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At least 19 recordsLinked to original sources
PubMed1978

Hyperbilirubinemia in inflammatory pancreatic disease: natural history and management.

Of 868 patients admitted with pancreatitis between 1971 and 1976, coexisting hyperbilirubinemia was noted in 125 (14%). The patient population was primarily composed of alcoholics (84%) with chronic pancreatic disease (75% Marsielles Class H or higher) which was of moderate severity (77% fewer than three prognostic signs). The hyperbilirubinemia in these 125 patients was due to extrahepatic obstruction in 22%, hepatocelluar disease in 31%, and was idiopathic in 47%. Transient hyperbilirubinemia (< 10 days duration) occurred most commonly in the idiopathic group. Transitory periductular pancreatic edema may account for the elevated bilirubin in some of these cases. Liver biopsy should be done whenever hyperbilirubinemia persists longer than ten days in patients with pancreatitis. If hepatocellular disease is not found, transhepatic or endoscopic retrograde cholangiography are indicated. If common bile duct obstruction is demonstrated, a brief trial of medical therapy is in order. Persistent conservative treatment, however, exposes the patient to the risk of cholangitis and biliary cirrhosis. In 13 of the 125 cases (10%), persistent extrahepatic obstruction proved to be due to compression of the common bile duct by inflammatory pancreatic tissue. In these circumstances, choledochoduodenostomy is recommended as the procedure of choice. In patients requiring biliary decompression, concommitant procedures upon the pancreas are occasionally indicated.

Acute Disease↗
PubMedDate not supplied

Cochlear and brain stem responses in hearing loss following neonatal hyperbilirubinemia.

The site of lesion in hearing loss following neonatal hyperbilirubinemia is unclear. Histopathological studies have implicated the brain stem auditory nuclei while other investigations have hinted at a lesion in the cochlea. In order to clarify this issue, attempts were made to record responses from the auditory pathway in 13 patients with hearing loss following neonatal hyperbilirubinemia. The neural response from the auditory nerve was absent in 11 of the 13 patients and present only in response to high intensity stimuli in 2 patients. However, the response of the cochlear hair cells (cochlear microphonic potential) was present in 9 of the 13 patients. In most other cases of sensorineural hearing loss, with no history of hyperbilirubinemia, the hair cell response was absent. This is functional evidence for auditory nerve damage in cases of hearing loss following neonatal hyperbilirubinemia while the hair cells are spared.

Adult↗
PubMedDate not supplied

Extreme hyperbilirubinemia in a patient with hereditary spherocytosis, Gilbert's syndrome, and obstructive jaundice.

Hyperbilirubinemia may be of several etiologies in the individual patient. An 18-year-old man presented with extreme hyperbilirubinemia (direct bilirubin 23.0 mg/dl, total bilirubin 60.0 mg/dl), hepatosplenomegaly, and anemia. Hematologic studies prelaparotomy documented the presence of hereditary spherocytosis. Intraoperative liver biopsy revealed moderately reduced levels of glucuronyl transferase activity (Gilbert's syndrome). Common bile duct obstruction secondary to choledocholithiasis was found, and a cholecystectomy and splenectomy were performed. This case stresses the potential confusion among several diseases which may present with hyperbilirubinemia.

Adolescent↗
PubMed1979

Chronic persistent hepatitis and unconjugated hyperbilirubinemia.

The authors studied 12 patients with chronic persistent hepatitis and persistent or intermittent mild unconjugated hyperbilirubinemia. Maximum serum total bilirubin concentration ranged from 2.1 to 3.6 mg/dl. Hemolysis was not evident. Hepatic bilirubin UDP-glucuronyltransferase activity assayed in each patient ranged from 0.16 to 0.39 U (mean +/- SEM = 0.27 +/- 0.02) compared to 0.68-1.99 (1.35 +/- 0.08) in 23 normals, 0.78-2.28 (1.41 +/- 0.05) in 53 patients with acute hepatitis, 0.34-1.74 (0.81 +/- 0.09) in 16 patients with anicteric chronic persistent hepatitis, and 0-0.62 (0.24 +/- 0.03) in 33 patients with Gilbert's syndrome. The mean UDP-glucuronyltransferase activity was significantly lower in anicteric chronic persistent hepatitis compared to normals, but higher than in Gilbert's syndrome. The incidence of unconjugated hyperbilirubinemia among first degree relatives was 0:32 in icteric chronic persistent hepatitis compared to 24:85 (28%) in Gilbert's syndrome. These results show that the likely cause for the unconjugated hyperbilirubinemia associated with chronic persistent hepatitis is an acquired depression of hepatic bilirubin UDP-glucuronyltransferase activity. The data suggest that the enzyme defect is related to chronic persistent hepatitis.

