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PubMed2004

[A case of gastric cancer with extraordinary liver metastasis effectively treated by adjuvant chemotherapy].

This was an extraordinary liver metastasis case with complication when the patient, a 70-year-old male, was diagnosed with stomach cancer for the first time. However, the patient has been in remission and is a long-term survivor due to an active chemotherapy after the operation. His chief complaints were stomachache and a loss of weight. He was diagnosed with stomach cancer by endoscopy. During the surgery, the mass was found to be 3 QFB palpable caused from hepatomegaly. The liver dysfunction was revealed in the blood biochemistry inspection. The abdominal CT revealed that the stomach cancer had spread to the whole liver. Distal gastrectomy was performed on May 22, 1997. In pathological findings, the tumor was diagnosed as a well-differentiated adenocarcinoma. Final findings: M, type3, T3 (SE), N2, H3, P0, CY0, and Stage IVb. The 5-FU based chemotherapy was performed and a complete response was temporarily obtained. However, it has recurred one year later and two or more kinds of chemotherapy have continued. He is alive for more than 7 years and comes to our hospital as an outpatient.

Adenocarcinoma↗
PubMed1991

Plasma glucagon concentration in cirrhosis is related to liver function but not to portal-systemic shunting, systemic vascular resistance, or urinary sodium excretion.

We tested the hypothesis that increased plasma glucagon concentration resulting from portal-systemic shunting or liver dysfunction causes arterial vasodilation and thereby stimulates sodium retention in cirrhosis. Twenty-seven studies were performed in patients with alcoholic liver disease, 11 of whom had ascites. Liver function was quantitated as the elimination rate of antipyrine, caffeine, and stable isotopes of cholic acid administered both orally (2,2,4,4-2H) and intravenously (24-13C). Portal-systemic shunt fraction was calculated as the ratio of the intravenous and oral clearances of the isotopes of cholic acid. Cardiac output was measured by using Doppler echocardiography. Plasma glucagon concentration was increased in patients with ascites when compared with that in patients without ascites (474 +/- 180 pg/ml vs 245 +/- 120 pg/ml, p = 0.0007) but was unrelated to urinary sodium excretion, heart rate, mean arterial pressure, cardiac output, and systemic vascular resistance (r = -0.48, 0.35, -0.13, 0.18, and 0.22, respectively). Plasma glucagon concentration correlated with the half-lives of all model compounds (r = 0.58, p = 0.002; r = 0.62, p = 0.0008; r = 0.62, p = 0.001; and r = 0.64, p = 0.0005; for caffeine, antipyrine, oral and intravenous cholic acid, respectively) but not with shunt fraction (r = 0.14). Increased plasma glucagon concentration in cirrhosis is probably a result of diminished hepatic clearance. However, increased plasma concentration of glucagon does not appear to cause a hyperdynamic circulatory state or sodium retention.

Glucagon↗
PubMed1991

Preoperative evaluation of the patient with liver disease.

Patients with underlying liver disease have an increased surgical risk. Prediction of surgical risk is based on the degree of liver dysfunction, the type of surgery, and the preoperative clinical status of the patient. The medical consultant must determine the type of liver disease (acute or chronic) and the degree of impairment of liver function (based on physical examination and laboratory data). Any abnormalities should be corrected prior to surgery. Elective surgery should be postponed in patients with decompensated cirrhosis (class B and C) and acute hepatitis until the patient improves. The consultant internist's care of the patient should continue during the early postoperative course to monitor any deterioration in liver function.

Anesthesia↗
PubMed1988

Acute rhabdomyolysis associated with cocaine intoxication.

Because an increasing number of patients were arriving at our emergency room with cocaine intoxication and rhabdomyolysis, we reviewed our experience with such patients. We identified 39 patients seen at our institution over an eight-year period with acute rhabdomyolysis after cocaine use. The patients' mean creatine kinase level was 12,187 U per liter (range, 1756 to 85,000). Thirteen of the 39 patients (33 percent) had acute renal failure; 6 of them died. In comparison to the patients with normal renal function, those with renal failure were more often admitted with profound hypotension (46 vs. 4 percent; P less than 0.001), hyperpyrexia (69 vs. 15 percent; P less than 0.001), and markedly elevated serum creatine kinase levels (mean, 28,084 vs. 7931 U per liter; P less than 0.01). Disseminated intravascular coagulation developed in seven patients with renal failure. All six deaths were in this group. Severe hepatic dysfunction was found in 11 patients with renal failure. We conclude that cocaine intoxication can cause acute rhabdomyolysis with acute renal failure, severe liver dysfunction, and disseminated intravascular coagulation and that the mortality rate among patients with this syndrome is high.

