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PubMed2001

Hepatic sarcoidosis with vanishing bile duct syndrome, cirrhosis, and portal phlebosclerosis. Report of an autopsy case.

A few cases of sarcoidosis are associated with progressive liver disease, with a wide variety of clinicopathologic features. Herein, we report an autopsy case (65-year-old man). During an examination for liver dysfunction, cirrhosis with cholestatic dysfunction and splenomegaly were found. Needle liver biopsy revealed cirrhosis with lymphocytic piecemeal necrosis, dense septal fibrosis, and ductopenia. In addition, noncaseating epithelioid granuloma was also seen in the periportal region. Ductal enzymes and immunoglobulin M (IgM) levels were elevated, although antimitochondrial antibodies were negative. Instead, angiotensin-converting enzyme was elevated. He died of pulmonary failure and lung cancer. The autopsy liver (1,220 g) showed multinodular cirrhosis with broad and dense septa that divided the parenchyma. Mild lymphoid cell infiltration was seen in the periportal region. About a half of the interlobular bile ducts were lost, and the remaining bile ducts showed prominent periductal fibrosis, resembling sclerosing cholangitis. Interestingly, a few interlobular bile ducts showed chronic nonsuppurative cholangitis with epithelioid granulomas. Intrahepatic portal veins showed luminal narrowing with prominent phlebosclerosis. Hepatobiliary pathologies that resemble primary biliary cirrhosis and primary sclerosing cholangitis and that are followed by vanishing bile duct syndrome, chronic active hepatitis-related cirrhosis, and intrahepatic portal venous phlebosclerosis occur in a single case of sarcoidosis.

Bile Ducts, Intrahepatic↗
PubMed1999

A high index of suspicion: the key to an early diagnosis of Wilson's disease in childhood.

BACKGROUND: To study the clinical features of Wilson's disease in childhood. METHODS: Retrospective review of the clinical, laboratory, and histologic features and prognosis of Wilson's disease in 26 Spanish children. RESULTS: The first medical visit, at age 9.8+/-3.4 years (range, 4-16 years), was prompted by liver dysfunction detected accidentally (61%), symptoms of liver disease (27%), family screening (8%), and extrapyramidal symptoms and personality changes (4%). There were laboratory data of hepatic failure in 27%. All copper metabolism test results (total serum copper, 24-hour urine excretion, serum ceruloplasmin) were abnormal in 62%, two in 27%, and one in 11%. All patients in whom extrahepatic involvement was found at diagnosis had severe liver disease. Histologic findings were portal fibrosis with steatosis (29%), cirrhosis (21%), portal fibrosis (17%), chronic active hepatitis (17%), and minimal changes or normality (17%). Penicillamine was administered to all but one patient. Four children underwent liver transplantation, three of them having received penicillamine for 12, 45, and 70 days. Three other patients recovered from liver failure after 1 year of treatment with penicillamine. After a follow-up of 4.5+/-3.3 years, all the children survived. Penicillamine caused severe toxicity in one patient. CONCLUSIONS: Wilson's disease in childhood is generally detected by maintaining a high suspicion of liver disease in patients who have no or nonspecific hepatic symptoms. Kayser-Fleischer ring is rare in childhood. Drug therapy is effective and well tolerated, even in some cases of hepatic insufficiency.

Adolescent↗
PubMed2000

Thyroid storm presenting as multiple organ dysfunction syndrome.

Thyroid storm is a rare disorder characterized by hypertension, hyperthermia, and multiple systems involvement. Early recognition and treatment of thyroid storm are essential in reducing morbidity and mortality from this disorder. We present the case of a patient with an atypical (normothermic, normotensive) presentation of thyroid storm, accompanied by multiple organ dysfunction syndrome, including lactic acidosis and liver dysfunction, both of which are very rare complications. This case highlights both the multiple organ systems that can be involved in thyroid storm and the importance of recognizing atypical presentations of thyroid storm.

Adult↗
PubMed1992

Multiple liver abscesses secondary to Yersinia enterocolitica.

