Fas (TNFRSF6) Gene Polymorphism in Pregnant Women With Hemolysis, Elevated Liver Enzymes, and Low Platelets and in Their Neonates

2006 ◽  
Vol 107 (3) ◽  
pp. 582-587 ◽  
Author(s):  
István Sziller ◽  
Petronella Hupuczi ◽  
Neil Normand ◽  
Amrita Halmos ◽  
Zoltán Papp ◽  
...  
Keyword(s):  
Gene Polymorphism ◽  
Pregnant Women ◽  
Liver Enzymes ◽  
Elevated Liver Enzymes

scholarly journals Hepatic capsular rupture in pregnancy

2016 ◽  
Vol 9 (4) ◽  
pp. 185-188 ◽  
Author(s):  
Charlotte J Frise ◽  
Peyton Davis ◽  
Graham Barker ◽  
Douglas Wilkinson ◽  
Lucy Mackillop
Keyword(s):  
Pregnant Women ◽  
Clinical Features ◽  
Liver Enzymes ◽  
Clinical Course ◽  
Rare Condition ◽  
Intrauterine Death ◽  
Elevated Liver Enzymes ◽  
Hepatic Haematoma ◽  
Capsular Rupture ◽  
In Pregnancy

The syndrome of haemolysis, elevated liver enzymes and low platelets is a rare condition specific to pregnancy, affecting approximately 5–20% of all pre-eclamptic pregnancies. Described here is a woman in her first pregnancy, who experienced an intrauterine death following a significant hepatic haematoma and capsular rupture, in the absence of classical clinical features suggestive of pre-eclampsia. The events that followed suggested haemolysis, elevated liver enzymes and low platelets syndrome as the likely diagnosis. The patient’s clinical course highlights the difficulties that may be encountered when making decisions about pregnant women with complicated medical and obstetric issues.

Are there Pre-Determinants for Elevated Liver Enzymes in Pregnant Women?

2017 ◽  
Vol 152 (5) ◽  
pp. S905-S906
Author(s):  
Michael E. Herman ◽  
Daniel Castaneda ◽  
Rupa L. Iyengar ◽  
Praneet Wander ◽  
Bharat Monga ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Liver Enzymes ◽  
Elevated Liver Enzymes

scholarly journals A 5-Year Clinical Experience of Haemolysis, Elevated Liver Enzymes and Low Platelet Count (HELLP) Syndrome at a Tertiary Care Teaching Hospital in North Karnataka – A Retrospective Analysis

2020 ◽  
Vol 9 (40) ◽  
pp. 2938-2941
Author(s):  
Aruna Mallangouda Biradar ◽  
Rajasri G Yaliwal ◽  
Shreedevi Somashekar Kori ◽  
Gamini B S ◽  
Shivakumar U Pujeri
Keyword(s):  
Intensive Care ◽  
Platelet Count ◽  
Maternal Mortality ◽  
Pregnant Women ◽  
Hellp Syndrome ◽  
Neonatal Intensive Care ◽  
Liver Enzymes ◽  
Class System ◽  
Elevated Liver Enzymes ◽  
Low Platelet Count