Adult↗
PubMed1977

Unconjugated hyperbilirubinemia in very low birth weight infants.

In very low birth weight infants, the occurrence of bilirubin-related brain damage has been repeatedly observed at low serum bilirubin concentrations in close association with altered pathophysiologic status (hypoxia, acidosis, hypothermia, and so on). This increased susceptibility is accompanied by increased severity and duration of unconjugated hyperbilirubinemia as compared with more mature infants. Clinical manifestations of kernicterus in very low birth weight infants are almost always nonspecific. No single biochemical or physiologic measurement is sufficient to predict the risk for development of the bilirubin-related brain damage in this group. Prevention of bilirubin-related brain damage in very low birth weight infants requires not only the maintenance of physiologic and biochemical milieu within normal limits, but also specific therapy to alleviate unconjugated hyperbilirubinemia. Although exchange transfusion has been the mainstay of therapy for unconjugated hyperbilirubinemia, the increased morbidity and mortality associated with exchange transfusion in these immature infants and the need to maintain very low serum bilirubin concentrations suggest that prophylactic phototherapy may be more beneficial for this group.

Bilirubin↗
PubMed1979

Conjugated hyperbilirubinemia in infants with erythroblastosis fetalis.

In an attempt to identify the incidence of conjugated hyperbilirubinemia in infants with erythroblastosis fetalis the records of 67 infants were reviewed. Twenty-two infants were found to have direct bilirubin concentrations greater than 1.0 mg./dl. Among 11 infants who underwent intrauterine exchange transfusion, nine (82%) had conjugated hyperbilirubinemia. Of the remaining 56 infants without the procedure, only 13 (23%) showed evidence of this complication. To predict infants at risk of developing conjugated hyperbilirubinemia, the ratio of hematocrit and total bilirubin concentration in cord blood (H/B ratio) was examined.

Bilirubin↗
PubMed1978

Hyperbilirubinemia and cholestasis.

Although the morphologist continues to describe cholestasis on the basis of precipitated bile seen on light microscopic sections of the liver or dilated canaliculi with loss of microvilli seen by electron microscopy, the physiologist can distinguish clearly between hyperbilirubinemia and cholestasis. Both bilirubin and bile acids are specifically removed from sinusoidal plasma by the normal hepatocyte and appear in bile in high concentration. Bilirubin conjugation and excretion appear to be governed by hepatocellular mechanisms that are, for the most part, separate from the conjugation and excretion of bile acids. Disturbances in bilirubin transport are recognized by hyperbilirubinemia which represents a number of clinical syndromes that can be classified by the nature of the block in the transport system. Serum bile acids appear to remain normal in hyperbilirubinemic syndromes. By contrast, cholestatic syndromes are characterized by marked bile acidemia with normal to slightly elevated bilirubin levels. Severe cholestasis, because of the marked reduction in bile flow, can however, engender jaundice. Further exploration of these excretory pathways will provide interesting new insights on the numerous cholestatic and hyperbilirubinemic syndromes that occur in nature.

Animals↗
PubMed1978

False-positive rubella hemagglutination-inhibition (HAI) titers in neonates and children with conjugated hyperbilirubinemia.

Two neonates, one with extrahepatic biliary atresia and one with cystic fibrosis, and a 9-year-old child with atresia of the common bile duct had conjugated hyperbilirubinemia and elevated rubella HAI titers when kaolin pretreatment of serum was used. A beta-lipoprotein fraction of the serum that is frequently found in association with biliary obstruction was shown to be the probable source of the rubella HAI inhibitor. This beta-lipoprotein was not removed by standard kaolin treatment of serum, but was removed almost completely by dextran sulfate--calcium chloride treatment. In the presence of conjugated hyperbilirubinemia, routine kaolin pretreatment of serum is an inadequate measure for the removal of interfering substances, as false-positive rubella HAI results are obtained consistently.

