in 42.2% and HBcAg in 20%) than in large hepatocellular carcinoma (HBsAg 23.7% and HBcAg 10.5%). These results suggest that replicative forms of hepatitis B virus DNA may exist in hepatocellular carcinoma more frequently than previously believed and that the malignant hepatocytes can support hepatitis B virus replication. A lymphocytic infiltration in hepatocellular carcinoma was more often observed in hepatocellular carcinoma expressing HBsAg (71%) or HBcAg (63%) than in hepatocellular carcinoma with no detectable HBsAg (26%) or HBcAg (37%), p less than 0.01. The reaction was mild in the majority (85%) of the cases. These findings suggest that hepatitis B virus antigen expression in hepatocellular carcinoma can provoke a local immune response. The most striking finding was that patients with hepatitis B virus antigens in small hepatocellular carcinoma had a 5-year survival rate (13%) lower than that (50%) of the antigen-negative patients (p less than 0.05). In contrast, patients with a marked local immune response in hepatocellular carcinoma, regardless of the viral antigen status, had significantly better 5-year survival rates (43%) than those with no or a mild lymphocytic reaction (18%). These findings indicate that a marked immune response in hepatocellular carcinoma is a favorable prognostic sign.(ABSTRACT TRUNCATED AT 250 WORDS)

Carcinoma, Hepatocellular↗
PubMed1989

Clonal origin of recurrent hepatocellular carcinomas.

Recurrence of hepatocellular carcinoma after treatment is frequent. To study the clonal origin of the recurrent tumors, we examined five pairs of hepatocellular carcinomas resected from individual hepatitis B surface antigen carriers. Using integrated hepatitis B virus DNA as a marker, tumor clonality was determined by Southern blot analysis. In 2 cases the second tumor contained the same integrated viral DNA as the first one. In the other 3 cases, the clonality of the second cancer differed. We conclude that recurrent hepatocellular carcinomas originate from the first tumor in some cases but represent de novo neoplasms in others.

Base Sequence↗
PubMed1988

Evolution of expression of hepatitis B surface and core antigens (HBsAg, HBcAg) in resected primary and recurrent hepatocellular carcinoma in HBsAg carriers in Taiwan. Correlation with local host immune response.

Studies were conducted on the evolution of hepatitis B virus (HBV) surface and core antigens (HBsAg and HBcAg) in the tumors of both primary and recurrent hepatocellular carcinoma (HCC) in 27 HBsAg carriers; these were followed for up to 8 years after the resection of the primary tumor. Twenty-seven primary and 34 recurrent tumors were included. HBV antigens were detected in the tumor of the primary HCC in ten cases (37%): six (22.2%) had both antigens (Group I) and four (14.8%) had HBsAg alone (Group II). The remaining 17 cases were negative for both antigens (Group III). Intrahepatic tumor recurrence occurred in 17 cases; both HBcAg and HBsAg were found in the recurrent HCC in four of five HBcAg-positive cases (Group I). In contrast, HBcAg was detected in none of the other 12 cases (Group II, 0 of one; Group III, 0 of 11), and HBsAg in only one (Group II, 0 of one; Group III, one of 11), P less than 0.03 and P less than 0.02, respectively. Groups I, II, and III had extrahepatic recurrence in two, four, and seven cases, respectively. HBcAg was detected in none, while HBsAg was found in only one case (7.7%). The frequent detection of both antigens in the primary HCC and even in the intrahepatic recurrences suggests that HBV replication in HCC may occur more commonly than previously perceived, especially in the small HCC. Failure to detect HBV antigens in the extrahepatic recurrences suggests that the switch-off of the viral gene expression, particularly the core gene, may be an event related to the extrahepatic growth of HCC. HBV antigen expression in HCC is associated with more evident lymphocyte infiltration; this local host immune response may in turn result in a negative selection and expansion of the antigen-negative HCC cell clones. This suggestion is in accord with the fact that HBV antigens, particularly HBcAg, are rarely detected in advanced HCC.

Carcinoma, Hepatocellular↗
PubMed1988

Tumor invasiveness and prognosis in resected hepatocellular carcinoma. Clinical and pathogenetic implications.

