World Rural Health Conference
Home Print this page Email this page Small font size Default font size Increase font size
Users Online: 482
Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents 
CASE REPORT
Year : 2019  |  Volume : 8  |  Issue : 1  |  Page : 280-284  

Abdelazim and AbuFaza ELLP syndrome as a variant of HELLP syndrome: Case reports


1 Department of Obstetrics and Gynecology, Ahmadi Hospital, Kuwait Oil Company, Ahmadi, Kuwait; Department of Obstetrics and Gynecology, Ain Shams University, Cairo, Egypt
2 Department of Obstetrics and Gynecology, Ahmadi Hospital, Kuwait Oil Company, Ahmadi, Kuwait

Date of Web Publication31-Jan-2019

Correspondence Address:
Ibrahim A Abdelazim
Department of Obstetrics and Gynecology, Ain Shams University, Cairo, Egypt and Ahmadi Kuwait Oil (KOC) Company Hospital, P.O. Box: 9758, Ahmadi - 61008

Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jfmpc.jfmpc_381_18

Rights and Permissions
  Abstract 


Background: The hemolysis, elevated liver enzymes, low platelet count (HELLP) syndrome is a serious complication in pregnancy occurring in 0.5–0.9% of all pregnancies and in 10–20% of cases with severe pre-eclampsia. Previous studies described HELLP syndrome without hemolysis without any further details. Objectives: This report represents the criteria for the diagnosis of Abdelazim and AbuFaza elevated liver enzymes, low platelet count (ELLP) syndrome as a variant of HELLP syndrome. Case Reports: A 39-year-old woman, pregnant 32 weeks' gestation, previous five cesarean sections, admitted with severe pre-eclampsia (blood pressure 160/110 mmHg, proteinuria +3, 700 mg proteins/24 h urine, and protein/creatinine ratio ≥0.9 in spot urine sample). Laboratory investigation showed elevated liver enzymes, low platelet (PLT) count, and no evidence of hemolysis. A 31-year-old woman, pregnant 33+4 weeks' gestation, previous one cesarean section, admitted with severe pre-eclampsia (blood pressure 170/120 mmHg, proteinuria +2, 1200 mg proteins/24 h urine, and protein/creatinine ratio 1.1 in spot urine sample). Laboratory investigations showed elevated liver enzymes, low PLT count, and no evidence of hemolysis. Both patients delivered by cesarean section after stabilization of their blood pressure and dexamethasone for induction of fetal lung maturity and MgSO4 for prevention of eclampsia. Both patients had uneventful intraoperative and postoperative stay in the hospital. The liver enzymes and the PLT count were completely normal on the 5th postoperative day, and they were discharged from the hospital in good general condition. Conclusion: Abdelazim and AbuFaza ELLP syndrome is variant of HELLP syndrome without hemolysis in women with severe pre-eclampsia. Abdelazim and AbuFaza ELLP syndrome diagnostic criteria are as follows: (1) Elevated liver enzymes; (2) Low PLT count; and (3) Absence of hemolysis (normal total and unconjugated bilirubin, absence of schizocytes, and polychromatic red cells in peripheral blood smear, and normal reticulocyte count).

Keywords: Abdelazim, AbuFaza, ELLP, HELLP, hemolysis


How to cite this article:
Abdelazim IA, AbuFaza M. Abdelazim and AbuFaza ELLP syndrome as a variant of HELLP syndrome: Case reports. J Family Med Prim Care 2019;8:280-4

How to cite this URL:
Abdelazim IA, AbuFaza M. Abdelazim and AbuFaza ELLP syndrome as a variant of HELLP syndrome: Case reports. J Family Med Prim Care [serial online] 2019 [cited 2019 Feb 22];8:280-4. Available from: http://www.jfmpc.com/text.asp?2019/8/1/280/251176