BACKGROUND Haemolysis (H), elevated liver enzymes (EL) and low platelet count (LP) i.e., HELLP syndrome is a vaguely understood condition of pregnancy which can present with rapid onset. It is commonly associated with pre - eclampsia. HELLP is also known to manifest itself without the clinical features of pre - eclampsia. The present study aims to assess the maternal and foetal complications associated with HELLP syndrome. METHODS This retrospective study included all the pregnant women who developed HELLP / partial HELLP with gestational age of ≥ 28 weeks. The variables analyzed were obstetric history, menstrual history, antenatal complications, laboratory investigations (haemolysis, ALT / AST, LDH, CBC), mode of delivery, postnatal complications, maternal outcomes and perinatal outcomes. RESULTS 72 patients were included in the present study. The mean age of pregnant women with HELLP syndrome was 23.6 ± 4.15 years. The average age of gestation was 33.17 ± 4.02 weeks. 58 % patients were primigravida. As per Mississippi triple-class system 82 % patients had partial HELLP, 18 % had complete HELLP. 4 %, 4 % & 10 % patients had HELLP class I, II & III respectively. Among the total cases, 74 % patients had antepartum onset, 10 % had intrapartum & 17 % postpartum onset of HELLP syndrome respectively. 65 % patients delivered vaginally & rest 35 % underwent caesarean section. High risk factors such as pre - eclampsia (65 %), eclampsia (3 %) & previous history of HELLP (8 %) were noted in study cases. Abruptio placentae (18 %), postpartum haemorrhage (17 %), pulmonary oedema (14 %), renal failure (14 %) & DIC (7 %) were the maternal complications noted. Maternal mortality was 7 %. The major perinatal morbidities noted were prematurity (67 %) & FGR (42 %). Intrauterine death was noted in 19 % babies. Neonatal intensive care (NICU) was required for 58 % babies, of which 42 % had respiratory distress. Neonatal death was noted in 17 %. CONCLUSIONS HELLP syndrome is a life threatening condition of pregnancy which has serious maternal and perinatal morbidities. Prompt referral, timely and appropriate interventions can save lives. Availability of Intensive Care Units (ICU) facilities, dialysis units and blood and its components along with Neonatal Intensive Care Unit (NICU) facilities can remarkably reduce the maternal and neonatal complications. KEY WORDS HELLP Syndrome, Preeclampsia, Maternal Mortality, Neonatal Mortality, Mississippi Triple - Class System

scholarly journals Cytomegalovirus may mimic the presentation of intrahepatic cholestasis and hemolysis, elevated liver enzymes and low platelets in immunosuppressed pregnant women

2016 ◽  
Vol 9 (3) ◽  
pp. 135-137 ◽  
Author(s):  
Gurleen Wander ◽  
Francesa Neuberger ◽  
Mandish K Dhanjal ◽  
Catherine Nelson-Piercy ◽  
May Ching Soh
Keyword(s):  
Liver Function ◽  
Pregnant Women ◽  
Intrahepatic Cholestasis ◽  
Congenital Abnormalities ◽  
Liver Enzymes ◽  
Liver Function Tests ◽  
Abnormal Liver Function ◽  
Function Tests ◽  
Elevated Liver Enzymes ◽  
Cholestasis Of Pregnancy

Most published cases of cytomegalovirus infection in pregnancy relate to congenital abnormalities in neonates infected in early pregnancy, while the mother remains asymptomatic. We describe a diagnostically challenging case of an immunosuppressed woman with scleroderma who developed deranged liver function tests attributed to intrahepatic cholestasis of pregnancy and haemolysis, elevated liver enzymes and low platelets syndrome but was ultimately found to have disseminated cytomegalovirus. Cytomegalovirus can present in a myriad of ways. Clinicians caring for immunocompromised pregnant women should consider cytomegalovirus as a possible differential diagnosis when reviewing abnormal liver function tests.

Hepatitis A Antigen in Liver, Bile and Stool

1975 ◽  
Vol 33 ◽  
pp. 340-341
Author(s):  
D.R. Jackson ◽  
J.H. Hoofnagle ◽  
A.N. Schulman ◽  
J.L. Dienstag ◽  
R.H. Purcell ◽  
...  
Keyword(s):  
Hepatitis A ◽  
Liver Enzymes ◽  
Hepatitis A Virus ◽  
Type A ◽  
Initial Study ◽  
Virus Like Particle ◽  
Elevated Liver Enzymes ◽  
Ag Particles ◽  
Ag Particle ◽  
Human Stool