Acute Disease↗
PubMed1993

Diagnosis of hepatic allograft rejection: role of liver biopsy.

The role of the liver biopsy for establishing a diagnosis of liver allograft rejection was investigated by examining under code 151 liver biopsies from 32 recipients and correlating the results with the clinical diagnosis determined by chart review. One-hundred-and-four biopsies were obtained to evaluate the cause of liver dysfunction and 47 were performed on a weekly protocol basis independent of the clinical status. A diagnosis of "definite histologic rejection" was made if a biopsy contained portal triaditis, bile duct injury, and endothelialitis, while biopsies were said to be suspicious for rejection if portal triaditis and bile duct injury were evident. A diagnosis of rejection using clinical and biochemical findings and response to therapy was made in association with 37 biopsies, of which 16 had definite histologic rejection and 13 were suspicious for rejection. Of the 114 biopsies performed in patients without clinical rejection, 71 had histology suspicious for rejection. Thus, biopsy was sensitive for the detection of rejection (78%), but was not very specific (33%). The positive predictive value was low (28%), while the negative predictive value was high (83%). These results indicate that liver biopsy is useful to evaluate graft dysfunction, to exclude rejection, to confirm clinically suspected rejection, and to diagnose other problems that can affect allograft function. Protocol biopsies appear to have little value.

Adolescent↗
PubMed1999

Hepatitis C virus infection and bone marrow transplantation: a cohort study with 10-year follow-up.

Before the introduction of routine blood donor screening in 1991, marrow transplant recipients were at significant transfusion-associated risk for infection with hepatitis C virus (HCV). We followed a cohort of 355 patients undergoing transplant in Seattle during 1987 to 1988 to determine (1) the impact of pretransplant HCV infection on the occurrence and severity of venocclusive disease (VOD); (2) the impact of HCV infection on liver dysfunction, other than VOD, occurring between 21 and 60 days after transplantation; and (3) the natural history of post-transplant HCV liver disease with a 10-year follow-up. HCV-RNA status was determined on serum stored before transplant and at day 100 post-transplant. Sixty-two (17%) patients were HCV-RNA positive before transplant, and 113 (32%) were HCV-RNA positive by day 100 post-transplant (or before death). Severe VOD developed in 22 of 46 (48%) evaluable patients with pretransplant HCV infection and in 150 of 229 (14%) evaluable patients without HCV (P <.0001). In multivariable analysis of risk factors for developing VOD, pretransplant HCV infection associated with elevated serum aspartate transaminase (AST) levels predicted the development of severe VOD (relative risk, 9.6; P =.0001). The presence of HCV with normal AST levels before transplant was not a risk factor for severe VOD. Between 21 and 60 days after transplant, HCV-RNA positive-patients had higher AST levels (median 101 U/L), but similar alkaline phosphatase and total bilirubin levels compared with HCV-negative patients, suggesting that cholestatic liver disease (particularly graft-versus-host disease [GVHD]) was not related to HCV infection. An acute flare of hepatitis (AST >10 times the upper limit of normal) developed at a mean of 136 +/- 58 days in 31% of HCV-positive patients; no patients developed fulminant hepatitis. Between 5 and 10 years after transplant, 57% of HCV-positive and 6% of HCV-negative patients had mild to moderate elevations of AST (P <. 0001), but HCV infection was not associated with excess mortality between 3 and 10 years after bone marrow transplantation. In summary, HCV infection with elevated AST levels is a significant risk factor for severe VOD after marrow transplant. However, the decision to proceed to transplantation in HCV-positive patients must balance the absolute risk of death from VOD against the risks of the underlying disease. In long-term survivors, HCV infection is not associated with excess mortality over 10 years of follow-up.

Adult↗
PubMed1989

Hereditary tyrosinemia type I (chronic form): pathologic findings in the liver.

Hereditary tyrosinemia type I presents with either acute hepatic failure in the neonatal period or later in infancy with progressive liver dysfunction secondary to cirrhosis. The inevitably fatal outcome in those children with the chronic form has been transformed with the advent of liver transplantation. Native livers from five children who received allografts were studied pathologically and compared with earlier hepatic biopsies in two of these patients that had been performed several years before transplantation. Our findings support the conclusion that a sequence of morphologic changes from the initial micronodular cirrhosis through an intermediate mixed cirrhotic pattern to macronodular cirrhosis occurs. The micronodular phase is transitory, over a period of only a few months, since mixed micronodular macronodular cirrhosis was already present in the livers of children who received transplants by 11 months of age. Focal hepatocellular dysplasia was present in one of the livers with mixed cirrhosis but was not identified in the other two cases. Macronodular cirrhosis accompanied two cases of hepatocellular carcinoma in this study. In order to preclude the latter complication, liver replacement is necessary before the age of 2 years.