A 37-year-old male, a poorly-controlled insulin-dependent diabetic patient, was admitted to our hospital with complaints of high fever and confusion. Laboratory data showed hyperglycemia, positive inflammatory reaction and liver dysfunction. Blood culture demonstrated Yersinia enterocolitica. Liver CT scan showed multiple low density areas. These data were consistent with a diagnosis of liver abscess secondary to Yersinia enterocolitica. He died of disseminated intravascular coagulation; subsequent autopsy confirmed the clinical diagnosis. Liver abscess secondary to Yersinia enterocolitica with septicemia is rare, but has been reported in compromised hosts. In the mechanism of this disease, the alimentary tract has been suggested to be the port of entry in most cases.

Adult↗
PubMed1991

The effect of pyruvate or dihydroxyacetone on parenterally induced liver lipid accumulation in the rat.

Orally fed pyruvate (pyr) and dihydroxyacetone (DHA) have been shown to decrease liver lipid accumulation in animal models. These compounds lessen the degree of fatty liver in ethanol-fed rats and in a genetic strain of hens predisposed to fatty liver. Total parenteral nutrition can result in liver dysfunction, including fatty infiltration of the liver. In this study, rats were assigned to either control, pyr, or DHA groups. All rats were fitted with jugular vein catheters, and following a 3-day recovery, were infused continuously for 7 days. The infusate provided adequate nutrition (including 7% kcal as fat) with 5% pyr or 5% DHA (g/liter) substituted for dextrose in the experimental groups. Plasma triglycerides were lower in the pyr groups relative to controls: 62.2 +/- 34.7 (SE) vs 96.8 +/- 44.3 mg/dl, though this was significant only at P less than 0.10. Neither pyr nor DHA decreased liver lipids. Pyr and DHA were administered intravenously in this study, and therefore passed through the heart and to peripheral tissues first. These compounds may need to be fed orally, passing via the portal system, to produce the liver lipid-lowering effects seen in other studies.

Animals↗
PubMed1999

[Clinical manifestations and histopathologic features of chronic liver disease with serum TT virus (TTV) DNA positive alone as measured by first generation primer sets].

To determine the clinical manifestations and histopathologic features of serum TTV DNA-positive chronic liver disease, we investigated eleven patients who showed serum TTV DNA alone, as detected by the polymerase chain reaction using first generation primer sets (RD primer series). Clinical manifestations were as follows: (1) biochemical abnormalities of the ALT-dominant and gamma-GTP-dominant types; (2) persistently elevated gamma-GTP despite normalization of ALT in gamma-GTP-dominant type patients; (3) association of TTV with pathogenesis of fatty liver or alcoholic liver dysfunction; and (4) response to liver-protective medicines. Histopathologic features were as follows: (1) inflammation-related cell infiltration scattered within the portal area, with distinguishable necroinflammation in the lobular region; (2) pathologic findings on biliary epithelium; (3) high incidence of steato-metamorphosis involvement; and (4) histologic characteristics undistinguishable from "viral" chronic hepatitis in some liver specimens.

Adult↗
PubMed1999

[Liver complications associated with short-term parenteral nutrition in children].

OBJECTIVE: Liver dysfunction (LD) with abnormalities in biochemical liver function tests is the most common metabolic complication of parenteral nutrition (PN). The aim of this study was to estimate the prevalence of LD in children receiving short-term PN and to identify risk factors. PATIENTS AND METHODS: Data were gathered retrospectively during a 2-year period. Ninety-four children older than 28 days received PN (mean age 5.4 +/- 5.1 years). PN related LD was defined as when serum levels of one or more of the following liver function tests were increased: ALT > or = 80 IU/L, GGT > or = 120 IU/L and total bilirubin > or = 1.8 mumol/L. Children with previous liver disease were excluded (n = 17), as well as those with incomplete data (n = 16). RESULTS: LD was present in 33 children (54%). The incidence rate was 5.8 cases/100 patient days of PN. It started 9.8 +/- 6.9 days after beginning PN. The nadir appeared during the second week of PN. The following variables did not appear to significantly influence the presence of PN: age, gender, nutritional status, PN caloric load or composition and underlying disease. Length of PN (9.6 +/- 4.4 vs 19.5 +/- 10.5 days; p < 0.001) and presence of sepsis (21% vs 55%, p = 0.014) were the only variables associated with LD. It was not necessary to discontinue PN because of LD in any case. CONCLUSIONS: Early LD is present in more than 50% of our children on PN. In preventing LD we should try to avoid infection and to reduce the time on PN.

