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PubMed2006

Relationship between sleep-disordered breathing and lifestyle-related illnesses in subjects who have undergone health-screening.

OBJECTIVE: Simplified sleep polysomnography was performed in 207 adult men to examine the relationship between the frequency of sleep-disordered breathing (SDB) and lifestyle-related illness. METHODS: Each subject was checked for SDB using a simplified sleep polysomnograph (Auto-Set Portable; Teijin Limited, Tokyo, Japan). Apnea and hypopnea were detected with a nasal cannula type airflow sensor. Hypoxemia was checked with a percutaneous oxygen saturation (SpO2) monitor. We analyzed the relationships between SDB and body mass index (BMI) and hypertension, hyperlipidemia, liver dysfunction, fatty liver, and abnormal glucose metabolism. RESULTS: Fifty-nine subjects (29%) showed SDB with apnea hypopnea index (AHI) over 15 times/h. The frequency of obesity (BMI > or = 25), hypertension, hypercholesterolemia, fasting blood glucose level, and HbA1c were significantly higher in patients with SDB than in normal individuals (AHI < 5 times/h). The frequencies of hypertension, hyperlipidemia, and abnormal glucose metabolism were compared between the obesity-free normal AHI group and the SDB group, and only that of hypertension was significantly different between the two groups. CONCLUSIONS: The present study revealed a high frequency of SDB among Japanese individuals. The results also suggest that as SDB becomes severe, it becomes more closely linked to the onset of lifestyle-related illnesses, such as hypertension, hypercholesterolemia and abnormal glucose metabolism.

Adult↗
PubMed1999

[A case of pulmonary tuberculosis with acute renal failure caused by readministration of rifampicin].

We report a case of pulmonary tuberculosis with acute renal failure caused by readministration of Rifampicin (RFP). A 73 year-old man was admitted to a certain hospital complaining with dyspnea on exertion. As his sputum smear was positive for acid-fast bacilli, he was transferred to our hospital for the isolation and treatment. He was diagnosed as lung tuberculosis and was administrated RFP, Isoniazid (INH) and Ethambutol (EB). On the 20th day after the initiation of treatment, the administration of drugs were suspended, because of liver dysfunction. After recovery of liver dysfunction, we have readministered antituberculous drugs, starting with EB, then INH, and finally RFP. On the 22nd day after the readministration of RFP, acute renal failure was observed. All medications were suspended and we started treatment with hydration and furosemide. His renal function recovered after 7 weeks. Histopathological examination of the kidney revealed interstitial infiltration and tubular nephritis. According to the histopathological examination and the clinical course, we concluded acute renal failure was induced by the readministration of RFP. This case suggests that we have to pay attention to renal side effect of RFP in the course of readministration.

Acute Kidney Injury↗
PubMed2003

Hepatic encephalopathy.

Hepatic encephalopathy (HE) is a brain disorder caused by chronic liver failure, particularly in alcoholics with cirrhosis, which results in cognitive, psychiatric, and motor impairments. In these patients, the number of functional liver cells is reduced, and some blood is diverted around the liver before toxins are removed. As a result, toxins such as ammonia and manganese can accumulate in the blood and enter the brain, where they can damage nerve cells and supporting cells called astrocytes. Positron emission tomography analyses have determined that ammonia levels are elevated in the brains of HE patients; ammonia accumulation can alter the expression of various important brain genes. Magnetic resonance images show that manganese is deposited in a brain area called the globus pallidus; manganese deposits may be responsible for structural changes in the astrocytes that are characteristic of HE. Treatment of patients with HE involves measures to lower ammonia levels in the blood, medications to counteract ammonia's effects on brain cell function, devices to compensate for liver dysfunction, and liver transplantation.

Brain↗
PubMedDate not supplied

Prospective evaluation of abnormal liver function tests in pregnancy.