Antibodies, Viral↗
PubMed1978

Familial lecithin: cholesterol acyltransferase deficiency complicated with unconjugated hyperbilirubinemia and peripheral neuropathy. The first reported cases in the Far East.

Three Japanese patients with lecithin: cholesterol acyltransferase (LCAT) deficiency, the offspring of a consanguineous marriage, are described. In addition to the characteristic clinical and laboratory findings of the disease, our patients had hitherto unreported manifestations, namely unconjugated hyperbilirubinemia, peripheral neuropathy and marked hypocholesterolemia. Although the mechanism of the unconjugated hyperbilirubinemia is not clear, the role of impaired hepatic bilirubin uridine-diphosphate-glucuronyl transferase activity combined with another unknown factor(s) was postulated. Non-random assortment was observed between LCAT deficiency and haptoglobin types, as previously reported. The discovery of Japanese patients with LCAT deficiency indicates that the distribution of this hereditary metabolic disorder is not confined to the Western hemisphere.

Adult↗
PubMed1979

A guide to the use of phototherapy in the management of neonatal hyperbilirubinemia.

Nomograms have been designed to provide rational and consistent guidelines for the use of phototherapy in the management of neonatal hyperbilirubinemia. In the management of 195 neonates in the first week of life, phototherapy, given according to these nomograms, was successful, except in some severe cases of Rhesus incompatability, in controlling hyperbilirubinemia in both premature and term neonates. When compared to the more random use before the introduction of the nomograms, phototherapy was reduced significantly without an increase in the requirement for exchange transfusions.

ABO Blood-Group System↗
PubMed1979

Renal function in infants with hyperbilirubinemia.

A total of 45 infants were studied on the fourth or fifth day of life: 13 term and 10 pre-term infants with serum bilirubin levels ranging between 257 and 390 mumol/l were compared with 12 term and 10 pre-term infants with serum bilirubin levels below 195 mumol/l. The groups did not differ with regard to mean gestational age or mean post-natal age. GFR and CPAH were determined with the single injection clearance method and ability to excrete Na+ was determined following an oral loading of sodium chloride. GFR was lower in infants with hyperbilirubinemia and correlated negatively to the highest recorded serum bilirubin value. CPAH was similar in hyperbilirubinemic infants and controls. The urinary sodium excretion was significantly higher in infants with hyperbilirubinemia.

Age Factors↗
PubMed1979

Evidence of riboflavin depletion in breast-fed newborns and its further acceleration during treatment of hyperbilirubinemia by phototherapy.

Phototherapy in the treatment of newborns with hyperbilirubinemia, resulting in degradation of bilirubin, also appears to have other photodynamic effects on metabolism. We studied flavin adenine dinucleotide (FAD) saturation of erythrocyte glutathione reductase, which should reflect riboflavin nutritional status, in 28 healthy newborns, and followed 37 newborns with hyperbilirubinemia prior to the start of and during phototherapy. The results indicate that healthy newborns on human milk feeding, relatively poor in riboflavin, have evidence of a transient riboflavin depletion soon after birth. This effect is made more pronounced by phototherapy and partially prevented by parenteral or oral administration of moderate amounts of riboflavin.

Bilirubin↗
PubMed1978

Hyperbilirubinemia connected with parenteral administration of higher amounts of fluids in premature infants.

During a study on the influence of different amounts of fluid intake on water and electrolyte metabolism in the first 3 days of life, a high incidence of hyperbilirubinemia was observed in infants receiving a large water load (150 ml/kg/24 h) intravenously. The amount of meconium excreted during the 3-day period in newborns with total parenteral alimentation was significantly lower than in controls. Hyperbilirubinemia is considered to be due to the enterohepatic circulation of bilirubin present in the retained meconium. The role of slight hemolysis and insufficient stimulation of choleresis is discussed.

Humans↗
PubMed1978

Agar in control of hyperbilirubinemia of full-term newborn infants with erythrocyte G-6-PD deficiency.

