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PubMedDate not supplied

Propafenone-induced liver injury.

OBJECTIVE: To describe propafenone-induced liver injury. DESIGN: Retrospective case report. SETTING: Referred care in a large tertiary care center. Laboratory tests were performed at the auxiliary site and the tertiary care center. PATIENT: A 71-year-old woman with atrial fibrillation developed elevations of greater than two times the upper limit of normal in alkaline phosphatase (ALK), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma glutamyltransferase (GGT) after initiation of propafenone therapy. INTERVENTIONS: Studies included serial measurements of ALK, ALT, AST, and GGT. RESULTS: The patient developed elevations of greater than two times the upper limit of normal in ALK, ALT, and AST, one month after initiating propafenone therapy. The propafenone dose was decreased from 900 to 675 mg/d and, ten days later, the ALK, ALT, and AST were decreased slightly, but still above the upper limit of normal. One month later, serum transaminases had returned to baseline, but propafenone therapy was discontinued because of recurrent atrial fibrillation, persistent elevation in ALK, and elevation in GGT. Two months after discontinuing propafenone, serum aminotransaminase and ALK concentrations had normalized and GGT had decreased and remained only slightly elevated. CONCLUSIONS: The occurrence of liver injury secondary to propafenone therapy is rare. Reported cases appear to be secondary to hepatocellular injury, cholestasis, or a combination of the two. In this case, the pattern demonstrated by elevations in liver enzymes may be classified as acute cholestatic liver injury. Because the reported incidence is 0.1-0.2 percent and there are no known fatalities secondary to propafenone liver injury, routine monitoring of liver function tests in all patients receiving propafenone cannot be recommended at this time. Baseline liver function tests prior to initiating propafenone therapy with follow-up laboratory studies one month later are recommended in patients with known liver dysfunction. If elevations are noted, a reduction in dose may result in lower liver enzyme concentrations, although discontinuation of therapy may be required in some cases.

Aged↗

PubMed2004

[Liver involvement in primary Sjogren's syndrome].

PURPOSE: To determine the prevalence of liver involvement in patients with primary Sjogren's syndrome (SS) and to evaluate the association of this complication with other extra-glandular manifestations and serologic markers. METHODS: We examined 155 Japanese patients (150 women and 5 men, mean age 66.6 years) who met the European Epidemiology Center Criteria for primary SS. Liver involvement was considered present when abnormal liver function tests (AST, ALT, ALP, GTP, or bilirubin) were detected more than three times. RESULTS: 20 patients (13%) had liver involvement including 2% with clinically overt liver disease. The causes of liver involvement were primary biliary cirrhosis (PBC) 6, autoimmune hepatitis (AIH) 2, hepatitis C virus (HCV) infection 2, concurrence of AIH and HCV infection 1, fatty liver 1. In 8 patients, the cause remained unclear. Of 6 patients complicated with PBC, four patients had PBC-specific antimitochondrial antibodies (AMA). Liver dysfunction was transient in two patients. Hepatocelluar carcinoma developed in a patient whose liver involvement was due to AIH and HCV. Patients with liver involvement were more likely to have cutaneous and neurological manifestations, when compared to SS without liver involvement. A positive antinuclear antibody, rheumatoid factor, and anticentromere antibody were also associated with liver involvement. Other autoantibodies did not correlate with the prevalence of liver involvement. CONCLUSION: Although symptomatic liver involvement is rare in SS patients, asymptomatic liver involvement is common. Clinicians must be aware of the possibility of liver involvement so that it can be treated as soon as possible.

Adult↗

PubMed1988

Allopurinol kinetics in humans as a means to assess liver function: evaluation of an allopurinol loading test.

A newly developed liver function test was performed on 18 apparently healthy individuals and 29 patients with liver disease. After intravenous injection of a low dose allopurinol (17.1 mumol/kg body mass), blood specimens were collected during 1 h. Plasma analyses of allopurinol and its metabolite oxipurinol were performed and the data were processed by means of a computer-based biodynamic model. This modelling approach makes it possible to estimate parameters, containing information about liver perfusion, hepatocyte membrane transport and hepatocyte cell mass. One parameter (kA31) showed complete discrimination between the reference sample group of healthy individuals and patients with severe liver dysfunction. In a reference sample group of patients with slightly to moderately reduced liver function, only a few patients (5/20) had a kA31 value over the decision limit. In this respect, the allopurinol loading test is superior to the conventional intravenous galactose tolerance test.