  Introduction Top


Weinstein in 1982 defined the HELLP syndrome (H = Hemolysis, EL = Elevated liver enzymes, and LP = Low platelets) syndrome.[1] HELLP syndrome considered a complication of severe pre-eclampsia.[2],[3],[4],[5] The diagnosis of HELLP syndrome requires the presence of the three major components of the syndrome, whereas partial or incomplete HELLP syndrome consists of only one or two elements of the triad (H or EL or LP).[6]

HELLP syndrome is a serious condition in its complete form and associated with maternal and fetal risks.[7],[8]

HELLP syndrome occurs in about 0.5–0.9% of all pregnancies and in 10–20% of severe pre-eclampsia.[9] The majority of women with the HELLP syndrome have had hypertension and proteinuria, which may be absent in 10–20% of the cases.[5]

Women with partial HELLP syndrome have absent one or two elements of the HELLP triad (H or EL or LP). However, partial or incomplete HELLP syndrome may progress to complete form of the disorder.[4]

The three components of the HELLP syndrome are hemolysis, elevated liver enzymes, and thrombocytopenia. Hemolysis is one of the major component of the disorder and is due to a microangiopathic hemolytic anemia. Red cell fragmentation caused by high-velocity passage through damaged endothelium of the small vessels. The presence of fragmented schizocytes in the peripheral blood smear reflects the hemolytic process.[10] Polychromatic red cells in blood smears and increased reticulocyte count reflect the compensatory release of immature red cells from the bone marrow.[11]

Hemoglobin released from hemolysis of the red cells converted to unconjugated bilirubin in the spleen or may be bound in the plasma by haptoglobin. The hemoglobin-haptoglobin complex is cleared quickly by the liver, leading to low or undetectable haptoglobin levels in the blood.[11] Low haptoglobin concentration can be used to diagnose hemolysis and is the preferred marker of hemolysis.[12],[13],[14] Thus, the diagnosis of hemolysis supported by high Lactate dehydrogenase (LDH) concentration and the presence of unconjugated bilirubin, but the low or undetectable haptoglobin concentration is more specific indicator of hemolysis.[12],[13],[14]

Hemolysis contributes substantially to the elevated levels of LDH, whereas increased asparate aminotransferase (AST) and alanine aminotransferase (ALT) levels are mostly because of liver injury. Plasma glutathione S-transferase-A1 (GST-A1) is more sensitive indicator for acute liver damage than AST and ALT.[14]

Thrombocytopenia [platelets (PLTs) <150 × 103/mm 3] in pregnancy may be caused by gestational thrombocytopenia, immune thrombocytopenic purpura (ITP), pre-eclampsia, and HELLP syndrome.[15] Decreased PLT count in the HELLP syndrome is due to increased PLT consumption.[10]

At present, there are two major definitions for diagnosing the HELLP syndrome. In the Tennessee Classification System, Sibai proposed strict criteria for “true” or “complete” HELLP syndrome, which includes PLTs ≤100 × 103/mm 3, AST ≥70 IU/L, and LDH ≥600 IU/L.[5] Intravascular hemolysis diagnosed by abnormal peripheral blood smear, increased serum bilirubin (≥20.5 μmol/l or ≥ 1.2 mg/100 ml), and elevated LDH levels (>600 IU/l).[16]

The Mississippi-Triple Class System of HELLP syndrome depending on the low PLT count during the course of the syndrome.[4] Class 1 and Class 2 associated with hemolysis (LDH >600 IU/l) and elevated AST (≥70 IU/l), whereas Class 3 requires LDH >600 IU/l and AST ≥40 IU/l, in addition to the specific PLT count.[17] Class 3 HELLP syndrome considered as a clinical transition stage or a progression phase of the HELLP syndrome.[17]

The HELLP syndrome can be diagnosed simply on biochemical evidence.[18],[19],[20] Some authors require the presence of severe pre-eclampsia together with the biochemical markers to diagnose HELLP.[20],[21],[22],[23]


  Case Reports Top


A 39-year-old woman, pregnant 32 weeks' gestation, previous five cesarean sections, diabetic on oral hypoglycemic medications, admitted to Ahmadi hospital, Kuwait oil company (KOC) with severe pre-eclampsia (blood pressure 160/110 mmHg measured twice 6 h apart, lower limbs edema, headache, exaggerated ankle and knee reflexes, proteinuria +3 using urine dipsticks, 700 mg proteins/24 h urine, and protein/creatinine ratio ≥0.9 in spot urine sample).