In order to elucidate the biologic behavior of hepatocellular carcinoma (HCC), the long-term prognostic impact of the pathologic features of 143 surgically resected HCC were studied. Seventy-four were smaller than 5 cm in diameter (small HCC), and 69 were larger (large HCC). This study confirmed that tumor size was an important but not the only determining prognostic factor in HCC. Although cirrhosis could cause hepatic failure, patient mortality was mainly attributable to tumor recurrence, which, in turn, was strongly correlated with the invasive nature of HCC. Tumor invasion to the liver and the intraportal spread were very frequent and particularly extensive in large HCC. In both small and large HCC the noninvasive groups not only had high 4-year actuarial survival (84.6% and 90%, respectively), but there was also no patient mortality from intrahepatic tumor recurrence. Therefore, it was concluded that invasiveness of an HCC is the most crucial factor in determining the long-term outcome for the patient, and that the clinical course of resected HCC is predictable in a great majority of the cases. In our small HCC series only 2.4% of HCC were regarded as having true multicentric origin. These findings suggest that the majority of HCC occur unicentrically, and that multiplicity and tumor recurrence result mostly from intrahepatic dissemination. In both small and large HCCs invasive tumors were accompanied by high patient mortality from tumor recurrence even when the tumor was small, indicating that intrahepatic spread may start very early during the growth of HCC.

Carcinoma, Hepatocellular↗
PubMed1988

Status of hepatitis B virus DNA in hepatocellular carcinoma: a study based on paired tumor and nontumor liver tissues.

To investigate the hepatitis B virus (HBV) DNA status in the liver when hepatocellular carcinoma (HCC) has developed, 35 paired nontumorous and tumorous liver tissues from 27 hepatitis B surface antigen (HBsAg)-seropositive and 8 HBsAg-negative patients with HCC were studied by Southern blot analysis. The hybridization patterns of HBV DNA were different in the nontumor and tumor parts in 26 (96.3%) of the 27 HBsAg-positive patients. In the nontumor parts, integration of HBV DNA into the host genome was significantly less when compared to the tumor parts (15/27 vs. 25/27, P less than 0.05), whereas free replicative viral forms were significantly more frequent (17/27 vs. 7/27). The integrated HBV DNA in the nontumor parts showed discrete band patterns in the majority of cases (13/15). Hepatitis B e antigen (HBeAg) was significantly associated with the expression of free replicative forms of HBV DNA in the tumor tissues. An integrated HBV DNA sequence was detected in the tumor part of one HBsAg-negative patient, but not in her nontumor counterpart. Our observation that discrete integrated HBV DNAs are present in the nontumor part, representing subclinical clonal expansion that precedes the development of HCC, suggests the risk of future new tumor growth from these cell clones.

Carcinoma, Hepatocellular↗
PubMed1987

Clearance of hepatitis B surface antigen (HBsAg) after surgical resection of hepatocellular carcinoma.

The serum HBsAg in 4 chronic HBsAg carrier patients with hepatocellular carcinoma (HCC) cleared within 4-38 months after surgical resection of their hepatic tumors. Two patients developed anti-HBs. During the follow-up period from 21 to 28 months after HBsAg clearance, none of the patients regained positive serum HBsAg. Two patients who had had tissue HBsAg present, exclusively in the tumor, showed quick HBsAg clearance after resection. The other 2 patients had a delayed HBsAg clearance. One had tissue HBsAg in both the tumor and nontumoral liver. Only 1 patient had tissue HBsAg in the liver, but not in the tumor. During the same period of observation of 323 chronic HBsAg carriers, who had a variety of histologically-verified chronic liver diseases and were followed for more than 6 months, only 1 cleared the antigen. The spontaneous HBsAg clearance in our HBsAg carriers (1/323) was significantly lower than that (4/64) of HBsAg-positive HCC patients with tumor resection, P less than 0.004. The mechanisms of HBsAg clearance in HCC patients after surgical resection of tumors are discussed.

Aged↗
PubMed1987

DNA clonal heterogeneity of hepatocellular carcinoma demonstrated by Feulgen-DNA analysis.