Adolescent↗
PubMed1998

Chronic liver injury promotes hepatocarcinogenesis of the LEC rat.

The Long-Evans rat with a cinnamon-like color (LEC) is a mutant rat that spontaneously suffers from chronic liver injury and subsequent hepatocellular carcinoma (HCC) caused by abnormal copper accumulation in the liver. We attempted to elucidate the role of prolonged liver cell injury on LEC rat hepatocarcinogenesis using a copper-deficient diet (CuDD) to inhibit the occurrence of consequent liver injury. The animals were fed the CuDD from the age of 4 weeks until being killed at the age of 10 months. Diethylnitrosamine (DEN) was administered at the age of 8 weeks. Groups fed a basal diet (BD) with or without the administration of DEN were also assigned as control groups. The animals fed the BD manifested liver injury, while those fed the CuDD did not show liver dysfunction until death. The number and volume of glutathione S-transferase placental form (GST-P)-positive preneoplastic lesions in the liver, which were calculated from the data on two-dimensional planes, were examined to clarify the promotive effect of chronic liver injury on the development of HCC. Regarding the size of the lesions, which indicated the intensity of the promotive effect, the lesions in the livers of rats fed the BD with DEN were much larger than those of rats fed the CuDD with DEN. Feeding the LEC rats with CuDD completely suppressed the manifestation of liver injury, and it was clearly shown that prolonged liver injury had a promotive effect on the LEC rat hepatocarcinogenic process.

Alanine Transaminase↗
PubMedDate not supplied

Qualitative evaluation of chronic diffuse liver disease by STIR MRI.

OBJECTIVE: The purpose of our study was to characterize the relationship between signal intensity on STIR MRI, histology, and liver function. MATERIALS AND METHODS: MRI was performed in 39 patients with chronic liver diseases [chronic persistent hepatitis (CPH), chronic active hepatitis (CAH), liver cirrhosis (LC)] and 11 patients without liver dysfunction (normal). RESULTS: On STIR images, very low signal intensities compared with those of the spleen were seen in all 11 normal livers (100%), and brighter intensities were seen in chronic diffuse liver diseases (10 patients with CPH, 11 patients with CAH, and 18 patients with LC) (100%). The higher the signal grade on STIR images (moderate, marked), the more advanced was the chronic diffuse liver disease (p < 0.02). The levels of serum glutamic-oxaloacetic and glutamic-pyruvic transaminase increased in parallel with increasing signal intensity on STIR images (both p < 0.01). CONCLUSION: We found that the signal intensity of liver on STIR images appeared to be associated with the degree of histologic and/or clinical severity in patients with chronic liver disease.

Adult↗
PubMed2001

Congestion of right liver graft in living donor liver transplantation.

BACKGROUND: Left liver graft from a small donor will not meet the metabolic demands of a larger adult recipient. One solution to this problem is to use a right liver graft without a middle hepatic vein (MHV). However, the need for drainage from the MHV tributaries has not yet been described. METHODS: Five right liver grafts without a MHV were transplanted in patients including two hepatitis B virus-cirrhosis, two fulminant hepatic failure and one secondary biliary cirrhosis. The graft weight ranged from 650 to 1,000 g, corresponding to 48 to 83% of the standard liver volume of the recipients. RESULTS: Two of five recipients were complicated with severe congestion of the right median sector immediately after reperfusion, followed by prolonged massive ascites and severe liver dysfunction. One of the patients died of sepsis with progressive hepatic dysfunction 20 days after the operation. CONCLUSIONS: Preservation and reconstruction of the MHV tributaries is recommended to prevent congestion of the right liver graft without MHV.

Body Weight↗
PubMed1995

Increased serum IgE in alcohol abusers.