Laboratory investigation showed elevated liver enzymes (ALT 211 IU/l, AST 432 IU/l, and LDH 670 IU/l), low PLT count 67 × 103, and no evidence of hemolysis.

Ultrasound fetal assessment showed single intrauterine pregnancy matching with her dates and estimated fetal weight (EFW) 1.700 Kg.

A 31-year-old woman, pregnant 33+4 weeks' gestation, previous one cesarean section on oral thyroxine for treatment of hypothyroidism, admitted to Ahmadi hospital, KOC with severe pre-eclampsia (blood pressure 170/120 mmHg measured twice 6 h apart, lower limbs edema, headache, epigastric pain, proteinuria +2 using urine dipsticks, 1200 mg of proteins/24 h urine and protein/creatinine ratio 1.1 in spot urine sample).

Laboratory investigations showed elevated liver enzymes (ALT 292 IU/l, AST 437 IU/l, and LDH 720 IU/l), low PLT count 56 × 103, and no evidence of hemolysis.

Ultrasound fetal assessment showed single intrauterine pregnancy matching with her dates with EFW 1.850 Kg.

Both patients delivered by cesarean section after stabilization of their blood pressure and dexamethasone for induction of fetal lung maturity [24] and MgSO4 for fetal neuroprotection and for prevention of eclampsia.[25] Both patients had uneventful intraoperative and postoperative stay in the hospital. The liver enzymes and the PLT count were completely normal on the 5th postoperative day, and they were discharged from the hospital in good general condition.


  Discussion Top


The HELLP syndrome may be misdiagnosed as viral hepatitis, cholangitis, and other serious conditions such as idiopathic thrombocytopenic purpura (ITP), acute fatty liver of pregnancy (AFLP), hemolytic uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), and systemic lupus erythematosus (SLE).[16]

AFLP typically occurs between the 30th and 38th gestational weeks with history of malaise, vomiting, epigastric or right upper abdominal pain, and jaundice, whereas hypertension and proteinuria are usually absent. AFLP usually associated with low grade disseminated intravascular coagulation (DIC), prolonged prothrombin time, and partial thromboplastin time, low fibrinogen, and anti-thrombin concentrations.[14]

ITP is a syndrome with thrombocytopenia, which may be manifested by bleeding disorder with purpura and petechiae. Pregnancy does not increase the incidence of ITP and even with a very low PLT count, most cases of ITP not associated with neither maternal nor fetal morbidity.[26],[27]

HUS and TTP are thrombotic microangiopathies that share some characteristics of the HELLP syndrome such as endothelial injury, PLT aggregation, micro-thrombi, thrombocytopenia, and anemia.[28]

The microvascular injury in HUS affects mainly the kidneys with signs and symptoms of renal failure. However, most cases of HUS appear in children and adolescents and caused by specific enterotoxin produced by  Escherichia More Details coli O157:H7.[29]

TTP is an extremely rare condition during pregnancy characterized by neurological dysfunction, abdominal pain, and bleeding. The spectrum of neurological abnormalities include headache, visual disturbances, transient paresis, and seizures.[30]

SLE is an autoimmune disorder characterized by deposits of antigen-antibody complexes in capillaries of multiple organs (kidneys, lungs, heart, liver, and brain). The clinical and laboratory findings in lupus nephritis are similar to those of severe pre-eclampsia. Antiphospholipid antibodies (APA; lupus anticoagulant and/or anticardiolipin antibodies) are present in 30–40% of the cases, whereas thrombocytopenia occurs in 40–50% and hemolytic anemia in 14–23% of women with SLE. Cerebral symptoms may develop because of vasculitis and/or cerebro-vascular occlusion that might lead to seizures.[5] APA associated with recurrent thrombosis and pregnancy loss. Antiphospholipid syndrome may also occur as a primary disease unrelated to SLE.[31]