To demonstrate DNA clonal heterogeneity of hepatocellular carcinomas (HCC), the DNA histographic pattern of both primary HCCs and their recurrent or metastatic lesions were studied among 36 patients (33 men and 3 women). Thirty-six paired aspirations or imprints taken from primary, recurrent or metastatic lesions were stained, using the modified Feulgen method, and the DNA content was measured with a scanning microdensitometer at a wavelength of 550 nm. Paired aspirations or imprints taken from different parts of the same HCC were examined in 17 cases; the DNA distribution patterns were similar in 15 (88%) and differed in only two (12%). A similar DNA histogram was also shown among different tumors in 10 (71%) of 14 patients with multiple HCCs, with a DNA ploidy discrepancy in only four (29%). Two of two subcutaneous metastases and two of three recurrent tumors showed DNA distribution patterns similar to those in their primary HCCs. In summary, a DNA clonal heterogeneity of HCC was found in 19% (7/36). In contrast, the similar DNA histographic patterns found in most instances among different parts of the HCC and between the primary and recurrent or metastatic lesions suggest that HCC may derive from a single cell clone in the majority of cases.

Adult↗
PubMed1987

Small hepatocellular carcinoma: intratumor ethanol treatment using new needle and guidance systems.

Intratumor injection of absolute ethanol to treat small hepatocellular carcinoma sometimes results in incomplete necrosis of the tumor. Causes of this include inhomogeneous distribution of the ethanol and difficulty in identifying the tumor after previous ethanol injections. To solve these problems, the authors designed a multiple-side-hole needle for ethanol injection and implanted one or more small steel coils into the tumor before treatment to serve as a landmark. Six patients thus treated all showed adequate necrosis on follow-up computed tomography, biopsy, and angiography studies; initially elevated serum alpha-fetoprotein levels present in five patients were decreased. A resected surgical specimen obtained in one patient showed extensive necrosis of the tumor as well as of the surrounding healthy liver; only a small locus of equivocally viable cancer cells remained in the tumor margin.

Aged↗
PubMed1987

Intratumor injection of absolute ethanol under ultrasound guidance for the treatment of small hepatocellular carcinoma.

For the treatment of small hepatocellular carcinoma, intratumor injection of absolute ethanol under ultrasound guidance was performed in 27 tumors in 23 patients, with a tumor diameter of between 1.0 and 3.3 cm. The initially elevated serum alpha-fetoprotein levels in 15 patients decreased during treatment, with 13 returning to normal after this regimen. In the 6 patients who finally received surgical resection, 4 had complete necrosis of the tumor, while the other 2 had a small peripheral residual cancer nest. In the remaining non-resected 17 cases, follow-up CT, multiple biopsies and angiography revealed evidence of viable tumor in only 3 cases. After additional ethanol injections, these 3 cases were successfully treated. Inhomogeneous distribution of the injected ethanol and difficulty in identifying the tumor after previous injections accounted for the incomplete necrosis of the tumor. To cope with these problems, a steel coil was implanted in the tumor before treatment, and a needle with multiple side holes was used in the last 3 cases, with satisfactory results. Ethanol injection is promising and may even be curative in the treatment of small hepatocellular carcinoma.

Adult↗
PubMed1987

Metastasis of hepatocellular carcinoma to the proximal jejunum manifested by occult gastrointestinal bleeding.

A 31-yr-old man, who had received left hepatic lobectomy for a ruptured hepatocellular carcinoma 17 months previously, began to have elevation of serum alpha-fetoprotein and occult gastrointestinal bleeding. Abdominal computed tomography, angiography, ultrasonography, upper gastrointestinal panendoscopy, colon-fiberscopy and endoscopic retrograde cholangiopancreaticography failed to disclose any recurrent intrahepatic tumor or bleeder in the gastrointestinal tract. However, a barium meal study revealed an intussusception with a suspicious nodular lesion in the proximal jejunum as the leading edge, which, after laparotomy, was proven to be a metastatic hepatocellular carcinoma and the cause of the gastrointestinal bleeding. The serosal side of this lesion was free from cancer involvement and there was no peritoneal implantation or lymph node involvement. The metastasis is probably hematogenous. The extremely unusual location involved by hepatocellular carcinoma in this patient signifies the ubiquitous nature of metastasis in this cancer.