Abnormalities in liver function tests (LFT) during pregnancy are a commonly encountered problem often associated with serious consequences especially when it occurs in the third trimester. The spectrum of abnormal liver functions in pregnancy can be fairly wide and diagnostic work up often challenging. There is insufficient prospective data on the spectrum and outcome of liver disease in pregnant population from south India. This study was performed to assess the causes of deranged liver function in the pregnant population and also to prospectively determine the outcome of liver dysfunction in pregnancy. All abnormal LFT results observed in serum samples from pregnant patients attending the obstetric unit of our hospital from January 2003 to January 2005 were evaluated and prospectively followed throughout pregnancy. Laboratory investigations included coagulation profile, renal function tests, serology for viral markers (HBsAg, anti-HCV, IgM anti-HEV and IgM anti-HAV) and other relevant biochemical tests. In those with liver dysfunction in the third trimester the maternal and perinatal outcome was evaluated. A total of 125 patients were identified with abnormalities in LFT results during this period. The majority of causes were related to pregnancy specific conditions (57.6%). Most episodes of abnormal LFT occurred in the third trimester (59.2%). Hyperemesis gravidarum (55.8%) and viral hepatitis (47%) were the most common causes of abnormal LFT in the first and second trimesters respectively. HELLP (28.3%) and AFLP (14.8%) were the most common causes of abnormal LFT in the third trimester. There were no mAternal deaths due to liver dysfunction in the first or second trimester. Liver dysfunction in the third trimester (74 patients) was associated with serious consequences. DIC was the most common complication (20.2%). The overall and perinatal mortality was 20.2% and 24.6% respectively. AFLP and HELLP syndromes were associated with poor maternal and fetal outcome. We conclude that liver dysfunctions were directly related to pregnancy in the majority of patients especially in the third namely trimester. Incidence of the most serious conditions AFLP and HELLP syndromes is much greater than what has been reported and is often associated with a high maternal mortality and poor perinatal outcome.

Adult↗
PubMed2004

Clinical significance of serum IGF-I, IGF-II and IGFBP-3 in liver cirrhosis.

AIM: To investigate the relationship between insulin-like growth factor-I, -II (IGF-I and IGF-II), IGF-binding protein 3 (IGFBP-3) and Child-Pugh score in patients with liver cirrhosis, and to search for potential clinical markers of liver function. METHODS: Forty-four patients with advanced liver cirrhosis of viral origin were divided into 3 groups according to severity of cirrhosis (Child-Pugh score) and 38 healthy subjects served as controls. Serum levels of IGF-I, IGF-II and IGFBP-3 were measured by immunoradiometric assay. RESULTS: Serum IGF-I, IGF-II and IGFBP-3 levels were significantly lower in patients with cirrhosis than in controls, and serum concentrations of IGF-I, IGF-II and IGFBP-3 were associated with the severity of liver dysfunction, and dropped sharply during the progression of liver failure. Among these 3 parameters, serum IGF-II was the most sensitive and effective indicator for liver dysfunction. Concentrations of IGF-I <30 ng/mL, IGF-II <200 ng/mL and IGFBP-3 <6 ng/mL implied a negative prognosis for patients with liver cirrhosis. CONCLUSION: Serum IGF-I, IGF-II and IGFBP-3 may provide a new dimension in the assessment of liver dysfunction. Combined detection of serum IGF-I, IGF-II and IGFBP-3 with Child-Pugh score is more effective in predicting prognosis than Child-Pugh score alone.

Adult↗
PubMed1995

Postoperative liver allograft dysfunction: the use of quantitative duplex Doppler signal analysis in adult liver transplant patients.