Adolescent↗
PubMed2002

[Multi-organ failure in a young soldier: a clinical-pathological meeting].

This clinical-pathological conference took place at the Sourasky Medical Center, Tel Aviv, on February 21, 2001. We present the case of a young and previously healthy soldier who developed multi-organ failure with predominant liver dysfunction following exertional heatstroke. The patient's clinical course consisted of an early phase of transient encephalopathy, associated with hyperthermia, hypophosphatemia, mild laboratory indications of renal failure, rhabdomyolysis and consumption coagulopathy. Following an intermediate convalescing phase that lasted a single day the patient deteriorated into a catastrophic course with hemodynamic instability, fulminant hepatic failure, respiratory distress, kidney failure, rhabdomyolysis, coagulopathy and coma. He died 4 days later. In this article we elaborate on the association of heatstroke with multiple organ dysfunction syndrome in general, and fulminant liver failure in particular. The nature of hypophosphatemia and the possible role of additional injury from acetaminophen are discussed.

Acute Kidney Injury↗
PubMed1986

Absorption of cyclosporine A after oral dosing.

Variability in the absorption of CsA seems to contribute to the observed lack of correlation between the size of the oral dose and the trough concentration at steady state. Absorption is probably improved by thorough dispersion of the oral solution of CsA in the drink the patient prefers. Evidence for GI metabolism of CsA has only been gathered in animal experiments. The importance of bile for absorption of CsA into the portal blood is established. The bioavailability of CsA does not seem to be determined by the metabolism during the first passage through the liver. Enterohepatic recycling is likely for CsA metabolites and unlikely for unchanged CsA. A pharmacokinetic model that assumes zero-order absorption of CsA describes human data better than a model with first-order absorption. According to the zero-order model, CsA is absorbed only in the upper part of the small intestine by a mechanism that operates under saturation. Two independent findings in transplantation patients support this model. First, it was shown that small doses of CsA produce disproportionally high blood concentrations, probably due to a better bioavailability. Second, accelerated transit times in the intestine (diarrhea) lead to unexpectedly low blood concentrations, probably due to poor bioavailability. Further factors have been identified that cause low absorption of CsA: liver dysfunction and external bile drainage after liver transplantation. The influence of food on the absorption of CsA is still not determined conclusively, but it seems that giving CsA together with a standard breakfast results in higher blood concentrations. The observed increase in the bioavailability of CsA with time after transplantation could be caused by the attempt to steadily lower the dose.

Administration, Oral↗
PubMed1981

Hepatitis B virus-associated liver disease after renal transplantation.

A retrospective analysis of the first 200 recipients of renal transplants at the Johannesburg Hospital showed that 23 (11,5%) were chronic carriers of the hepatitis B virus (HBV) and a further 10 (5%) had previously been exposed to the virus as evidenced by detectable concentrations of antibody to the hepatitis B surface antigen in their serum. In no patient did graft function appear to suffer as a result of chronic HBV infection. However, 7 of the patients with hepatitis B surface antigenaemia had biochemical evidence of liver dysfunction. In 3 of these patients liver tissue was examined histologically; 2 had a macronodular cirrhosis and 1 chronic persistent hepatitis. One further patient developed acute fulminant B virus hepatitis and was the only one who died of liver failure in either group. Chronic infection with HBV may cause liver disease in renal transplant recipients, and strict techniques to limit the spread of the virus in renal transplant and dialysis units should continue to be enforced.

Carrier State↗
PubMed1995

[Hepatitis virus infection and bone marrow transplantation].

Hepatitis virus infection is a special problem in China and the role of Hepatitis virus infection in allogeneic bone marrow transplantation (BMT) is not well-defined. In this study, 106 BMT patients were included for analysis of the role of virus infection in allo-BMT. Seven and 65 of 106 patients were found to have HBV infection and HCV infection, respectively. Neither HBV infection and HCV infection interfered with the engraftment of bone marrow cells nor increased the rate of AGVHD, CGVHD, VOID. Neither HBV infection nor HCV infection prohibited allo-BMT. But Hepatitis virus infection can cause mild to moderate liver dysfunction, even death because of acute liver function failure, active prevention and treatment of hepatitis virus infection remains necessary. In this respect, rh-interferon is useful.

