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PubMed1990

Glucose-based versus fat-based total parenteral nutrition (TPN): effects on hepatic function in septic patients complicated with cholestatic jaundice.

A prospective study of two types of total parenteral nutrition (TPN) was carried out in 34 patients suffering from sepsis and complicated liver dysfunction. Group 1 (18 patients) received non-protein energy as glucose plus fat emulsion in a caloric ratio of 19:1, while group 2 (16 patients) received the same energy intake but with a ratio of 1:1. Group 1 exhibited higher levels of bilirubin and alkaline phosphatase with values of 93.5 +/- 25.5 mumol/l and 160 +/- 30 IU/l respectively compared to Group 2, in which the corresponding values were 81.6 +/- 32.3 mumol/l and 120 +/- 10 IU/l (p < 0.05). On the other hand, group 1 had lower levels of serum albumin and serum transferrin with values 25 +/- 1.3 g/l and 40 +/- 20% of normal, compared to group 2 in whom the corresponding values were 28 +/- 8 g/l and 48 +/- 30% of normal (p < 0.05). There were no differences between the two groups, in the absolute number of T-lymphocytes and in transaminase levels. In sepsis complicated by liver dysfunction a 50:50 glucose: fat regimen caused less disturbance of liver function than one consisting almost entirely of glucose.

Journal Article↗
PubMed2003

Severe alcoholic hepatitis accompanied by Fournier's gangrene.

Fulminant necrotizing soft-tissue infection of the external genitalia and perineum (Fournier's gangrene) occurred in a patient with severe alcoholic hepatitis. By means of radical débridement and disinfection of the necrotizing tissue, use of broad-spectrum antibiotics and prednisolone, and other supportive measures, Fournier's gangrene and severe alcoholic hepatitis eventually subsided with broad skin defects in the waist and external genitalia. Later, the skin defects were successfully reconstructed with skin grafts. Although the route of bacterial intrusion could not be defined, Fournier's gangrene presumably developed in a background of impaired immunological defences, principally associated with habitual massive alcohol consumption and profound liver dysfunction. This present case highlights not only the underlying immunocompromised condition but also the need for concern regarding the urogenital and anorectal areas as potential foci of life-threatening infection in patients with liver dysfunction, especially when related to alcohol intake.

Fournier Gangrene↗
PubMed1987

Direct hyperbilirubinemia and hepatic fibrosis: a new presentation of Jeune syndrome (asphyxiating thoracic dystrophy).

Jeune syndrome (asphyxiating thoracic dystrophy) is an autosomal recessive skeletal dysplasia with multisystem involvement. The disorder is usually considered lethal, with death resulting from respiratory insufficiency during infancy, or from renal failure during childhood. Hepatic dysfunction, diagnosed on the basis of direct hyperbilirubinemia and hepatic fibrosis, led to early diagnosis of Jeune syndrome in a newborn infant. Review of the literature indicates that the specific pathologic lesion (biliary dysgenesis with portal fibrosis and bile duct proliferation) has been observed as an incidental finding at autopsy, but that clinically significant liver dysfunction has not been appreciated as an important manifestation in this disorder. The characteristic histopathologic abnormality has been present in every patient studied, and may advance during infancy; in contrast, clinical liver dysfunction resolves over the first few months of life. Whereas many patients with Jeune syndrome die early, several have survived into adolescence, suggesting that aggressive treatment is appropriate, especially for those with minimal respiratory and renal involvement. Longitudinal evaluation of liver function and pathology in these survivors is needed to define the long-term prognosis.

Asphyxia Neonatorum↗
PubMed2004

Acute hepatic failure in pregnancy.

Severe liver dysfunction in late pregnancy is an unusual but dramatic event because it can progress very rapidly to fulminating disease and also because two lives, that of the mother and foetus, are involved. We report a descriptive study of a pregnant woman presenting with severe liver dysfunction.

Adult↗
PubMedDate not supplied

Serum interleukin-6 and hepatocyte growth factor levels in patients after hepatectomy.