40 patients after orthotopic liver transplantation were prospectively analysed by serial quantitative duplex Doppler signal analysis (DDSA) to quantify the abnormalities of Doppler waveform of the hepatic artery (HA), the portal vein (PV) and the hepatic vein (HV) under various conditions of graft dysfunction. Quantitative analysis of the HA, PV and HV was obtained before, during and after allograft dysfunction by different Doppler angle independent parameters. The results obtained later on were correlated with clinical and laboratory data, cytological and histological findings of liver core biopsy and quantitative DDSA data of healthy transplanted volunteers. The increase of the resistive index of Pourcelot calculated for the hepatic artery (HA-RI) was found to be significant in early graft reperfusion reaction (p < 0.01). No correlation was found between the HA-RI and acute allograft rejection. Different patterns of damping quantified by the damping index (DI = minimum velocity shift/maximum velocity shift) for the portal vein (PV-DI) and the hepatic vein (HV-DI) Doppler signal were observed under various conditions of allograft dysfunction. Acute rejection was identified by premature decrease of PV-DI and increase of HV-DI (p < 0.01) with a sensitivity of 75%, a specificity of 91%, a positive predictive value (ppv) of 75% and a negative predictive value (npv) of 91%. Chronic allograft rejection was not associated with an increase of HV-DI but only with a significant decrease of PV-DI (p < 0.01), with a sensitivity of 80%, a specificity of 95%, ppv of 95%, npv of 98%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1976

Kinin activation in the blood of patients with sepsis.

To determine whether or not kinin activation in the blood during severe infection with gram-negative bacteria may be related to hemodynamic abnormalities encountered, blood prekallikrein, kallikrein inhibitor and kinin values in 2l surgical patients with sepsis were compared with those in normotensive and hypotensive states. Because of reduced prekallikrein synthesis in patients with hepatic insufficiency, the normotensive and hypotensive groups were each subdivided according to the presence or absence of liver dysfunction, as indicated by elevated blood bilirubin, serum glutamic-oxalacetic transaminase or alkaline phosphatase levels. The mortality was zero in group 1, normotensive normal liver function; 80 per cent in group 2, hypotensive-normal liver function; 20 per cent in group 3, normotensive liver dysfunction, and 67 per cent in group 4, hypotensive liver dysfunction. Ultimately, the majority of deaths were due to respiratory failure. Although the blood prekallikrein level, was below normal in all groups and was significantly less in all patients with liver dysfunction, it was reduced proportionately in hypotensive patients to less than 30 per cent of the values noted in the two normotensive groups. This finding suggests prekallikrein consumption in the hypotensive groups to be the result of the process of activating kallikrein and bradykinin. This concept is supported by finding elevated kinin values, above 3 nanograms per milliliter of plasma, in only 28 per cent of those in group 1 and 12 per cent of those in group 3, while in the hypotensive patients, groups 2 and 4, the kinin level was elevated in 60 and 66 per cent, respectively.

Alkaline Phosphatase↗
PubMed2003

The impact of liver metastasis on mortality in patients initially diagnosed with locally advanced or resectable pancreatic cancer.

BACKGROUND: Liver metastases are frequent in pancreatic cancer, although their impact on patient mortality is still unclear. METHOD: The extent of liver metastasis (H-III [diffuse], H-II [moderate], H-I [limited], H-0) and the magnitude of liver dysfunction (lf-III [failure], lf-II [severe], lf-I [moderate], lf-0) were reviewed in 89 locally advanced and resectable pancreatic cancer patients in order to determine possible relationships with mortality and survival. RESULTS: The extent of liver metastasis (H-III, 18; H-II, 20; H-I, 12; H-0, 39) and the magnitude of liver dysfunction (lf-III, 12; lf-II, 8; lf-I, 11; lf-0, 58) were quite variable. Based on the aforementioned two categories, pancreatic cancer patients could be divided into four groups: (A) extensive liver metastasis affecting patient mortality, 14% (12/89); (B) liver metastases that do not cause severe liver dysfunction, 38% (34/89); (C) severe liver dysfunction, not associated with liver metastasis, 9% (8/89); (D) spared liver function, with no liver metastasis, 39% (35/89). The median survival period of H-III patients (195 d) was quite short compared with those of H-I (288 d) and H-0 (240 d) patients. CONCLUSION: Considering patients with locally advanced and resectable pancreatic cancer, the fraction of cases with diffuse liver metastases is relatively small. Moreover, only a minor proportion of pancreatic cancer patients die from hepatic failure as a direct result of liver metastasis.

Adult↗
PubMed2005

Change of components of the metabolic syndrome in a workers' health checkup after five years--relation with elevated liver enzymes, gene polymorphisms for ALDH 2, beta3-AR and lifestyle.