Adolescent↗
PubMed1994

Enucleation combined with hepatic vascular exclusion is a safe and effective alternative to hepatic resection for liver cell adenoma.

Liver cell adenomas are benign, rare tumors that occur primarily in women with a history of oral contraceptive use. Surgical treatment is recommended to reduce the risk of sudden, unpredictable hemorrhage or malignant transformation, but mortality rates of 5 to 8 per cent are reported for major hepatic resections. This report summarizes an experience of eight patients with liver cell adenoma treated by enucleation or resection, alone or combined with hepatic vascular exclusion (HVE). The latter technique, originally described in the mid-1960s, markedly reduces operative blood loss associated with hepatic resection. All eight patients were women of child-bearing age, and seven reported previous oral contraceptive use. The majority of patients were asymptomatic at the time of presentation. Six patients (75%) had a single adenoma and the remaining two had multiple lesions. HVE was used successfully in four patients with no perioperative mortality and reduced by nearly 50 per cent the intraoperative blood loss compared to conventional hepatic resection (1635 mL versus 3875 mL, respectively). Six evaluable patients were followed for an average of 65 months, with no evidence of liver dysfunction or adenoma recurrence. Enucleation of liver cell adenoma appears to be a safe alternative to formal hepatic resection and provides excellent long-term results. HVE markedly reduces operative blood loss, has no adverse effect on metabolic function, decreases the potential health risk associated with transfusion, and should be used whenever possible.

Adenoma, Liver Cell↗
PubMed1997

Course of asymptomatic liver involvement in sarcoidosis: role of therapy in selected cases.

AIM: Although granulomatous involvement of the liver with functional abnormalities is widely known, the course of these abnormalities is not clearly known. The study was designed to find out the incidence and course of asymptomatic liver function abnormalities. METHODS: From 1990-1995, during the five year period, 44 (35.2%) of 125 patients with sarcoidosis at LAC + USC Medical Center had liver involvement. Liver enzyme abnormalities aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (AP) were taken as criteria for liver involvement: 41 (93%) patients had elevated AP, 22 (50%) showed elevated ALT, and 24 (54.5%) had elevated AST. RESULTS: 25 of 44 patients received treatment; 12 (48%) showed improvement in liver enzymes and 13 (52%) remained unchanged. Ten (7%) of 13 patients, who did not receive any treatment, also improved. During the same period at USC University Hospital 18 (25%) of 72 had liver involvement. Twelve patients received treatment; 6 (50%) patients showed improvement in liver enzymes. One of 3 patients, who did not receive treatment, improved. 5 (41%) developed complications due to steroids. CONCLUSION: Liver involvement is common in African American patients with sarcoidosis. Social and economic status do not seem to influence the liver involvement. In men the age distribution has an early peak. The outcome of patients who receive treatment remains similar, as far as liver function is concerned, suggesting that most of the patients with liver involvement undergo natural remission. Unless the patient has progressive liver dysfunction, it is advisable to monitor liver enzymes periodically and obtain liver biopsies only if clinically indicated. In patients who need treatment, it is reasonable to try options other than steroids in view of severe corticosteroid related complications.

Adult↗
PubMed2003

Autonomic neuropathy in end-stage cirrhotic patients and evolution after liver transplantation.