Adolescent↗

PubMed2000

[Indications for liver biopsy in liver tumors].

Significant progress has been made in the assessment of liver dysfunction by application of non-invasive physical and biochemical test procedures. However, liver biopsy remains an important tool for diagnosis, evaluation and prognosis of chronic liver diseases and hepatic neoplasms. Liver biopsy results are most useful when the biopsy is performed for well-defined indications following a complete work-up of the patient. In case of lesions highly suspicious for hepatocellular carcinoma, a biopsy should be performed in case surgical (curative) treatment is no option. Thus for the planning of a surgical intervention, biopsy of the tumor is not necessary. In case of concomitant liver cirrhosis, a biopsy taken from the non-neoplastic (cirrhotic) liver may help to assess the functional capacity or to clarify the etiology. Metastases of the liver with unknown primary tumor should be biopsied to obtain information of the primary tumor and the potential for cytostatic therapy. In case of hemangioma or focal nodular hyperplasia, diagnosed and confirmed by radiology or ultrasound, biopsy is usually not necessary. Concern has been expressed about seeding of the needle tract with malignant cells. Indeed, such instances have been recorded with various carcinomas, but they remain rare events and are seldom of clinical importance. With the use of needles with diameter < 1.3 mm to minimise also the risk of bleeding, the procedure is simple, safe and painless.

Biopsy, Needle↗

PubMedDate not supplied

Disappearance of hepatic encephalopathy and improvement of liver function after surgical treatment of portal-systemic shunt in a patient with liver cirrhosis.

Large portal-systemic shunts in cirrhotic patients often cause recurrent hepatic encephalopathy and might promote liver dysfunction because of the reduced portal blood flow. We report a case of liver cirrhosis in which hepatic encephalopathy disappeared and liver function improved together with an increase of hepatopetal portal blood flow and liver volume after shunt resection. A 70-year-old woman with liver cirrhosis was admitted because of recurrent disorientation. Serum ammonia levels ranged from 174 to 321 micrograms/dL. Computed tomography demonstrated an atrophic liver and a large shunt. Portography disclosed that this shunt originated from the superior mesenteric vein and flowed into the inferior vena cava, common iliac vein and ovarian vein. Portal blood flow was poor because of the deviation into this shunt. After the surgical resection of the shunt, ammonia levels were normalized and hepatic encephalopathy no longer occurred. Portography and computed tomography after surgery demonstrated that hepatopetal portal blood flow evidently improved and the liver volume increased (before 369; after 574 cm3). Two years after surgery, hepaplastin test and serum albumin level improved from 41 to 76% and from 2.7 to 3.4 g/dL, respectively. This case supports the effectiveness of shunt resection for hepatic encephalopathy and the deteriorated liver function in cirrhotic patients with large portal-systemic shunt.

Adult↗

PubMed1992

[Investigation of lipid peroxidation in regenerating rat liver].

The purpose of this study was to estimate the effects of lipid peroxidation in regenerating rat liver. Partial 70% hepatectomy was performed in rat according to Higgings and Anderson. EPC (alpha Toc: Ascorbic acid = 6:4, radical scavenger) was injected intravenously (5mg/kg weight) one hour before operation. Lipid peroxidation in regenerating liver reached a peak at 24 hours after operation. The administration of EPC markedly suppressed the increase of lipid peroxide in the plasma and remnant liver and that of GPT after hepatectomy, with subsequent good liver regeneration ratio. Moreover, the pretreatment with EPC remarkably elevated the activity of thymidine kinase (index of DAN synthesis). The EPC administration had not notable effects on the level of plasma ketone body ratio in animal but pathologically caused early advent of glycogen granule in the remnant liver tissue after partial hepatectomy, which reflected restoration of mitochondrial energy level. The results of the present study suggest that scavenger may be useful not only for impairment of liver dysfunction but also for recovery of mitochondrial energy level and DNA synthesis after liver resection.

Alanine Transaminase↗

PubMed1987

Vitamin K-dependent blood clotting changes in female rats treated with oestrogens.