BACKGROUND/AIMS: To examine whether serum hepatocyte growth factor and interleukin-6 levels are early parameters of postoperative liver dysfunction after hepatectomy. METHODOLOGY: The serum levels of hepatocyte growth factor and interleukin-6 were measured in 16 hepatectomized patients on the day of surgery (before surgery, immediately after hepatectomy, after completion of surgery) and on postoperative days 1, 3, and 5. Serum liver function tests were determined for 14 days after surgery and their results were correlated with serum interleukin-6 and hepatocyte growth factor levels. RESULTS: Serum interleukin-6 and hepatocyte growth factor levels were elevated after surgery and these values were higher in patients who underwent hepatectomy greater than lobectomy in magnitude. The mean maximum value of interleukin-6 appeared on day 0 and was earlier than that of hepatocyte growth factor, which was found on day 1. Serum total bilirubin and alanine aminotransferase levels reached the maximum within 5 days after surgery. Multiple regression analysis showed that serum levels of interleukin-6 and hepatocyte growth factor on day 0 after surgery were significantly correlated with the postoperative maximum total bilirubin level (P < 0.0001). The maximum interleukin-6 level but not hepatocyte growth factor significantly correlated with the postoperative maximum bilirubin level (P < 0.02). CONCLUSIONS: Both the serum interleukin-6 and hepatocyte growth factor levels are likely early indicators of postoperative liver dysfunction in patients after hepatectomy.

Adult↗
PubMed1982

The predictive value of the lymphocyte transformation test in isoniazid-associated hepatitis.

Sixty-one patients receiving isoniazid (INH) for chemotherapy or chemoprophylaxis were assessed by the lymphocyte-transformation test (LTT) shortly after starting treatment. Thirty-eight per cent exhibited stimulation with INH, isonicotinic acid (INA) or human-serum albumin conjugates of these haptens. In the LTT-positive group, liver dysfunction subsequently developed in 58.8%, as compared to 22.7% in the LTT-negative group (P less than 0.01). The difference was not accountable on the basis of age, ethnic background, sex or chemotherapy vs chemoprophylaxis. Although there was an excess of alcohol abusers in the LTT-positive group, the probability of developing liver dysfunction amongst alcohol abusers in that group was twice as great as for LTT-negative alcohol abusers. The specificity of the LTT in predicting liver damage was 83-90% (depending upon the criteria used for determining positivity), while the sensitivity of the test was only 50%.

Adult↗
PubMed1990

Soluble interleukin-2 receptor and soluble CD8 in liver cirrhosis and obstructive jaundice.

Activated lymphocytes secrete soluble interleukin-2 receptor (sIL-2R); CD8-positive lymphocytes secrete soluble CD8 (sCD8). Liver dysfunction in cirrhosis and obstructive jaundice is known to result in depressed cellular immunity. To evaluate whether this is due to real inactivation of the immune system, we measured sIL-2R and sCD8 in the serum of 46 patients with liver cirrhosis, 25 patients with obstructive jaundice, 32 patients with alcoholic liver disease without evidence of cirrhosis, 23 healthy persons and 43 patients with unrelated disease. sIL-2R in patients with cirrhosis (mean +/- s.e.m. 1499 +/- 140 U/ml) and obstructive jaundice (1517 +/- 204) was significantly increased compared with healthy subjects (363 +/- 29) and patients with unrelated diseases (685 +/- 92); sCD8 was significantly increased in patients with cirrhosis (737 +/- 63) but not in patients with obstructive jaundice (419 +/- 32) compared with healthy subjects (322 +/- 23) and patients with unrelated diseases (375 +/- 22). No difference was found between patients with cirrhosis due to alcohol abuse (n = 15) and chronic hepatitis B (n = 6). The Child-Pugh score had no significant influence on the sIL-2R or sCD8 value. In obstructive jaundice, sIL-2R correlated with alkaline phosphatase as marker of cholestasis (r = 0.43). These data show that in spite of the apparent depressed cellular immune defense both in liver cirrhosis and obstructive jaundice there is a general activation of the immune system but the CD8+ cell compartment is only activated in liver cirrhosis. The great changes of sIL-2R and sCD8 in liver dysfunction are important for the interpretation of studies using these serum proteins as markers for immune activation.

Adult↗
PubMed2001

Two hyperandrogenic adolescent girls with congenital portosystemic shunt.