Using immune electron microscopy Feinstone et. al. demonstrated the presence of a 27 nm virus-like particle in acute-phase stools of patients with viral hepatitis, type A, These hepatitis A antigen (HA Ag) particles were aggregated by convalescent serum from patients with type A hepatitis but not by pre-infection serum. Subsequently Dienstag et. al. and Maynard et. al. produced acute hepatitis in chimpanzees by inoculation with human stool containing HA Ag. During the early acute disease, virus like particles antigenically, morphologically and biophysically identical to the human HA Ag particle were found in chimpanzee stool. Recently Hilleman et. al. have described similar particles in liver and serum of marmosets infected with hepatitis A virus (HAV). We have investigated liver, bile and stool from chimpanzees and marmosets experimentally infected with HAV. In an initial study, a chimpanzee (no.785) inoculated with HA Ag-containing stool developed elevated liver enzymes 21 days after exposure.

Differential diagnosis of elevated liver enzymes: case reports

2008 ◽  
Vol 46 (05) ◽  
Author(s):  
T Korom ◽  
I Nagy ◽  
É Csajbók ◽  
T Wittmann
Keyword(s):  
Differential Diagnosis ◽  
Liver Enzymes ◽  
Case Reports ◽  
Elevated Liver Enzymes

THE NUCLEAR FACTOR OF HEPATOCYTES 1β (HNF1β)–ASSOCIATED DISEASE. CLINIC, DIAGNOSTIC, TREATMENT (LITERATURE REVIEW AND CLINICAL OBSERVATION)

2019 ◽  
Vol 23 (2) ◽  
pp. 100-108
Author(s):  
S. V. Papizh ◽  
O. R. Piruzieva
Keyword(s):  
Sanger Sequencing ◽  
Clinical Observation ◽  
Liver Enzymes ◽  
Renal Ultrasound ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Renal Hypoplasia ◽  
Unilateral Renal Agenesis ◽  
Elevated Liver Enzymes ◽  
Medullary Nephrocalcinosis

Hepatocyte nuclear factor 1β (HNF1β)-associated disease is a rare autosomal dominant disease caused by various mutations in the HNF1β gene coding the hepatocyte nuclear factor 1β. HNF1β is a transcription factor that is critical for the development of kidney urogenital tract, pancreas, liver, brain, and parathyroid gland. Renal phenotype or HNF1β- nephropathy appeared to be extremely heterogenic: multicystic renal dysplasia, renal hypoplasia, unilateral renal agenesis, horseshoe kidney, atypical familial juvenile hyperuricemic nephropathy, urinary tract malformations and tubular dysfunction. Extrarenal phenotype of HNF1β-associated disease could be maturity-onset diabetes of the young (MODY), pancreatic atrophy and exocrine pancreatic dysfunction, elevated liver enzymes, neonatal cholestasis, congenital abnormalities of the genital tract, hyperparathyroidism, neurological symptoms. The multisystem phenotype makes clinical verification of the diagnosis extremely difficult. In this article, we present a clinical observation of a child with HNF1β – associated disease. The first clinical presentation of HNF1β-associated disease was ultrasound changes in the kidneys (hyperechogenic kidneys?), which were detected by prenatal ultrasonography in pregnancy. Renal ultrasound revealed polycystic kidney disease in the first days of life and bilateral medullary nephrocalcinosis by the age of three. The clinical examination showed a reduced renal function and developed Fanconi syndrome (glycosuria, low molecular proteinuria, hypophosphatemia, aminoaciduria, hyperuricosuria) in the first year of life. Also the child had a non-constant asymptomatic elevation of liver enzymes, hyperparathyroidism, osteoporosis. The diagnosis was confirmed by the results of next generation sequencing which revealed novel heterozygous mutation in exon 4 of the HNF1b gene (chr17: 36091813C>T), p.Cys273Tyr (c.818G>A). The identified mutation was validated by Sanger sequencing. Validation by Sanger sequencing did not reveal a chr17: 36091813C>T mutation in parents, which suggested the appearance of a mutation in the child de novo.

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