BACKGROUND: It has been reported that total serum IgE is increased in patients with alcoholic cirrhosis, but it is not clear if this fact is related to alcoholic liver disease or to alcohol intake. OBJECTIVE: To measure serum IgE in a group of chronic alcoholics with different stages of liver injury in order to elucidate if IgE increase in related to alcoholic liver damage. PATIENTS AND METHODS: Total serum IgE was determined by enzyme immunoassay in 186 chronic alcoholic patients (137 male/49 female) and 101 healthy controls. Patients and controls with known reasons for IgE elevation were excluded. Among alcoholic patients, 24 had fatty liver, 28 hepatic fibrosis, 29 alcoholic hepatitis, and 67 liver cirrhosis (38 patients were not evaluable concerning liver injury). RESULTS: Total serum IgE was found to be increased in alcoholics (median 154.5 IU/mL, range 1-7329 IU/mL) with respect to healthy controls (median 20 IU/mL, range < 1-1417 IU/mL) (P < 0.001). IgE increase was moderate (180-1000 IU/mL) in 60 alcoholics (32.3%) and marked ( > 1000 IU/mL) in 27 (14.5%). Male alcoholics had higher IgE levels than females (median 191 IU/mL and range 1-7329 IU/mL vs 105 IU/mL and range 2-2189 IU/mL) ( P = 0.009). On logistic regression analysis, alcoholism, male sex and younger age (but not smoking) were independently associated with higher IgE levels. No clear relationship was noted between serum IgE and severity of alcoholic liver disease. Thus, no correlation was observed between IgE and parameters of liver function (serum bilirubin, albumin or prothrombin index). Likewise, IgE concentrations were not significantly different in patients with liver cirrhosis with respect to patients with less severe liver disease. Serum IgE was increased ( > 180 IU/mL) in 47.8% of cirrhotics and in 44% of patients without liver cirrhosis. In contrast, other immunoglobulins (IgG, IgA and IgM) were significantly correlated with liver dysfunction. CONCLUSION: Chronic alcoholism should be considered as a cause of increased total serum IgE, regardless of the severity of the underlying liver disease.

Adolescent↗
PubMed2002

Rapidly progressive fibrosing cholestatic hepatitis--hepatitis C virus in HIV coinfection.

Fibrosing cholestatic hepatitis (FCH) is a severe and progressive form of liver dysfunction seen in organ transplant recipients infected with hepatitis B virus or hepatitis C virus (HCV) and has been attributed to cytopathic liver injury. To date, no case of FCH due to HCV has been reported in HIV-positive individuals. We describe two cases of HCV-induced FCH in two patients coinfected with HIV, culminating in rapidly progressive liver failure and death. Histological features and progression in both cases were not consistent with drug effect or obstruction. Late institution of interferon-based therapy was ultimately unsuccessful. The HCV RNA was not markedly elevated in these cases, suggesting that the cytopathic effect of HCV in these patients was not simply a consequence of viral load. FCH may in part explain the accelerated development of cirrhosis previously observed among coinfected patients. Clinicians should remain vigilant for FCH in the HIV/HCV population and consider antiviral treatment in this setting.

Adult↗
PubMed1985

Conjugated bile acids in serum and secretions in response to cholecystokinin/secretin stimulation in children with cystic fibrosis.

More than 80% of patients with cystic fibrosis have poor pancreatic function, and have large daily faecal bile acid losses. This has been postulated to lower luminal bile acid concentrations and adversely affect fat absorption. We studied, for the first time, quantitative individual conjugated duodenal bile acid secretion rates into the duodenum during cholecystokinin/secretin infusion in 55 cystic fibrosis patients and six controls, using a quantitative non-absorbable marker technique. We were able to show adequate duodenal total bile acid concentrations and normal secretion rates in these children. The bile acid secretion pattern in cystic fibrosis patients showed a marked increase in bile acid concentration during cholecystokinin/secretin infusion, to levels which were above the critical micellar concentration indicating that the gall bladder is a functional organ in this disease. The subsequent fall in secretion rate was similar to controls. We have documented a significantly raised glycine/taurine bile acid conjugation ration in duodenal juice from cystic fibrosis patients and suggest that the combined effects of lowered ileal pH and increased glycine conjugated proportion of bile acids may cause precipitation of bile acids leading to decreased fat absorption and large faecal bile acid losses. To further investigate bile acid secretion in children with cystic fibrosis, we modified the high performance thin layer chromatography/densitometry method to enable measurement of individual glycine and taurine conjugates in serum. In comparing cystic fibrosis patients and controls, we were able to determine a group of 18 (36%) with bile acid evidence of liver damage who also showed reduced bile acid secretion into the duodenum. We were unable to study changes in serum bile acids during cholecystokinin/secretin infusion because of the high level of bile acid contamination in Boots Secretin. Some patients showed raised fasting serum bile acid concentrations more than two years before changes in conventional liver function tests or clinically evident liver disease. We have shown fasting serum bile acids to be a sensitive measure of liver dysfunction in cystic fibrosis and postulate that raised proportions of glycine conjugated bile acids may be responsible for the high incidence of liver disease in cystic fibrosis.