Clinical symptoms such as headache, visual changes, epigastric pain, and nausea-vomiting have been suggested to be better predictors of adverse maternal outcome in HELLP syndrome.[32]

Spontaneous rupture of a sub-capsular liver hematoma in pregnancy is a rare, but life threatening complication that occurs in about 1% to < 2% of the cases with the HELLP syndrome.[33]

Abruptio-placentae, DIC, and subsequent severe post-partum bleeding are more common serious maternal complications with HELLP syndrome.[5] Bilateral permanent visual loss associated with retinopathy is a rare ophthalmic complication of HELLP syndrome.[34] In the literature, there are several case reports of cerebral bleeding associated with the HELLP syndrome.[35],[36] Wound hematoma and infection are frequent complications in women with the HELLP syndrome undergoing cesarean delivery.[37]

Abruptio-placentae associated with the HELLP syndrome increases the risk of DIC as well as the risk of renal failure and blood transfusion.[38] Cerebral hemorrhage or stroke found to be the primary cause of death in 26% of HELLP syndrome.[39] The perinatal mortality rate related to the HELLP syndrome is ranging from 7.4% to 34%.[39] According to Gulet al., the perinatal mortality was 34% before 32 weeks' gestation and 8% after the 32nd week.[40] Prematurity, placental insufficiency, with or without intrauterine growth restriction, and abruptio-placentae are the main causes of neonatal death.

The studied women had severe pre-eclampsia diagnosed by (1) High blood pressure ≥160/110 mm Hg measured twice 6 h apart. (2) Significant proteinuria using urine dipsticks, ≥500 mg of proteins/24 h urine, and protein/creatinine ratio ≥0.9 in spot urine sample. (3) Symptoms in form of headache, epigastric pain, and/or exaggerated ankle and knee reflexes.

Laboratory investigations of the studied women showed elevated liver enzymes (ALT, AST, and LDH) and low PLT count. The presence of hemolysis excluded by normal bilirubin (total and unconjugated) and absence of schizocytes, and polychromatic red cells in blood smear, and normal reticulocyte count.[10]

Chhabraet al., described the partial HEELP as a syndrome contains only one or two of the three components HELLP syndrome.[41] Roelofsenet al., described the ELLP syndrome as HELLP syndrome without hemolysis in a retrospective study investigating the maternal-fetal outcome after pregnancies complicated by (H) ELLP syndrome.[42]

A number of studies have included women with HELLP syndrome without evidence of hemolysis without further details.[43],[44]

Abdelazim and AbuFaza ELLP syndrome is variant of HELLP syndrome without hemolysis in women with severe pre-eclampsia. Abdelazim and AbuFaza ELLP syndrome diagnostic criteria are as follows: (1) Elevated liver enzymes; (2) Low PLT count; and (3) Absence of hemolysis (normal total and unconjugated bilirubin, absence of schizocytes, and polychromatic red cells in peripheral blood smear, and normal reticulocyte count).

In general, there are three major options for the management of women with severe pre-eclampsia and HELLP syndrome.[14]

These include (1) Immediate delivery if HELLP syndrome diagnosed at ≥34 weeks' gestation; (2) Delivery after stabilization of the maternal condition within 48 h if HELLP syndrome diagnosed at 27–34 weeks' gestation; and (3) Expectant (conservative) management for >48–72 h may be considered if HELLP syndrome diagnosed before 27 weeks' gestation.[14]

Both studied women delivered by cesarean section after stabilization of their blood pressure and dexamethasone for induction of fetal lung maturity [24] and MgSO4 for fetal neuroprotection and for prevention of eclampsia.[25] Both patients had uneventful intraoperative and postoperative stay in the hospital. The liver enzymes and the PLT count were completely normal on the 5th postoperative day, and they were discharged from the hospital in good general condition.