UNLABELLED: We describe two adolescent girls with a congenital portosystemic shunt who exhibited hyperandrogenism in addition to insulin resistant hyperinsulinaemia. Case 1 was referred to our clinic to undergo a routine clinical work-up prior to tonsillectomy at 14 years of age. Mild liver dysfunction was identified and hypogenesis of the portal vein with a congenital portosystemic shunt diagnosed. Primary amenorrhoea and virilization were evident and an endocrinological evaluation revealed hyperandrogenism and insulin resistant hyperinsulinaemia. Case 2 was referred at 15 years of age because of cardiomegaly. Mild liver dysfunction and hyperbilirubinaemia led to a diagnosis of agenesis of the portal vein with a congenital portosystemic shunt. Virilization was evident and an endocrinological evaluation revealed hyperandrogenism and insulin resistant hyperinsulinaemia. The haemodynamics of these patients were similar to those of secondary portosystemic shunt due to liver cirrhosis, which is often associated with hyperinsulinaemia and/or non-insulin dependent diabetes mellitus. On the other hand, hyperandrogenism is associated with certain insulin-resistant conditions with hyperinsulinaemia, including the polycystic ovary syndrome (PCO). Hyperinsulinaemia is believed to cause hyperandrogenism in patients with PCO by stimulating androgen production in both the ovary and adrenal gland. Therefore, in congenital portosystemic shunts, hyperinsulinaemia is also thought to cause hyperandrogenism due to the same mechanism. CONCLUSION: A certain percentage of female patients with hyperandrogenism, likely including those with polycystic ovary syndrome may also have congenital portosystemic shunts. Our results indicate that serum levels of total bile acids and ammonia are prognostic indicators of this hepatic vascular anomaly.

Adolescent↗
PubMed2004

Deficient phospholipase C activity in blood polimorphonuclear neutrophils from patients with liver cirrhosis.

BACKGROUND/AIMS: Circulating neutrophils from cirrhotic patients have a reduced capacity to generate superoxide anion (O(2)(-)), which might contribute to frequent bacterial infections in these patients. We studied the signal transduction pathways involved in the generation of O(2)(-) in neutrophils from 98 cirrhotic patients and 46 healthy controls. METHODS: We measured O(2)(-) production in neutrophils induced by fMLP, opsonized zymosan, TNF alpha, NaF, AlF(4)(-), A23187 and phorbol myristate acetate. Furthermore, we measured phospholipase C activity in neutrophils from healthy controls and end-stage cirrhotic patients. RESULTS: O(2)(-) production was decreased in neutrophils from patients in response to fMLP, opsonized zymosan and TNF alpha. Likewise, response of these cells to G-protein stimulation by fluorides was also decreased. These reduced responses correlated significantly with the degree of liver dysfunction. On the contrary, neutrophils from patients responded normally to A23187 and phorbol esters stimulation indicating that Ca(2+)- and PKC-dependent pathways are intact in these cells. Finally, phospholipase C activity was markedly reduced in neutrophils from end-stage liver cirrhosis. CONCLUSIONS: These data confirm that O(2)(-) generation by neutrophils is decreased in patients with cirrhosis, particularly in those with more severe liver dysfunction, and suggest that this defect involves phosphatidylinositol specific phospholipase C activity.

Adult↗
PubMed1998

Sero-epidemiologic study of hepatitis C virus infection in Fukuoka, Japan.

We conducted an epidemiological study of 509 residents of H town, Fukuoka, Japan, to investigate the high mortality rate from liver disease. Antibodies to hepatitis C virus (HCV) (anti-HCV) were detected in 120 residents (23.6%); HCV RNA in 91 (17.9%), and hepatitis B surface antigen (HBsAg) in 13 (2.6%). Multivariate logistic regression analyses showed that presence of anti-HCV, male gender, and history of liver disease were associated with the presence of liver dysfunction, and that age of more than 40 years and a particular district were associated with the presence of anti-HCV. HCV RNA was more frequently detected in anti-HCV-positive men than women (41, or 85.4% versus 50, or 69.4%) (P < 0.05). The incidence of liver dysfunction was significantly higher in HCV RNA-positive men than women (32, or 66.7% versus 22, or 30.6%) (P < 0.05). These findings suggest that: (1) HCV was correlated with the high mortality rate from liver diseases, (2) there were district-related differences in the incidence of HCV, and (3) the lower frequency of elimination of HCV from men may explain why they showed a high mortality from liver disease.

Adult↗
PubMed1990

Effects of glycyrrhizin (SNMC: Stronger Neo-Minophagen C) in hemophilia patients with HIV-1 infection.