Adult↗
PubMed1987

Clinicopathologic studies of asymptomatic HBsAg carriers: with special emphasis on carriers older than 40 years.

To investigate the clinicopathologic features of asymptomatic carriers of hepatitis B surface antigen (HBsAg), liver biopsies were obtained in 140 carriers followed-up for more than 6 months. They included 47 older than 40 years and 75 with elevated SGPT values at least once during the follow-up period. Among the 93 carriers younger than 39 years, milder histologic changes than chronic persistent hepatitis (CPH) were seen in most of those with normal SGPT values, while more severe histologic changes (chronic lobular hepatitis, chronic active hepatitis and active cirrhosis) were found in 18 out of 50 with elevated SGPT values. In contrast, when the carriers were more than 40 years of age, the histologic liver changes became "bipolar", i.e., either very mild or quite severe, since among 47 subjects in this group, 37 (79%) had hepatic lesions milder than CPH, and the remaining 10 (21%) had cirrhosis. The positive rate of hepatitis B e antigen (HBeAg) was not significantly different among those with milder and those with more severe histologic changes in the younger group. However, that of the older carriers was significantly higher among those with liver cirrhosis (50% vs. 16.2%, p less than 0.05). The results imply that, in Taiwan where chronic HBsAg carriage usually occurs in early childhood, a poorer prognosis may exist in asymptomatic HBsAg carriers when HBeAg persists beyond the age of 40.

Adult↗
PubMed1986

Serum HBsAg, HBeAg, anti-HBe, and hepatitis B viral DNA in asymptomatic carriers in Taiwan.

Plasma samples from 89 asymptomatic hepatitis B surface antigen (HBsAg) positive volunteer blood donors were titrated for HBsAg by radioimmunoassay using the parallel line method. HBsAg titers ranged widely from 0.01 to 325 micrograms/ml. The titers correlated well with hepatitis B viral DNA (HBV DNA) and hepatitis B e antigen (HBeAg) in the serum. The HBsAg titers in 55 HBV DNA positive carriers were 90.7 +/- 61.7 micrograms/ml (Mean +/- SD) vs. 6.3 +/- 12.2 micrograms/ml in the 34 carriers without HBV DNA in the serum. The titers were 93.9 +/- 59.1 micrograms/ml in 56 carriers with HBeAg, 6.4 +/- 10.1 micrograms/ml in 24 anti-HBe-positive carriers, and 4.9 +/- 4.6 micrograms/ml in 9 HBeAg/anti-HBe-negative carriers. 50 (89.3%) of the 56 HBeAg-positive carriers had HBV DNA, in contrast to four (16.7%) of 24 anti-HBe-positive carriers. The study indicated that high-titered HBsAg carriers were much more likely to be infectious, and confirmed that HBeAg is a practical marker of infectivity. Absence of HBeAg, however, did not exclude infectivity in asymptomatic HBsAg carriers, inasmuch as one-sixth of the carriers had HBV DNA.

Adult↗
PubMed1986

Noninvasive diagnosis of advanced pancreatic cancer by real-time ultrasonography, carcinoembryonic antigen, and carbohydrate antigen 19-9.

One-hundred-forty patients with clinical impression of pancreatic cancer were examined prospectively with three noninvasive tests: real-time ultrasonography, determination of serum carcinoembryonic antigen (CEA), and carbohydrate antigen (CA 19-9). Among them, 24 (17.1%) patients were found to have pancreatic cancer. The sensitivity of ultrasonography, CEA, and CA 19-9 was 72.9%, 70.8%, and 83.3%, respectively; the specificity was 94.0%, 77.6%, and 90.5%, respectively, and the diagnostic accuracy was 91.4%, 76.4%, and 89.3%, respectively. The combination of ultrasonography and determination of serum CA 19-9 had better sensitivity (95.8%), comparable specificity (84.5%), and comparable diagnostic accuracy (86.4%) to any individual test alone or any other combination. It was suggested that combined use of real-time ultrasonography and determination of serum CA 19-9 provided excellent noninvasive screening for patients suspected of having pancreatic cancer.

Adult↗