Autonomic neuropathy (AN), which is frequently observed in cirrhosis patients, has been associated with a higher mortality. We have prospectively evaluated the prevalence of AN, its relationship with the degree of liver dysfunction and circulatory disturbances, and the evolution of AN after liver transplantation (LT) in 62 end-stage liver cirrhosis patients. AN was evaluated by seven cardiovascular tests assessing sympathetic or parasympathetic function before and 6 months after LT. Patients were classified as showing absent (A), early (E), or definite dysfunction (D). AN appeared in 67.7% of cases (E: 24.2%, D: 43.5%) without relation to liver disease etiology. Parasympathetic dysfunction was more prevalent than sympathetic dysfunction (59.7% vs. 20.9%). AN was significantly related to Child-Pugh score. Hyperdynamic circulation was more marked in the D than the A group as shown by a greater cardiac output (CO)(9 vs. 7.3 L/min) and a lower peripheral resistance (SVR)(666 vs. 866 dyn.s.cm(-5)). Moreover, AN scores significantly correlated with CO and SVR. Overall the prevalence of AN decreased 6 months after LT (67.7% vs 48%) due to a significant reduction in definite AN (43.5 vs. 14.8%; P<.05). AN improved in 70% of cases after LT. Sympathetic dysfunction remained in only one patient. We conclude that AN is frequent in liver transplant candidates; its severity is associated with the degree of liver failure. Systemic circulatory disturbances seem to correlate with the severity of AN. AN is clearly improved by LT. The evaluation of AN may contribute to a better selection of LT recipients.

Autonomic Nervous System Diseases↗
PubMed2026

Epigenetic regulation of fatty acid chain elongation in MAFLD and its implications in the liver-brain axis dysfunction.

Lipid metabolism plays a crucial role in cellular health and physiology by acting as an energy storehouse, cell membrane component, brain development and signaling molecules. Crucial steps to metabolize dietary fat take place within the hepatic tissue. Any abnormalities in the hepatic fatty metabolic pathways cause abnormal accumulation of lipid inside the liver, causing MAFLD, ranging from simple steatosis to more complex steatohepatitis and fibrosis. During high-fat-diet-induced hepatic inflammation, systemic proinflammatory cytokines disrupt the blood-brain barrier, resulting in neuroinflammation, cognitive impairment, brain damage and even neurodegeneration. Further, during this altered metabolic scenario, circulating metabolites pass through the impaired BBR and deregulate the epigenetic landscape of the central nervous system. Thus, it becomes crucial to understand the epi-metabolic crosstalk between two crucial organs of our body: the liver and the brain. Here in this chapter, we demonstrate the approach that we are using in our laboratory to study the epigenetic reprogramming in the context of metabolic gene expression in the liver, which is the causal for life style disorders like MAFLD. Remarkably, we intend to understand how liver dysfunction can have an implication in the brain function. Here, we discuss the concept of developing a diet-induced steatosis and steatohepatitis mouse model to understand the disease progression and its interconnection with brain physiology. Further, we also demonstrate 2D and 3D cell culture models to study the liver-brain cross-talk in greater molecular detail. Collectively, these approaches can provide a template for studying the role of epi-metabolic cross-talk in liver-guided brain dysfunction upon MAFLD.

Animals↗
PubMed2006

Vascular endothelial growth factor increases in serum and protects against the organ injuries in severe acute pancreatitis.

BACKGROUND: We have demonstrated that apoptosis was detected in liver and kidney cells in severe acute pancreatitis and that cellular injury because of apoptosis may be involved in the mechanism of multiple organ dysfunction syndrome. Vascular endothelial growth factor (VEGF) is a glycoprotein with potent angiogenic, mitogenic, and vascular permeability-enhancing activities specific for endothelial cells. It has been reported that VEGF is implicated in many diseases such as cancer and inflammation. METHODS: Serum VEGF concentrations were determined in patients with acute pancreatitis at the time of admission, and the relationships with severity, blood biochemical parameters on admission, organ dysfunction during the clinical course, and prognosis were analyzed. Moreover, to clarify the role of VEGF in acute pancreatitis, effects of VEGF were investigated in experimental severe acute pancreatitis. RESULTS: Serum VEGF levels were significantly elevated in patients with acute pancreatitis. Serum VEGF levels were not related to severity or prognosis. In male patients, among the various blood biochemical parameters, serum lactate dehydrogenase, and blood urea nitrogen levels were positively correlated with serum VEGF levels. Serum VEGF levels with organ dysfunction (liver and kidney) were higher than those without organ dysfunction. In rat experimental severe acute pancreatitis, serum VEGF levels were significantly elevated. Recombinant VEGF did not affect the lung water content, volume of ascitic fluid, hematocrit, or serum amylase, but improved the hepatic and renal dysfunctions. Apoptosis of liver and kidney was significantly inhibited by the administration of VEGF. CONCLUSIONS: These results suggest that VEGF is closely related to organ dysfunction in severe acute pancreatitis, and that VEGF may function as not a vascular permeability factor, but a protective factor via the anti-apoptotic effect against the organ injuries in this disease.