Forty-two hemophiliacs with HIV infection were treated with high-dose glycyrrhizin, Stronger Neo-Minophagen C (SNMC). The dose was 100-200 ml of SNMC in 21 patients and 400-800 ml in the other 21. The patients were divided into an asymptomatic carrier (AC) group and AIDS related-complex (ARC)/AIDS group. SNMC was administered intravenously daily for the first 3 weeks, and every second day for the following 8 weeks to the 42 HIV-infected hemophilia patients, in accordance with the protocol proposed by the Japanese National Research Committee. The CD4/CD8 ratio and CD4 positive lymphocyte counts did not change during the treatment period. However, significant improvement was noted in some cases. A slight increase in mitogenic responsiveness to phytohemagglutinin, Concanavalin A and pokeweed mitogen was noted in most patients of both groups, especially significant improvement was seen in the AC group administered over 400 ml of SNMC. Furthermore, complete improvement was noted in liver dysfunction, which has been thought to be one of the major problems for hemophiliacs treated with blood products. Thus, prophylactic administration of high-dose SNMC to HIV positive hemophiliacs who have impaired immunological ability and liver dysfunction was considered to be effective in preventing the development from AC/ARC to AIDS.

AIDS-Related Complex↗
PubMed1999

Neonatal oxidative liver metabolism: effects of hydrogen peroxide, a putative mediator of septic damage.

BACKGROUND/PURPOSE: Surgical neonates are at risk for sepsis and liver dysfunction. These complications are more common in preterm neonates and in those who receive total parenteral nutrition. Elevated levels of reactive oxygen species (eg, hydrogen peroxide) have been reported in these "at-risk" patients and may be the mediators of liver impairment via their effect on oxidative energy metabolism. The aim of this study was to test the hypothesis that elevated levels of hydrogen peroxide (H2O2) impair neonatal liver oxidative energy metabolism. METHODS: An in vitro model to test this hypothesis was developed in hepatocytes isolated from neonatal (11-day to 15-day) rats. The cells, respiring on palmitate (0.5 mmol/L in 2% bovine serum albumin), were exposed to H2O2. Oxygen consumption was measured polarographically. In experiment A, H2O2 was added to the cell preparation at different concentrations (0.5 mmol/L, 1 mmol/L, 1.5 mmol/L, 2 mmol/L) to assess the effect on oxygen consumption. In experiment B, H2O2 (2 mmol/L) was added to hepatocytes in the presence of inhibitors of mitochondrial respiration to define the site of action of H2O2. In experiment C, electron microscopy was performed on hepatocytes after incubation with 1 mmol/L and 2 mmol/L of H2O2. RESULTS: In experiment A, H2O2 significantly reduced hepatocyte oxygen consumption at 1.5 and 2 mmol/L. In experiment B, in the presence of inhibitors of mitochondrial respiration, myxothiazol (inhibitor of substrate oxidation), and oligomycin (inhibitor of adenosine triphosphate (ATP) synthase), no further inhibition by H2O2 occurred, indicating that the effect of H2O2 was intramitochondrial and affecting the synthesis of ATP. In experiment C, microscopic alterations of mitochondria were noticed exclusively in hepatocytes incubated with 2 mmol/L H2O2. CONCLUSIONS: Results of this study demonstrate that H2O2 impairs neonatal liver oxidative metabolism. H2O2 probably directly inhibits ATP synthase. The authors hypothesize that H2O2 may play a role in the biochemical pathogenesis of liver dysfunction associated with sepsis. Identification of the precise target site of H2O2 may be valuable in directing therapy in septic neonates.

Adenosine Triphosphate↗
PubMed1985

Effects of volatile anesthetics or fentanyl on hepatic function in cirrhotic rats.

