Systemic Disease and the Liver

Farrell, Michael; Bucuvalas, John C.

doi:10.1017/cbo9780511547409.040

Cited by 9 publications

(10 citation statements)

References 443 publications

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“…Patients may progress to cirrhosis and show the signs of liver failure. Unlike adults, children may have only firm hepatomegaly and ascites may be absent [128].…”

Section: Budd-chiari Syndrome (Bcs)mentioning

confidence: 99%

Study of Serum Copper and Iron in Children with Chronic Liver Diseases

Ibrahim¹

2013

Anat Physiol

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Trace elements have a major role as both oxidants and antioxidants, promoting and protecting from tissue damage respectively. As the liver has a pivotal role in trace elements metabolism and consequenyly their bioavailability, we aimed to measure serum levels of essential trace elements in children with chronic liver diseases (CLDs) regardless the etiology and to study their correlation with liver function tests. Serum zinc (Zn), copper (Cu) and iron (Fe); together with other trace elements parameters; were measured in 50 children with CLDs using spectrophotometry and their levels were compared with those age and sex matched healthy children as controls. Serum Cu, Fe, ferritin and transferrin saturation (TS) were significantly higher in the CLDs group than that in the control group; while serum Zn and total iron binding capacity (TIBC) were significantly lower in the CLDs than that in the control group. Serum Fe, Cu, TS and ferritin were positively correlated with biochemical parameters of liver damage; while serum Zn and TIBC were negatively correlated with biochemical parameters of liver damage. These results encourage inclusion of serum Zn, Cu and Fe as biomarkers for monitoring the severity of liver damage during routine assessment of children with CLDs. We recommended caution to avoid excess Fe and Cu intake in children with CLDs. Moreover, Zn supplementation could be encouraged in children with CLDs regardless its etiology.

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“…Patients may progress to cirrhosis and show the signs of liver failure. Unlike adults, children may have only firm hepatomegaly and ascites may be absent [128].…”

Section: Budd-chiari Syndrome (Bcs)mentioning

confidence: 99%

Study of Serum Copper and Iron in Children with Chronic Liver Diseases

Ibrahim¹

2013

Anat Physiol

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“…Patients receiving hyperalimentation are susceptible to developing cholestasis because of the diminished stimulus to bile flow associated with the absence of oral feeding and release of hormones that stimulate bile flow, 17 as well as direct oxidant stress to the liver. 18 Cholestasis associated with hyperalimentation is particularly common in infants 19,20 and in adult patients on long-term hyperalimentation. In the latter group, up to 50% of patients receiving hyperalimentation for 1 or 2 years develop intrahepatic cholestasis, fibrosis, and early biliary cirrhosis.…”