Acute Disease↗
PubMed1993

Clinicopathologic features of late hepatic dysfunction in orthotopic liver transplants.

Orthotopic liver transplantation (OLT) has been used with increasing frequency as a definitive treatment for end-stage liver disease. Whereas the spectrum of pathology in the early posttransplant period is well documented, the clinicopathologic features of patients with late hepatic dysfunction are less clearly defined. In a series of 100 OLTs we identified 12 patients with progressive liver dysfunction 4 months after transplantation. Four patients succumbed rapidly to fulminant hepatitis 4 to 6 months following transplantation, three of whom had recurrent hepatitis B infection. One patient lost two successive grafts owing to hepatitis C. Liver biopsies were diagnostic for hepatitis in all cases. The outcome of the remaining eight patients with late hepatic dysfunction was grim. Their clinical courses were notable for intractable and progressive cholestasis. Five patients died and two others required retransplantation. Only one patient responded to increased immunosuppression with FK506. Ductopenia was a common feature of liver biopsies in these cases, but severe ductopenia (vanishing bile duct syndrome) was seen in the liver biopsies of only four patients. In contrast, occlusive arteriopathy and secondary ischemic changes were ubiquitous. In summary, the liver biopsy is a useful adjunct in the diagnosis of late OLT dysfunction, particularly in distinguishing recurrent viral hepatitis from chronic graft rejection. Centrilobular ischemic changes occur frequently in chronic rejection, whereas ductopenia may be difficult to document consistently.

Adolescent↗
PubMed1997

Effect of calpain inhibitor I, an inhibitor of the proteolysis of I kappa B, on the circulatory failure and multiple organ dysfunction caused by endotoxin in the rat.

1. We compared the effects of calpain inhibitor I (inhibitor of the proteolysis of I kappa B and, hence, of the activation of nuclear factor kappa B (NF kappa B) and dexamethasone on (i) the circulatory failure, (ii) multiple organ dysfunction and (iii) induction of the inducible isoforms of nitric oxide (NO) synthase (iNOS) and cyclo-oxygenase (COX-2) in anaesthetized rats with endotoxic shock. 2. Injection of lipopolysaccharide (LPS, E. coli, 10 mg kg-1, i.v.) resulted in hypotension and a reduction of the pressor responses elicited by noradrenaline. This circulatory dysfunction was attenuated by pretreatment of LPS-rats with calpain inhibitor I (10 mg kg-1, i.v., 2 h before LPS) or dexamethasone (1 mg kg-1, i.v.). 3. Endotoxaemia also caused rises in the serum levels of (i) urea and creatinine (renal dysfunction), (ii) alanine aminotransferase (ALT), aspartate aminotransferase (AST) (hepatocellular injury), bilirubin and gamma-glutamyl transferase (gamma GT) (liver dysfunction), (iii) lipase (pancreatic injury) and (iv) lactate. Calpain inhibitor I and dexamethasone attenuated the liver injury, the pancreatic injury, the lactic acidosis as well as the hypoglycaemia caused by LPS. Dexamethasone, but not calpain inhibitor I, reduced the renal dysfunction caused by LPS. 4. Endotoxaemia for 6 h resulted in a substantial increase in iNOS and COX-2 protein and activity in lung and liver, which was attenuated in LPS-rats pretreated with calpain inhibitor I or dexamethasone. 5. Thus, calpain inhibitor I and dexamethasone attenuate (i) the circulatory failure, (ii) the multiple organ dysfunction (liver and pancreatic dysfunction/injury, lactic acidosis, hypoglycaemia), as well as (iii) the induction of iNOS and COX-2 protein and activity in rats with endotoxic shock. We propose that prevention of the activation of NF-kappa B in vivo may be useful in the therapy of circulatory shock or of disorders associated with local or systemic inflammation.

6-Ketoprostaglandin F1 alpha↗