Halothane, enflurane, isoflurane, and fentanyl were examined for their potential to exacerbate liver dysfunction in rats with preexisting cirrhosis. Male Wistar rats given sodium phenobarbital for 2 weeks are assigned randomly to two groups. One group (cirrhotic) was exposed by inhalation to carbon tetrachloride (CCl4) in air at weekly intervals for 12 weeks to induce cirrhosis. The other group (noncirrhotic) was handled similarly but received air only. Five weeks after the last exposure to CCl4, cirrhotic and noncirrhotic rats were given three hours of 1 MAC halothane, enflurane, or isoflurane in 50% oxygen, or 350 micrograms fentanyl per kg of body weight and 50% oxygen, or 50% oxygen only. Blood gas tensions and blood glucose levels were measured before, during, and at the end of exposure. Forty-eight hours after exposure, serum chemistries were measured in each rat for comparison with preexposure values. Rats were then killed by CO2 overdose, and liver, kidney, and testis were prepared for microscopic examination. Enflurane, isoflurane, and halothane, but not fentanyl, produced mild respiratory acidosis and no change in serum glucose levels. All anesthetics resulted in a mild but similar degree of acute liver dysfunction as indicated by small increases in SGOT or SGPT in both cirrhotic and noncirrhotic rats. Liver histology revealed mild to moderate portal cirrhosis with fibrosis and well-developed micronodules in rats exposed to CCl4, but no superimposed acute hepatocellular damage was noted. It is concluded that all the anesthetics used in this study were associated with the same minimal degree of postanesthetic hepatic dysfunction and that the dysfunction was similar in both cirrhotic and noncirrhotic rats.

Alanine Transaminase↗
PubMed1998

The impacts of experimental necrotizing pancreatitis on hepatocellular ion homeostasis and energetics: an in vivo nuclear magnetic resonance study.

BACKGROUND: Liver dysfunction may be an early event or the end result of multiple organ dysfunction (MOD) in necrotizing pancreatitis. This study measured the early changes in hepatocellular ions and energetics associated with such conditions. METHODS: Twenty-five rats, prepared with a 23Na and 31P double-tuned nuclear magnetic resonance surface coil secured over the dome of the liver, were randomized into 5 groups: control, 10 and 20 minutes of total inflow ischemia, pancreatitis induced by deoxycholic acid (DCA), and sham-DCA (saline injection). Dysprosium-TTHA3- solution was used to separate the intracellular and extracellular sodium peaks. RESULTS: In rat liver, 20 minutes of total inflow occlusion caused irreversible depletion of high-energy phosphates. Changes at 2 hours after the onset of DCA-pancreatitis are compared with changes after 20 minutes of ischemia (mean +/- SEM). Although the DCA-pancreatitis animals did not become hypotensive until 1 hour after the induction of pancreatitis, the changes in hepatic intracellular ions and energetics began soon after such an insult. At 2 hours after the onset of pancreatitis, hepatocellular pHi and [NA+]i were 6.99 +/- 0.16 and 78.4 +/- mmol/L, respectively (P < .01, compared with sham animals). A similar pattern of changes in hepatic bioenergetics also occurred. After the onset of pancreatitis, the hepatic cytostolic phosphorylation potential decreased with time (y = 0.654 - 0.004t, where t is time in minutes and r2 = 0.967 and the rate of hepatic hydrolysis of adenosine triphosphate increased progressively (y = 0.702t + 91.363, where t is time in minutes and r2 = 0.969. These changes correlated well with the accumulated [Na]i. CONCLUSIONS: Unresuscitated necrotizing pancreatitis caused severe hepatocellular acidosis, profound sodium accumulation, and bioenergy depletion early in its course. These effects were as severe as those induced by total liver ischemia. Liver dysfunction may be an early, not terminal, event of MOD in necrotizing pancreatitis.

Adenosine Triphosphate↗
PubMed2003

Pre-operative hepatitis in a woman treated with Chinese medicines.

A 37-year-old Hong Kong Chinese female with cervical cancer was scheduled for radical hysterectomy and lymphadenectomy. Her past health was good. Pre-operatively, she was found to have a fatty liver, prolonged prothrombin time and abnormal liver function tests. Surgery was not postponed and she was anaesthetised uneventfully, using a general anaesthetic technique. The procedure lasted 4 h. Postoperatively, she developed a large pelvic haematoma and a wound infection. Her coagulation and liver function tests gradually returned to normal. No obvious medical cause for her liver dysfunction could be found. However, it emerged that she had received a 6-week course of traditional Chinese medicines prior to admission. The prescriptions contained over 60 different ingredients, some of which were known to be hepatotoxic, cytotoxic or to cause bleeding. This was the most likely explanation for her liver dysfunction.

Adult↗
PubMed2006

Novel diagnostic approach to citrin deficiency: analysis of citrin protein in lymphocytes.