Adolescent↗
PubMed2000

Report of the Spanish Gaucher's disease registry: clinical and genetic characteristics.

BACKGROUND AND OBJECTIVES: Since 1993 the demographic, clinical, analytical, genetic and follow-up data of Spanish patients with Gaucher's disease (GD) have been collected in an anonymous national database. Some statistical analyses of these data are reported concerning the distribution, clinical and genetic characteristics of GD in Spain and the response to enzyme replacement therapy (ERT) is evaluated. DESIGN AND METHODS: We performed a cohort study in Spanish GD patients by national inquiry, submitted by mail to 75 Spanish hospitals (over 300 beds) directed to internal medicine, hematology and pediatric departments. The questionnaire included 30 questions (gender, height, weight, date of birth, date of diagnosis, abode and number of relatives affected, bone crises, neurologic symptoms, other symptoms, liver and spleen size, hemoglobin, leukocyte and platelet count, tartrate resistant acid phosphatase, ALT/AST, chitotrioxidase activity, total plasma cholesterol, triglycerides, high density lipoprotein cholesterol, enzymatic activity of acid -glycosides, mutation, X-ray examination, magnetic resonance imaging-MRI-evaluation, spleen removal, and orthopedic procedures (ERT, date of first infusion). Each case with a presumed diagnosis was considered an enrolled patient. Written informed consent was obtained from all patients. The cases without enzymatic or genetic diagnosis were studied in a reference laboratory (the same for all the samples). Clinical status was evaluated by Zimran's severity score index. The enzymatic activity of acid -glycosides was determined in cellular extracts of peripheral blood granulocytes by a fluorescent method using an artificial substrate (4-methyl-umbelliferyl -D-glycoside). Polymerase chain reaction (PCR) molecular analysis was performed in DNA samples to characterize the mutations (N370S, L444P, IVS2+1, 84GG, D409H, R463C and G377S) of the glycoside genes. Two groups were created according to age at diagnosis: children under 15 years and adults, in order to evaluate clinical, genetics and follow-up. Effectiveness of ERT was evaluated using objective parameters (hemoglobin, platelets, liver and spleen size, skeletal lesions), before and after therapy. In patients under ERT, quality of life (QOL) was assessed by a SF-36 modified inquiry, including 22 questions. Statistical analysis including descriptive and frequency distribution for each variable was performed, the ANOVA test was used to identify differences between groups. Paired t-tests (before and during therapy) were carried out. The degree of linear association among measured variables was estimated by Pearson's correlation. RESULTS: By December 1999 one hundred and fifty-five patients from 117 families had been included from 66 Spanish Hospitals; the inquiry was complete for 114 patients. Mean age at diagnosis: 24.0+/-16.9 years, M/F: 72/83. No symptoms were present at diagnosis in 19.3%; visceral disease was present in 95.6% and bone disease in 62.4%. Hemoglobin levels, leukocyte and platelet counts were below the normal range in 62.3% of cases. Higher acid phosphatase levels were observed in 99% of cases; biochemical liver dysfunction tests were found in 42.9%. The test for acid glycosidase showed a marked decrease in enzymatic activity. Morphologic documentation (spleen or liver tissue, bone marrow biopsy or aspirate) of GD was obtained in 71% of the patients. The most frequent mutations observed were N370S (46.3% of the alleles detected), and L444P (18.5%). In 18.7% of the cases the disease was stable or progressing slightly; in 23.8% the spleen had been removed between 1-14 years after diagnosis and 60.6% were under ERT. Children showed both greater liver enlargement and higher SSI (p = 0.0001). There was a correlation between SSI and clinical or analytical data in adults patients for spleen size (Z: 3.142; CI: 0. 173-0.637; p= 0.0017). In 35 patients on ERT, clinical and analytic data improved as did self-evaluated QOL (p< 0.0001). (A

Adolescent↗
PubMed2004

[Procalcitonin as an indicator of infection in patients with liver cirrhosis].