Hexoestrol, diethylstilboestrol and ethinyloestradiol administered orally at a dose of 60 mg/kg/day to groups of five rats caused decreases in vitamin K-dependent blood clotting as measured by the Thrombotest reaction. These changes were self-limiting over a twenty-day study period and were not associated with external signs of bleeding. Pretreatment with testosterone and vitamin K1 did not significantly affect the clotting changes, but the antioestrogen clomiphene citrate exacerbated these, in several cases to lethal effect. Death was associated with haemorrhage. Hexoestrol-treated rats receiving clomiphene citrate in a sub-experiment did not show the increase in liver weight seen in animals given hexoestrol alone. In another sub-experiment, the level of clotting factor VII activity in the plasma of rats receiving hexoestrol at 60 mg/kg/day for four days was shown to be about half that of controls. There was probably no abnormal clotting inhibitor activity. It was deduced that the reduction in factor VII activity was more likely to be due to a decrease in synthesis as a result of liver dysfunction than changes in vitamin K availability. Clomiphene citrate may exacerbate the liver-dependent clotting disorders induced by oestrogens by preventing an adaptive increase in liver mass. It is concluded that the rat is a poor model species for investigating the blood clotting disorders seen in humans treated with oestrogens.

Administration, Oral↗

PubMed1994

[Percutaneous ethanol injection (PEI) for small hepatocellular carcinoma--study on its therapeutic effect and prognosis based on long-term observation].

Percutaneous ethanol injection (PEI) was performed on 183 tumors in 147 patients with small hepatocellular carcinoma (HCC), of no larger than 3 cm in size and less than three in number, during 9 years and 4 months between August 1983 and December 1992. The 1-, 3- and 5-year survival rates of all 147 patients calculated by the Kaplan-Meier method were 96.3%, 62.5% and 40.7% respectively. Multivariate analysis (Cox's proportional hazard model) demonstrated that the most significant factor contributing to the prognosis of the patients was the severity of liver dysfunction (clinical stage) before treatment. Recurrence was seen in different areas of the liver from the original lesion in 26.9% in one year and 61.5% in three years. Multivariate analysis demonstrated that the most significant factor contributing to the recurrence was the number of tumors before treatment. Regrowth of the original tumor occurred in two patients (1.4%). There was no serious complication due to PEI. To evaluate the therapeutic effect of PEI, contrast-enhanced CT with intravenous bolus injection was considered to be indispensable. We conclude that PEI can be indicated in most patients with small HCC and is also effective.

Adult↗

PubMed1996

Evaluating asymptomatic patients with abnormal liver function test results.

Asymptomatic patients with abnormal results on liver function test pose a diagnostic challenge. In general, determinations of routinely ordered tests of liver function are neither sensitive nor specific for liver disease. Fatty liver, alcohol-related liver damage and chronic viral hepatitis are the most common causes of abnormal liver function test results in asymptomatic patients. Causes of asymptomatic liver disease include hemochromatosis, Wilson's disease, drug toxicity, chronic autoimmune hepatitis, biliary cirrhosis, sclerosing cholangitis, alpha1-antitrypsin deficiency and sarcoidosis. The most efficient screening tests for liver damage are alanine transaminase, alkaline phosphatase and bilirubin. Repeat testing when results are abnormal, and use of ancillary tests, such as creatine phosphokinase or gamma-glutamyl-transferase, may confirm liver damage. Imaging studies help exclude biliary obstruction or neoplasm. Treatable illnesses should be ruled out. Three to six months of observation for progressive symptoms and liver dysfunction may follow. After the period of observation, further laboratory tests, a diagnostic liver biopsy and/or referral to gastroenterologist may be needed.

Aftercare↗

PubMed1998

[Inflammatory mediator and organ dysfunction syndrome].

Inflammatory mediators include endotoxin (ETX), cytokines (interleukins [ILs], tumor necrosis factors [TNFs], and interferons), eicosanoids (prostaglandins and thromboxanes), reactive oxygen species (O2-, NO, and ONOO-), complements (C3 and C4), and stress hormones (catecholamine, cortisol, vasopressin, and growth hormone). These mediators work to maintain homeostasis under stressful conditions through a complex chain reaction or cascade that results in transient tissue damage known as the inflammatory response. The inflammatory response is decreased by a negative feedback system, which consists not only of the self-inhibitory action of ETX, TNF-alpha, IL-1, and IL-8, but also of the production of antiinflammatory mediators such as IL-4, -10, -11, and -13, TGF-beta, IL-Ra, and sTNFR. If excessive stress or a second attack of stress results in a higher level of inflammation-producing mediators than of inflammation-inhibiting mediators, tissue destruction occurs due to activation and infiltration of inflammatory cells or necrosis due to endothelial injury is seen, followed by disruption of homeostasis, organ dysfunction, and organ failure (multiple organ dysfunction syndrome [MODS] or multiple organ failure [MOF] induced by SIRS). In experimental liver dysfunction after 95% hepatectomy, massive apoptosis of hepatocytes is induced by prolonged hypercytokinemia, ONOO- production, decreased mitochondrial membrane potential of hepatocytes, and decreased Bc12 levels. On the other hand, if the antiinflammatory response is greater than the inflammatory response (CARS) a compromised state and refractory infection are seen, followed by progressive, irreversible organ dysfunction (MODS or MOF induced by CARS).