Citrin deficiency induces two clinical features; namely neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD) and adult-onset type II citrullinemia. Hypercitrullinemia is the most characteristic feature, whereas there are non-citrullinemic individuals. Diagnosis of citrin deficiency is performed by genetic analysis, although the 12 known mutations in the alleles are not detected in about 15% of cases. Thus, we aimed to examine citrin protein in lymphocytes isolated from peripheral blood as an alternative diagnostic method. We examined 38 children having an episode of cholestatic liver dysfunction, 8 heterozygotes, and 11 healthy individuals. All subjects were evaluated for citrin protein by Western blotting and for the 12 known mutations by gene analysis. Citrin protein was detected in 15 of 38 children with cholestatic liver dysfunction. Fourteen of them were negative for 12 known mutations in both alleles, whereas one patient was found to have a known mutation in one allele. Citrin protein was absent in 23 of the 38 patients. Among these 23, gene analysis diagnosed citrin deficiency in 19, whereas 2 patients were later revealed to be NICCD with novel mutations. In the remaining 2 patients, who exhibit the clinical features of NICCD, a known mutation was detected in one allele but no mutation was identified in another allele. Citrin protein was also detected in the 8 heterozygotes and 11 healthy individuals. We disclosed that citrin was deficient in lymphocytes among patients with citrin deficiency. Analysis of citrin is useful to diagnose citrin deficiency even in patients without known mutations or hypercitrullinemia.

Blood Preservation↗
PubMedDate not supplied

Bosentan.

Bosentan is the first endothelin (ET) receptor antagonist approved by the Food and Drug Administration for the management of pulmonary arterial hypertension (PAH). In patients with World Health Organization Class III and IV PAH, bosentan has demonstrated improvement in dyspnea and exercise tolerance. ET also plays an important role in the pathophysiology of different vascular diseases. Therefore, bosentan also may have the potential to alter the outcome of many other diseases, such as heart failure, hypertension, ischemic heart disease, and renal disease, as well as cerebrovascular disorders. Because of the rarity and the poor prognosis of patients with PAH, as well as the requirement of close monitoring of bosentan (due to its potential of causing liver dysfunction and its teratogenic effects), bosentan is currently available only through a special access program and is distributed by certain selected pharmacies. Patients who are receiving bosentan should be taught to recognize early signs and symptoms of liver dysfunction and possible pregnancy. In addition, bosentan is not only a substrate but also an inducer of CYP3A4 and CYP2C9. Therefore, it is anticipated that numerous drug interactions may occur. Patients should be advised to consult their physicians or pharmacists should they need to consume other prescription or nonprescription medications.

Antihypertensive Agents↗
PubMed1988

[Werner's syndrome associated with meningioma: case report].

We present two cases of Werner's syndrome associated with intracranial meningioma. Characteristic clinical features of Werner's syndrome include short stature with slender extremities, premature senility, juvenile cataract, skin changes, a tendency to diabetes mellitus and familial occurrence. A 44-year-old female, who had been treated for diabetes mellitus, was diagnosed as having Werner's syndrome because of various characteristic features. A falx meningioma was incidentally found on CT scan, and was surgically removed. Her diabetes mellitus improved. The second case was a 28-year-old male was diagnosed as having Werner's syndrome, diabetes mellitus, juvenile cataract, together with diabetes insipidus, and liver dysfunction. He developed severe headache, gait disturbance and then became unconscious with right hemiparesis. He was found to have a parasagittal meningioma by CT scan and angiography. After removal of the tumor, diabetes mellitus, diabetes insipidus and liver dysfunction improved. The reported incidence of neoplasms associated with Werner's syndrome is about 10%. The majority of associated tumors were mesenchymal in origin. Ten meningiomas, 1 neurinoma and 2 gliomas are reported as associated tumors in the central nervous system. Most of the associated meningiomas were asymptomatic and found incidentally at autopsies or CT scans. Diabetes mellitus associated with Werner's syndrome is generally mild with high immunoreactive insulin value and is controllable by diet therapy and oral antidiabetic drugs. Daily profile of blood sugar improved after the removal of tumor in our cases. In 50 gm glucose tolerance test, tendency of delayed appearance of peak value, which is common in Werner's syndrome, was not altered in our cases. Discussion is made as to the association of Werner's syndrome with meningioma and diabetes mellitus.

Adult↗