We previously reported that the prevalence of elevated alanine aminotransferase (ALT) increases with accumulation of metabolic syndrome components, and a greater degree of involvement of aldehyde dehydrogenase 2 (ALDH2) than beta3-adrenergic receptor gene (beta3-AR) polymorphisms. The present study was designed to clarify the effect of aging, lifestyle and the two gene polymorphisms on the relationship between 4 components of the metabolic syndrome (obesity, hypertension, dyslipidemia and impaired glucose tolerance) and elevated ALT values in a subset of 73 out of 148 male workers who were 35 years of age in the baseline study and 40 years old in the present study. Study subjects completed questionnaires about drinking and smoking habits, and underwent urinalysis, physical examination and peripheral blood tests, blood chemistry, electrocardiogram and chest X-rays each year as required by Japanese law. Information from the questionnaires and physical examinations, including liver function tests, were compared with previously reported ALDH2 and beta3-AR genotypes for the 73 workers. Of the 73 workers studied, 14 (19%) demonstrated decrease in metabolic syndrome components, 39 (53%) demonstrated no change, and 20 (27%) demonstrated an increase. Ten workers (14%) showed liver dysfunction at age 35 and 20 workers (27%) at age 40. Fourteen workers were newly diagnosed as having liver dysfunction at their 40-year checkup, thus being associated with the BMI and an active ALDH2 genotype. Accumulation of components of the metabolic syndrome were associated with the presence of liver dysfunction at 35 years. In conclusion, these findings indicate that ALDH2 genotyping as well as lifestyle habits may be important factors in causing metabolic syndrome with liver dysfunction.

Adult↗
PubMed1991

[Hepatitis C virus (HCV) infection in childhood].

We studied the prevalence of hepatitis C virus (HCV) infection in childhood by determining HCV antibody (Ortho Diagnostic Systems, USA). Among patients with post-transfusion non-A, non-B hepatitis, anti-HCV was positive in 8 (72.7%) out of 11 patients. On the other hand, only 1 (25.0%) out of 4 patients of the children with acute non-A, non-B hepatitis, and only 1 (20.0%) out of 5 with chronic non-A, non-B hepatitis patients were positive for anti-HCV. Among the infants with non-A, non-B hepatitis, anti-HCV was positive in 3 (7.5%) out of 40 infants. To demonstrate mother-to-infant transmission of HCV, we examined 7 infants born to 4 anti-HCV positive mothers for their GPT values and anti-HCV. Liver dysfunction occurred in all the infants but one. And 1 infant was positive for anti-HCV. This infant with positive anti-HCV and liver dysfunction was considered to be a case of mother-to-infant transmission of HCV. And in the infants with liver dysfunction and negative anti-HCV, it was suggested that liver dysfunction occurred in association with HCV infection.

Child↗
PubMed2004

Functional liver recovery parallels autologous gut salvage in short bowel syndrome.

BACKGROUND/PURPOSE: Parenteral nutrition (PN) is life saving in short bowel syndrome. However, long-term parenteral nutrition is frequently complicated by a syndrome of progressive cholestatic liver disease that is considered to be irreversible beyond the early stages of cholestasis, particularly in the presence of any degree of fibrosis in the liver. The purpose of this study was to examine apparent improvement in PN-associated liver dysfunction in a cohort of children with short bowel syndrome. METHODS: A retrospective case-record review of all patients managed within a dedicated Intestinal Rehabilitation Program (IRP) identified 13 patients with short bowel who had PN-associated liver dysfunction, defined for this purpose as hyperbilirubinemia or an abnormal liver biopsy. RESULTS: At referral, 12 of the 13 patients were exclusively on PN, and one was on 50% PN. At current follow-up, 3 patients have achieved complete enteral autonomy from PN, and 7 patients have had smaller decrements in PN requirements. Specific operative procedures to improve intestinal function were undertaken in 11 patients; 4 patients also underwent cholecystectomies with biliary irrigation at the time of intestinal reconstruction. The median highest bilirubin level in these 13 patients was 10.7 mg% (range, 3.2 to 24.5 mg%). Liver biopsy results indicated that 5 patients were cirrhotic, 3 had bridging fibrosis, and 4 had severe cholestasis or lesser degrees of fibrosis. Of 10 survivors in this series, 9 patients currently have a serum bilirubin less than 1 mg% with a median bilirubin in the group of 0.6 mg% (range, 0.3 to 6.4 mg%). Twelve of the 13 patients in this series were initially referred for liver-small bowel transplantation. CONCLUSIONS: This preliminary experience suggests that PN-dependent patients with advanced liver dysfunction in the setting of the short bowel syndrome may, in some instances, experience functional and biochemical liver recovery. The latter appears to parallel autologous gut salvage in most cases. As a corollary, the authors believe that even advanced degrees of liver dysfunction should not preclude attempts at autologous gut salvage in very carefully selected patients. Such a policy of "aggressive conservatism" may help avoid the need for liver/intestinal transplantation in some patients who appear to be not responding to PN.