40 full-term newborn infants with erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) deficiency were used for a study concerning the effectiveness of agar per os in preventing severe hyperbilirubinemia. 20 randomly selected neonates were given agar (1 g/kg/day) orally in 4 daily doses from their 1st to their 5th day of life. 20 infants were not treated and served as controls. Three exchange transfusions were performed in the experimental as well as in the control group. According to these results, agar does not seem to be effective in preventing severe hyperbilirubinemia, which frequently occurs in newborn infants with erythrocyte G-6-PD deficiency.

Administration, Oral↗
PubMed1979

[Psychoneurologic status of preschool children who have sustained hyperbilirubinemia during the newborn period].

A study of the neurological and mental state (as well as of the functional state of some system) with the aid of EMG, REG and EEG in 110 children permitted the authors to conclude that the residual period of hyperbilirubinemia is characterized by a morphofunctional brain immaturity. Clinically it may be expressed in frequent vegetovascular disorders and different psychopathological syndromes, decreasing the adaptational possibilities of the functional systems and disturbing the social adjustment of children. The residual period of hyperbilirubinemia of the newborn is being considered as a period of a relatively favourable and unstable compensation. The authors recommend a certain system of organizational, pedagogical and medical measures ensuring mental and physical health of these children.

Autonomic Nervous System↗
PubMed1978

[Glucose-6-phosphate dehydrogenase deficiency of the mediterranean type B minus. 2. Etiological basis for severe hyperbilirubinemia in the newborn].

After having described in detail the pathophysiology, symptomatology, X-chromosomal inheritance and some laboratory methods in detecting G-6-PD-deficiency by demonstrating a case of favism (Schulz et al. 1977), the authors now discuss the particularities of the enzyme deficiency in the newborn. These are complicated by additional physiological and transient deficiency of the enzymes catalase, NAD-diaphorase, glutathione peroxidase, and glucuronyl transferase. Several chemical substances, acidosis, hypoxia, hypoglycemia, and immaturity may cause a severe hyperbilirubinemia in G-6-PD-deficient newborns. The development of a kern-icterus in these cases may be prevented by early exchange transfusion. From clinical findings and some observations in different regions of Greece an additional factor influencing the liver function has been postulated which favors the development of hyperbilirubinemias in G-6-PD-deficient newborns. The nature of this possible factor is discussed. The authors emphasize the necessity of screening for G-6-PD-deficiency during pregnancy in families of mediterranian descent.

Cephalexin↗
PubMed1978

Amniotic fluid infections, neonatal hyperbilirubinemia, and psychomotor impairment.

A large prospective study found that infants born with evidence of recent amniotic fluid infections subsequently had an increased frequency of mental, motor, visual, and hearing impairment. These infections also potentiated the neurotoxicity of neonatla hyperbilirubinemia. This potentiation of bilirubin neurotoxicity of neonatal hyperbilirubinemia. This potentiation of bilirububin neurotoxicity increases with the severity of the amniotic fluid infections. With or without such infections, an increased frequency of long-term mild mental retardation started at peak neonatal bilirubin levels of only 7 mg/dl in both term and preterm infants. Significant neurologic abnormalities began at peak bilirubin levels of 12 to 13 mg/dl.

Amniotic Fluid↗
PubMed1979

CNS changes in hyperbilirubinemia. Functional implications.

Hyperbilirubinemia is a recognized etiologic factor in motor and hearing disorders associated with cerebral palsy. Its role in more subtle forms of neurological impairment is more controversial. Using a mutant animal model, which develops symptoms and signs closely resembling the human kernicterus syndrome, neurons of hippocampus, cerebral cortex, cochlear nuclei, losuc ceruleus, and olfactory bulb were examined by electron microscopy. Pathological changes, observed in all areas studied, consisted of mitochondrial and endoplasmic enlargement and vacuolation, with glycogen deposition; increased extracellular space; myelin figures; and degenerating changes in nerve terminals. If we make the assumption that pathologic changes in the human infant with neonatal jaundice are similar to changes in the animal model, then the widespread involvement of CNS neurons in all cortical areas examined may well help to explain the syndromes of minimal cerebral dysfunction reported in clinical studies.

Age Factors↗