Section: Clinical Discussionmentioning

confidence: 99%

Clinicopathology conferences: Inflammation-induced cholestasis

Crawford

Boyer

1998

Hepatology

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Intrahepatic cholestasis may arise from many sources, and it therefore presents a particular challenge when it develops in the seriously ill patient. A 54-year-old patient with a myeloproliferative disorder is presented, who developed jaundice in the setting of a severe decubital infection, polypharmacology, multiple blood transfusions for anemia, renal insufficiency, parenteral alimentation, and a history of long-standing alcohol abuse, a positive purified protein derivative, and recent biopsy-proven laryngeal squamous cell carcinoma. The thesis is advanced that many insults may cause local and systemic activation of the inflammatory cytokine system, and that these proinflammatory events are potent inducers of intrahepatic cholestasis. CASE HISTORYA 54-year-old male civil engineer was admitted with a 1-month history of headaches, fever, sore throat, sinusitis, myalgias, and general malaise. He had a long history of heavy drinking (up to 0.5 pints of liquor per day) and heavy smoking (Ͼ100 pack years), extending up to the time of his admission. He was known to be purified protein derivativepositive. On admission, he was a well-developed 83-kg white male with hoarseness, a temperature of 100°F, orthostatic hypotension, and 2ϩ pitting edema to his mid-calves. There was no hepatosplenomegaly. A chest roentgenogram showed mild chronic obstructive pulmonary disease with no evidence of active tuberculosis. His hematocrit was 35.7%, and the peripheral white blood cell count was 22,000/mm 3 with 2% myeloblasts. The erythrocyte sedimentation rate was 126 mm/h. His serum glutamate pyruvate transaminase was 25 IU/L (normal, 5-40 IU/L), serum glutamate oxaloacetate transaminase was 13 IU/L (normal, 5-40 IU/L), serum alkaline phosphatase was 95 IU/L (normal, 35-125 IU/L), serum lactate dehydrogenase was 230 IU/L (normal, 20-200 IU/L), serum total bilirubin was 0.5 mg/dL (normal, Ͻ1.0 mg/dL), and serum albumin was 2.3 g/dL (normal, 3.5-5.5 g/dL). Viral serologies were negative for hepatitis A and hepatitis B (this case antedated hepatitis C testing). A bone marrow aspirate and biopsy indicated a myeloproliferative syndrome, but not acute myelogenous leukemia. The liver and spleen were of normal size by liver-spleen scan, but uptake throughout the liver was mottled, suggesting parenchymal disease. Abdominal computed tomography scan was unremarkable.The presenting symptoms persisted following admission. Continued anemia over several weeks necessitated multiple transfusions, up to as many as 4 units of packed red blood cells three times a week. Persistent throat soreness prompted biopsy of a false vocal cord lesion in week 2, which revealed squamous cell carcinoma. Spiking fevers to as high as 104°F presaged the development of a presacral decubitus ulcer in week 6, from which Proteus mirabilis was ultimately cultured. Broad spectrum antibiotic therapy was initiated, but did not prevent the progression of the decubital ulcer to development of sacral osteomyelitis by week 8. Because of progressive weight loss, parenteral hyperalim...

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“…Classic hepatic VOD has become extremely rare in children since the 80s, when VOD became more commonly seen in adults as a complication of stem cell or bone marrow transplantation. 35 , 36 This marked reduction in the incidence of the disease in Egyptian children may be attributed to improved sanitary and hygienic conditions that predispose to the disease.…”

Section: Hepatic Venous Outflow Obstructionmentioning

confidence: 99%

Splanchnic Vein Thrombosis in the Mediterranean Area in Children

El‐Karaksy¹,

El-Raziky²

2011

Mediterr J Hematol Infect Dis

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Abdominal venous thrombosis may present as splanchnic venous thrombosis (SVT) (occlusion of portal, splenic, superior or inferior mesenteric veins) or Budd- Chiari Syndrome (BCS) (thrombosis of inferior vena cava and/or hepatic veins). The aim of this review is to report the scanty data available for SVT in the South Mediterranean area. In one Egyptian study, the possible circumstantial risk factors for portal vein thrombosis (PVT) were found in 30% of cases: 19% neonatal sepsis, 8.7% umbilical catheterization, 6% severe gastroenteritis and dehydration. Another Egyptian study concluded that hereditary thrombophilia was common in children with PVT (62.5%), the commonest being factor V Leiden mutation (FVL) (30%). Concurrence of more than one hereditary thrombophilia was not uncommon (12.5%). The first international publication on hepatic veno-occlusive disease (VOD) in Egypt was in 1965 in children who rapidly develop abdominal distention with ascites and hepatomegaly. This disease was more frequent in malnourished children coming from rural areas; infusions given at home may contain noxious substances that were hepatotoxic and infections might play a role. VOD of childhood is rarely seen nowadays. Data from South Mediterranean area are deficient and this may be attributable to reporting in local medical journals that are difficult to access. Medical societies concerned with this topic could help distribute this information.

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Systemic Disease and the Liver

Cited by 9 publications

References 443 publications

Study of Serum Copper and Iron in Children with Chronic Liver Diseases

Study of Serum Copper and Iron in Children with Chronic Liver Diseases

Clinicopathology conferences: Inflammation-induced cholestasis

Splanchnic Vein Thrombosis in the Mediterranean Area in Children

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