Adolescent↗
PubMed2000

Gastro-intestinal complement activation during human liver transplantation: impact on postoperative liver function.

BACKGROUND: Liver transplantation elicits a systemic inflammatory response and eventually a multiple organ failure syndrome. Gastro-intestinal inflammatory activation with release of proinflammatory cytokines and complement activation may occur. This study evaluates gastro-intestinal complement activation and the association with postoperative parenchymatous liver cell injury and liver dysfunction. METHODS: In 17 patients undergoing liver transplantation, blood samples were collected from radial artery and portal vein for analysis of complement SC5b-9 and endotoxin concentration. Portal venous-arterial SC5b-9 plasma concentration gradients at 30 min after reperfusion were calculated. Outcome parameters included postoperative organ failure and serum concentrations of aspartate aminotransferase, alanine aminotransferase, bilirubin and factor II-VII-X. RESULTS: Patients with gastro-intestinal SC5b-9 release (n=7) had higher postoperative serum aspartate aminotransferase and alanine aminotransferase concentrations [49 (32-80) microkat/l vs 8 (6-14) microkat/l, P<0.01 and 33 (15-54) microkat/l vs 8 (4-23) microkat/l, P<0.04, respectively] and lower factor II-VII-X concentrations [46 (21-48)% vs 60 (47-69)%, P<0.02] compared to patients without gastro-intestinal SC5b-9 release (n=10). The ICU stay was prolonged in patients with gastro-intestinal complement release. There was no difference in number of organ failures and serum bilirubin concentration between the groups. The endotoxin concentration in arterial and portal vein blood was low and the association between endotoxaemia and complement activation was poor. CONCLUSION: Gastro-intestinal complement activation may contribute to postoperative parenchymatous liver cell injury and liver dysfunction in patients undergoing liver transplantation.

Adult↗
PubMed2005

Mycophenolate mofetil for renal dysfunction in liver transplant recipients on cyclosporine or tacrolimus: randomized, prospective, multicenter pilot study results.

BACKGROUND: Liver transplantation (LTX) recipients with renal dysfunction may benefit from mycophenolate mofetil (MMF) and reduction or discontinuation of nephrotoxic calcineurin inhibitors (CNI). The authors report the first randomized, multicenter pilot studies of this approach (one study for patients on cyclosporine [CsA] and one for those on tacrolimus [Tac]). METHODS: Patients 3 to 27 months post-LTX with greater than 20% reduced renal function since LTX, and creatinine 1.8 to 4.0 mg/dL, creatinine clearance 20 to 60 mL/min, or both, were randomized to discontinuation (group 1) or 50% reduction (group 2) of CNI dose, together with MMF 1.5 g administered twice daily and prednisone. Endpoints included measured glomerular filtration rate (GFR) 52 weeks after study entry and biopsy-proven rejection. RESULTS: In the CsA and Tac trials, 15 and 12 patients, respectively, completed the 52-week follow-up. In the CsA trial, the mean GFR at baseline and week 52 were 35.0 and 57.8 mL/min (>15% improvement, five of six; unchanged, one of six) for group 1 and 46.0 and 63.8 mL/min (>15% improvement, four of nine; unchanged, three of nine; >15% deterioration, two of nine) for group 2. In the Tac trial, GFRs were 55.4 and 56.0 mL/min (>15% improvement, two of five; unchanged, three of five) for group 1 and 46.7 and 60.2 mL/min (>15% improvement, four of seven; unchanged, three of seven) for group 2. Mild or moderate rejection occurred in 38% and 9% of patients in groups 1 and 2 of the CsA trial and in 14% of each group of the patients in the Tac trial. CONCLUSIONS: These pilot studies show that in LTX recipients with renal dysfunction, MMF allows CNI dose reduction or discontinuation, improving or stabilizing GFR in most patients.