Incidence of bacterial infections in hospitalised patients with liver disease is high. Due to a liver dysfunction immune reactivity is significantly impaired and bacterial infections are more frequent. Also incidence of nosocomial infections is higher in patients with liver disease compared to patients hospitalised for other conditions. To make a differential diagnosis of infectious and non-infectious aetiology of an inflammation is very difficult. Characteristic laboratory tests for bacterial infection include test of a number of leucocytes in peripheral blood, differential count of leucocytes, erythrocyte sedimentation, procalcitonin, C-reactive protein, tumor necrosis factor alpha, interleukin-1, interleukin-6, interleukin-8, and complement fragment C3a. Clinically the most significant are C-reactive protein test and procalcitonin test. Procalcitonin is a protein, a calcitonin precursor, which is in healthy individuals produced by cells of thyroid gland. A half-life of procalcitonin in serum is 20-24 hours which makes it suitable for daily monitoring and enables to control a course of treatment and to distinguish bacterial infection from other types of inflammations. Procalcitonin levels rise in bacterial, parasite, and yeast infections. Elevated procalcitonin levels appear only in inflammations of an infectious etiology with systemic signs. In patients with liver cirrhosis bacterial infections are more frequent. They usually include spontaneous bacterial peritonitis, infection of the respiratory system, urinary infections, and bacteremia. A timely proof of a bacterial infection and an appropriate and effective antibiotic therapy lead to an improvement of the general state of a patient and to his/her better prognosis. Procalcitonin determination is appropriate for diagnosing infections and control of treatment.

Bacterial Infections↗
PubMed1989

[Clinical examination of serum bile acids for the diagnosis of hepatobiliary diseases].

There are four major clinical methods for determination of serum total bile acids (TBA) levels. The first is fasting TBA (FTBA), which increases specifically in liver disorders. It increased more sensitively and normalized faster than transaminases in acute hepatic injury. Secondly, the bile acid loading test is useful to examine the degree of liver cell damage. This test improved the detection rate of FTBA for the liver dysfunction and reflects the severity of the diseases. The third is the profiles and dynamic changes of individual bile acids (IBA). In liver cirrhosis synthesis of cholic acid (CA) was lowered and the ratio of CA + deoxycholic acid (DCA)/chenodeoxycholic acid (CDCA) + lithocholic acid (LCA) was less than 1. On the other hand in cholestasis, secondary bile acids were reduced and CA increased markedly due to the regulation of bile acid metabolism, so that the ratio of CA + DCA/CDCA + LCA was more than 1. This phenomenon can be used for the differential diagnosis of liver cell damage and cholestasis. The last is the detection of unusual bile acids, such as 3 beta-hydroxy-5-cholenoic acid is useful for the marker of hepatic cell carcinoma and the screening of congenital biliary atresia.

Bile Acids and Salts↗
PubMed1989

Some problems in the laboratory findings in multiple myeloma.

The clinical usefulness of alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) levels in serum and pathogenetic mechanism of hypoalbuminemia and hypocholesterolemia in multiple myeloma (MM) were investigated. In cases of MM with a history of pathological fracture, the level of serum ALP was significantly higher than normal. Thus, elevated ALP in MM patients may be an indicator of the occurrence of a pathological fracture within the past 2 months. The levels of serum LDH in about 80% of the MM patients were within normal limits despite the presence of a malignant tumor. These patients showed a normal pattern of isoenzymes and more mature types according to the Greipp classification. In contrasts, the patients with elevated serum levels of LDH showed the tumor pattern of the isoenzymes and the plasmablastic type. The total cholesterol concentration was correlated with the total protein levels and the serum cholinesterase. These findings were the same as those in patients with nephrotic syndrome and polyclonal hypergammaglobulinemia without liver dysfunction. These results suggest that the decreased cholesterol in MM is due to a reduction in the synthesis of albumin in the liver.

Humans↗
PubMed1975

Role of HBs Ab in development of hepatitis.

24% of a healthy control population had antibody to hepatitis-B surface antigen (HBsAb) detectable by passive haemagglutination. The frequency was higher in other population groups in proportion to the intensity of contract with individuals or material positive for HBsAg. Data obtained during an outbreak of type-B hepatitis indicate that immunity to the disease is directly dependent on the titre of circulating HBsAb. A close relationship was found between the presence of HBsAb and liver dysfunction in carriers of HBsAg. This supports the hypothesis that immune response to the antigen may be necessary for the development of liver damage in type-B hepatitis. Nevertheless, since a good antibody response to HBsAg was found in uraemic patients, in whom hepatitis had a clinical course quite different from the population at large, it is thought that immune mechanisms other than the humoral response may account for the pathogenesis of the disease.

Adolescent↗