Animals↗

PubMed1991

A retrospective analysis of therapy for acute graft-versus-host disease: secondary treatment.

We have reviewed results of secondary therapy in 427 patients with acute graft-versus-host disease (GVHD) who did not have a durable satisfactory response after primary treatment. At the beginning of secondary treatment, 320 patients (75%) had rash, 252 (59%) had liver dysfunction, and 228 (53%) had gut dysfunction. Secondary treatment was with glucocorticoids (n = 249), cyclosporine (n = 80), antithymocyte globulin (n = 114), or monoclonal antibody (n = 19) either singly (n = 390) or in combination (n = 37). Parameters of GVHD severity were recorded weekly, and responses were determined according to values at the initiation of tertiary treatment or, for patients without such treatment, using values on day 29 of secondary treatment or the last recorded values before death, whichever occurred first. Minimal criteria for improvement or deterioration were defined for each organ, but no attempt was made to define liver or gut outcome if another complication such as venocclusive disease or infectious enteritis was present. Improvement or resolution of GVHD in the respective organ was seen in 45% of patients with skin disease, 25% of patients with evaluable liver disease, and in 35% of patients with evaluable gut disease. Overall complete or partial responses were seen in 40% of patients. The highest complete response rate with secondary therapy (23%) was seen when GVHD recurred during the taper phase of primary glucocorticoid treatment and was managed by increasing the dose of glucocorticoids. Multivariate analyses were performed to identify patient, disease, or treatment factors associated with likelihood of complete response or overall improvement. A similar analysis was performed to identify covariates associated with time to treatment failure (defined as initiation of tertiary therapy or death not due to relapse of malignancy). Severe dysfunction in the skin, liver, and gut at the beginning of treatment was associated both with a decreased likelihood of complete response and an increased treatment failure rate. The times to treatment failure and the proportions of patients in various response categories were similar for primary and secondary treatment, suggesting that the potential efficacy of new immunosuppressive agents for treatment of acute GVHD can be assessed meaningfully in patients who have not responded adequately to initial therapy.

Adult↗

PubMed1995

Pharmacological correction of neonatal lethal hepatic dysfunction in a murine model of hereditary tyrosinaemia type I.

Hereditary tyrosinaemia type I, a severe autosomal recessive metabolic disease, affects the liver and kidneys and is caused by deficiency of fumarylacetoacetate hydrolase (FAH). Mice homozygous for a FAH gene disruption have a neonatal lethal phenotype caused by liver dysfunction and do not represent an adequate model of the human disease. Here we demonstrate that treatment of affected animals with 2-(2-nitro-4-trifluoro-methylbenzyol)-1,3-cyclohexanedione abolished neonatal lethality, corrected liver function and partially normalized the altered expression pattern of hepatic mRNAs. The prolonged lifespan of affected animals resulted in a phenotype analogous to human tyrosinaemia type I including hepatocellular carcinoma. The adult FAH-/- mouse will serve as useful model for studies of the pathophysiology and treatment of hereditary tyrosinaemia type I as well as hepatic cancer.

Amino Acid Metabolism, Inborn Errors↗

PubMed2026

Waist-to-height ratio as a practical indicator for screening pediatric metabolic dysfunction-associated steatotic liver disease in diverse populations and genetic backgrounds.

BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the leading chronic liver disease in children and adolescents; this parallels the global obesity epidemic. The contribution of genetic susceptibility to pediatric MASLD, and its interaction with anthropometric and biochemical indices used for non-invasive screening remains poorly understood. We aimed to evaluate waist-to-height ratio (WHtR) as a simple, equitable, and scalable tool for early identification of pediatric MASLD and relate this to genetic risk. METHODS: We combined school-based data from 1010 Chinese children with analyses of the Global Burden of Disease, the 1000 Genomes Project, and the US National Health and Nutrition Examination Survey (NHANES). Thirteen MASLD-related single-nucleotide polymorphisms (SNPs) were genotyped to construct a genetic risk score (GRS). We examined global epidemiological patterns, quantified inter-population allele divergence, and assessed how GRS modifies cutoffs and performance of nine anthropometric and biochemical indices. RESULTS: Genetic analysis revealed minimal frequency divergence across most ancestries (mean Fixation index < 0.05), except for the African ancestry where there was moderate divergence. Higher GRS were associated with lower cutoffs across indices. When GRS Z-score increased from -3 to 3, visceral adiposity index showed the sharpest changes (Z-score decreased from 1.5 to -1.8), while BFP (1.2 to 0.1) and WHtR (1.5 to 0.1) showed gradual change. Furthermore, incorporating GRS into the base anthropometric models yielded only marginal improvements in overall screening performance [area under the receiver operating characteristic curve (AUC) and Youden Index]. Validation in NHANES showed WHtR ≥ 0.48 retained high discrimination (AUC > 0.87) across most genetic variants. CONCLUSIONS: This study suggests that WHtR is a consistent and practical tool for screening pediatric patients with MASLD across diverse populations. While genetic variation may influence optimal thresholds, WHtR ≥ 0.48 appears broadly applicable, supporting its potential use as a frontline screening metric in diverse settings.

Humans↗

PubMed1992

Oral bile acid treatment and the patient with Zellweger syndrome.

The cerebrohepatorenal syndrome of Zellweger is a congenital syndrome of multiple manifestations, including hepatomegaly and liver dysfunction. Treatment is generally of a supportive nature, aimed at improving nutrition and growth, controlling the central nervous system symptoms and limiting progression of liver disease. Because the liver disease in Zellweger syndrome may be attributed to an overproduction and accumulation of cholestanoic acids, exacerbated by diminished primary bile acid synthesis, we hypothesized that primary bile acid administration would be beneficial in improving liver function by a mechanism involving down-regulation in the synthesis of these atypical bile acids. We report here the clinical and biochemical responses to primary bile acid administration in a 2-mo-old boy who was seen with the typical signs of Zellweger syndrome. Liver disease was evident from hepatomegaly and elevated serum liver enzymes and bilirubin. The diagnosis was supported by markedly elevated serum very long chain fatty acids and the bile acids dihydroxycholestanoic acid and trihydroxycholestanoic acid. Confirmation of the lack of peroxisomes was established by electron microscopy. When the patient was 6 mo old, the primary bile acids cholic acid and chenodeoxycholic acid, (100 mg each/day) were administered orally. A significant improvement in biochemical indices of liver function occurred with a normalization of the serum bilirubin and liver enzymes and a histological improvement in the extent of inflammation and bile duct proliferation and disappearance of cannalicular plugs. Serum and urinary cholestanoic acids showed a significant decrease within a few days. A striking and sustained increase in growth was observed after therapy, and an improvement in neurological symptoms was noted. In conclusion, this study indicates that primary bile acid therapy improves liver function and growth in the patient with peroxisomal dysfunction and should be considered in the supportive therapies for this condition.

Administration, Oral↗

PubMed2002

Selective bowel decontamination in elective liver transplantation: no improvement in endotoxaemia, initial graft function and post-operative morbidity.

Peri-operative endotoxaemia during liver transplantation has been linked to compromised graft function and infection. Selective decontamination of the digestive tract (SDD) could prevent endotoxaemia by eradicating Gram-negative bacteria from the intestine. In a randomized placebo controlled study we investigated the effects of endotoxaemia and the efficacy of SDD to prevent its occurrence. Thirty-one patients undergoing elective orthotopic liver transplantation received either SDD ( n=15) or placebo ( n=16), which was started at least 7 days before transplantation. Endotoxin levels were measured in blood peroperatively. Patients were scored daily for signs of liver dysfunction and infection. Endotoxaemia was neither associated with initial poor function nor any routine liver function test. Infections were more prominent in patients without endotoxaemia. SDD did not prevent endotoxaemia. Endotoxaemia does not affect post-operative graft function or the incidence of post-operative infections. SDD cannot prevent peri-operative endotoxaemia. Translocation of endotoxin may not be relevant in liver transplantation.

Adult↗

PubMed2004

PBC-AIH overlap syndrome with concomitant ITP and Hashimoto's disease with positivity for anti-centromere antibody.