Adult↗
PubMed2000

Activated protein C prevents multiple organ injury following extensive hepatectomy in cirrhotic rats.

BACKGROUND/AIMS: Extended hepatectomy for cirrhotic liver in patients with hepatocellular carcinoma often triggers posthepatectomy liver failure. It has been shown that the microcirculatory disturbance caused by microthrombus formation and sinusoidal endothelial cellular injury is one of the causes of post-hepatectomy liver dysfunction. We therefore investigated the effect of activated protein C (APC), a potent antithrombotic serine protease with anti-inflammatory effects, on posthepatectomy liver dysfunction and multiple organ injury in cirrhotic rats. METHODS/RESULTS: Dimethylnitrosamine-induced cirrhotic rats underwent 70% hepatectomy and received lipopolysaccharide (200 microg/kg) 48 h later to prepare a lethal posthepatectomy acute liver failure model. APC (1500 U/kg), given intravenously 15 min before and 1 h after endotoxin challenge, attenuated liver dysfunction and decreased serum tumor necrosis factor-alpha concentration. APC significantly improved the survival rate of rats at 12 h after endotoxin challenge. Histological examination revealed that APC treatment inhibited not only intrasinusoidal fibrin deposition and massive hepatocellular necrosis but also pulmonary injury and glomerular fibrin deposition. Immunohistochemically, expression of intercellular adhesion molecule-1 on sinusoidal cells and renal glomeruli was decreased in the APC-treated animals. CONCLUSIONS: APC administration prevented acute liver dysfunction and attenuated multiple organ injury following extended hepatectomy in cirrhotic rats, possibly via anticoagulant and anti-inflammatory effects.

Animals↗
PubMed1992

Interindividual variability in the concentrations of albumin and alpha-1-acid glycoprotein in patients with renal or liver disease, newborns and healthy subjects: implications for binding of drugs.

The concentrations of human plasma albumin (HPA) and alpha-1-acid glycoprotein (AAG) were measured in the serum obtained from 84 healthy subjects, 56 umbilical cords, 41 patients with renal failure, 65 patients maintained on chronic hemodialysis and 46 patients with liver cirrhosis. Severity of liver dysfunction was assessed with the use of Pugh et al. [1973] classification. Of the cirrhotic patients, 12, 22 and 12 patients were classified as mild, moderate and severe liver dysfunction, respectively. The coefficient of variation of AAG was greater than HPA in all groups of subjects, and the variability of HPA and AAG is increased in patients compared to healthy subjects. As the liver dysfunction progresses, HPA concentration decreases whereas, the average AAG concentration is not changed in mild, moderate and severe liver dysfunction. The coefficients of variation for HPA and AAG in moderate and severe liver disease is over twice those for healthy subjects. The concentration of HPA is normally distributed in all groups of subjects, with the exception of the cord serum. The frequency distribution of AAG was normal in healthy subjects whereas, it was asymmetric, being positively skewed, in newborn, in renal and liver patients. The wide interindividual variability and the not-normal frequency distribution of AAG in liver or renal patients make its mean of little value in defining a group. Neither HPA nor AAG correlated with the clearance of creatinine in renal patients. In liver disease, HPA and AAG did not correlate with GPT and GOT activities, prothrombinic activity and bilirubin concentration. HPA did not correlate with AAG in any group.

Adolescent↗
PubMed2004

Abnormal liver function tests following bone marrow transplantation: aetiology and role of liver biopsy.

INTRODUCTION: Liver dysfunction is common in bone marrow transplant recipients. Common causes are graft-versus-host disease, drugs, veno-occlusive disease, sepsis and iron overload. We studied the prevalence and aetiology of abnormal liver function tests following bone marrow transplantation and the role of liver biopsy. METHODS: All allogeneic and autologous bone marrow transplantations undertaken in our institution over a 2-year period were studied. Subsequent liver function tests, the use and timing of liver biopsy and the final cause of liver dysfunction were determined in each case. RESULTS: We studied 121 patients (58 allogeneic, 63 autologous). Abnormal liver function tests were found in 52% of bone marrow transplant recipients (72% allogeneic and 33% autologous; P = 0.015). The most common causes of liver dysfunction were graft-versus-host disease, drugs and iron overload in the allogeneic group, and drugs and sepsis in the autologous group. Nineteen patients (16%; 18 allogeneic) underwent liver biopsy. The majority of liver biopsies were carried out in the late post-transplant period to exclude or confirm graft-versus-host disease, although only one case was confirmed. Sixteen of the 19 patients who underwent biopsy had significant hepatic iron overload, but no biopsy revealed evidence of fibrosis or cirrhosis. CONCLUSION: Liver dysfunction following bone marrow transplantation is common and most diagnoses can be ascertained without resorting to liver biopsy. In our series, hepatic iron overload was the most common finding in those who underwent liver biopsy.

Adult↗
PubMed1988

[Clinical significance of sGOT elevation and thrombocytopenia in preeclampsia patients].

To assess the clinical significance of an elevated liver enzyme (sGOT) on the outcome of preeclamptic pregnancy, the charts of 145 preeclamptic/eclamptic patients who had sGOT determination during 7 days before and 2 days after delivery were reviewed. Of these, 60 patients exhibited a sGOT value above 30U/L (elevated sGOT group). This group was compared with the remaining 85 patients who showed a normal sGOT value related to clinical backgrounds and clinical outcome. The elevated sGOT group had a significantly low platelet count (16.4 +/- 8.4 vs. 21.4 +/- 6.7 X 10(4)/cumm, p less than 0.001) as well as a significantly high perinatal mortality rate (23.8 vs. 6.3%, p less than 0.01). There was a trend to a higher boy-to-girl ratio in the elevated sGOT group than in the normal sGOT group (1.10 vs. 0.83). In a group of 31 patients who were complicated with both elevated sGOT and thrombocytopenia, the perinatal mortality rate increased further to 42.4% and the boy-to-girl ratio was significantly higher than in the group of 66 patients who showed both a normal sGOt and normal platelet count (2.00 vs. 0.85, p less than 0.05). These results may indicate that 1) preeclamptic pregnancies complicated with liver dysfunction may tend to have a low platelet count; 2) liver dysfunction and thrombocytopenia are more likely to become complicated in preeclamptic pregnancies with a male fetus; 3) closer observations would be needed for preeclamptic pregnancy with liver dysfunction and thrombocytopenia.

Adult↗
PubMedDate not supplied

Subclinical liver disease in systemic lupus erythematosus.

In a detailed retrospective analysis of 81 patients with systemic lupus erythematosus (SLE), elevated serum "liver enzymes" were recorded in 45 (55%) subjects. In 9 cases, the cause was non-hepatic and in 14 cases liver dysfunction was probably drug induced. Aspirin was the most common offender. Of the remaining 22 patients, 3 had congested livers secondary to heart failure and 19 had no obvious cause for liver dysfunction other than SLE itself. Liver histology was reviewed in 7 of these 19 patients. An inflammatory infiltrate of the portal areas was seen in 5, fatty liver in one and chronic active hepatitis in one. The frequency of liver dysfunction and the associated portal inflammation support the view that subclinical liver disease is a concomitant feature of SLE.

Adolescent↗