We report a case of primary biliary cirrhosis (PBC)-autoimmune hepatitis (AIH) overlap syndrome with concurrent idiopathic thrombocytopenic purpura (ITP) and Hashimoto's disease with positivity for anticentromere antibody. The patient was a 64-year-old woman with symptoms of jaundice and general fatigue. About 30 years earlier, she had been diagnosed as having ITP and had undergone splenectomy. As part of her present history, she had exhibited liver dysfunction in 1995, during the follow-up of Hashimoto's disease, and a liver biopsy led to the diagnosis of PBC. In March 2000, she was admitted to hospital because of general fatigue and jaundice. Blood tests revealed: total protein (TP), 6.6 g/dl; gamma-globulin (glb), 35.9%; total bilirubin (T-bil), 9.41 mg/dl; direct bilirubin (D-bil), 7.52 mg/dl; aspartate aminotransferase (AST), 957 U/l; alanine aminotransferase (ALT), 651 U/l; alkaline phosphatase (ALP), 595 U/l; gamma-guanosine triphosphate (GTP), 129 U/l; IgG, 2620 mg/dl; IgM, 223 mg/dl; hepatitis B surface antigen (HBsAg), negative; anti-hepatitis C virus (HCV), negative; antinuclear antibody, positive; antimitchondrial antibody (AMA), negative (by the immunofluorescence [IF] method); and anti-pyruvate dehydrogenase complex (PDC)-E2 antibody, positive (by Western blotting). Anticentromere antibody (ACA), which is an alternative diagnostic marker for PBC, was detected in this patient. Prednisolone was administered after admission and liver function test results improved markedly. The liver biopsy in 1995 had revealed infiltration of lymphocytes and plasma cells in the portal areas with fibrous expansion and periportal necrosis. Destructive cholangitis was observed, as well as scattered epitheloid cell granulomas in some portal areas. Liver biopsy after the steroid treatment revealed alleviated necrotic inflammatory responses of hepatocytes, while the destructive cholangitis persisted. This is a very rare case of PBC-AIH overlap syndrome accompanied by ITP and Hashimoto's disease which provides a possible insight into the mechanisms and interplay of autoimmune diseases.

Antibodies↗

PubMed2003

Simultaneous operations for abdominal aortic aneurysm and liver cancer complicated by severe ischemic heart disease: report of a case.

We performed successful simultaneous operations for an abdominal aortic aneurysm (AAA) and liver cancer in a patient complicated by severe ischemic heart disease. A 59-year-old man with a history of liver dysfunction presented with acute epigastric pain. Abdominal computed tomography findings of ascites and a liver tumor indicated a diagnosis of ruptured hepatocellular carcinoma. He had a concomitant 65-mm AAA and a 48-mm right common iliac aneurysm. Elective surgery was scheduled because of his good general condition. Although triple-vessel disease was detected preoperatively, there were no graftable coronary arteries. The aneurysms were repaired first to utilize intra-aortic balloon pumping (IABP) during resection of the liver cancer, followed by left lateral segmentectomy. Perioperative hemodynamics were maintained by administering catecholamines and vasodilators, without the need for IABP. The patient was discharged on the 21st postoperative day without any complications, and no recurrence of liver cancer has been found in the 5 months since his operation.

Aortic Aneurysm, Abdominal↗

PubMed2002

A patient with small-cell carcinoma of the stomach with long survival after percutaneous microwave coagulating therapy (PMCT) for liver metastasis.

A 66-year-old man was admitted to our hospital with epigastralgia. Preoperative examinations revealed an 8.0 x 8.0-cm, Borrmann type 2 tumor in the posterior wall of the cardia, without distant metastases. Total gastrectomy with pancreato-splenectomy and regional lymph node dissection was performed curatively. Histologically, the tumor was composed mainly of small cells with hyperchromatic nuclei and scant cytoplasm, which showed positive staining for Grimelius, gamma-neuron-specific enolase (gamma-NSE), chromogranin A, and serotonin. About 10 months after the operation, a solitary tumor was revealed in S8 of the liver by abdominal computed tomography (CT), and it was histologically confirmed by needle biopsy to be a metastasis of the small-cell carcinoma from the stomach. Instead of hepatectomy, percutaneous microwave coagulating therapy (PMCT) was indicated, because of the patients' liver dysfunction (ICG R15, 39.9%); CT showed complete necrosis of the metastatic focus in the liver after the PMCT. Now, 33 months after the first detection of the liver metastasis (43 months after the gastrectomy), the patient is still alive without any growth of the liver metastasis. The 67 previously reported cases of small-cell carcinoma of the stomach in Japan, including ours, are also reviewed.

Aged↗