This report represents the diagnostic criteria of Abdelazim and AbuFaza ELLP syndrome as a variant of HELLP syndrome without hemolysis, and large studies are going on to confirm the diagnostic criteria of the syndrome.


  Conclusion Top


Abdelazim and AbuFaza ELLP syndrome is variant of HELLP syndrome without hemolysis in women with severe pre-eclampsia. Abdelazim and AbuFaza ELLP syndrome diagnostic criteria are as follows: (1) Elevated liver enzymes; (2) Low PLT count; and (3) Absence of hemolysis (normal total and unconjugated bilirubin, absence of schizocytes, and polychromatic red cells in peripheral blood smear, and normal reticulocyte count).

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Acknowledgments

The authors are grateful to the studied women for their agreement and consent to participate in this presentation [signed consent taken from the studied women].

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Weinstein L. Syndrome of hemolysis, elevated liver enzymes, and low platelet count: A severe consequence of hypertension in pregnancy. 1982. Am J Obstet Gynecol 2005;193:859.  Back to cited text no. 1
    
2.
Celik C, Gezginc K, Altintepe L, Tonbul HZ, Yaman ST, Akyurek C, et al. Results of the pregnancies with HELLP syndrome. Ren Fail 2003;25:613-8.  Back to cited text no. 2
    
3.
Ertan AK, Wagner S, Hendrik HJ, Tanriverdi HA, Schmidt W. Clinical and biophysical aspects of HELLP-syndrome. J Perinat Med 2002;30:483-9.  Back to cited text no. 3
    
4.
Martin JN Jr, Rose CH, Briery CM. Understanding and managing HELLP syndrome: The integral role of aggressive glucocorticoids for mother and child. Am J Obstet Gynecol 2006;195:914-34.  Back to cited text no. 4
    
5.
Sibai BM. Diagnosis, controversies, and management of the syndrome of hemolysis, elevated liver enzymes, and low platelet count. Obstet Gynecol 2004;103:981-91.  Back to cited text no. 5
    
6.
Barton JR, Sibai BM. Diagnosis and management of hemolysis, elevated liver enzymes, and low platelets syndrome. Clin Perinatol 2004;31:807-33.  Back to cited text no. 6
    
7.
Matsuda M, Mitsuhashi S, Watarai M, Yamamoto K, Hashimoto T, Ikeda S. Hemolysis, elevated liver enzymes and low platelet (HELLP) syndrome associated with systemic lupus erythematosus. Intern Med 2003;42:1052-3.  Back to cited text no. 7
    
8.
Murphy MA, Ayazifar M. Permanent visual deficits secondary to the HELLP syndrome. J Neuroophthalmol 2005;25:122-7.  Back to cited text no. 8
    
9.
Karumanchi SA, Maynard SE, Stillman IE, Epstein FH, Sukhatme VP. Preeclampsia: A renal perspective. Kidney Int 2005;67:2101-13.  Back to cited text no. 9
    
10.
Baxter JK, Weinstein L. HELLP syndrome: The state of the art. Obstet Gynecol Surv 2004;59:838-45.  Back to cited text no. 10
    
11.
Wilke G, Rath W, Schutz E, Armstrong VW, Kuhn W. Haptoglobin as a sensitive marker of hemolysis in HELLP-syndrome. Int J Gynaecol Obstet 1992;39:29-34.  Back to cited text no. 11
    
12.
Rath W, Faridi A, Dudenhausen JW. HELLP syndrome. J Perinat Med 2000;28:249-60.  Back to cited text no. 12
    
13.
Deruelle P, Coudoux E, Ego A, Houfflin-Debarge V, Codaccioni X, Subtil D. Risk factors for post-partum complications occurring after preeclampsia and HELLP syndrome. A study in 453 consecutive pregnancies. Eur J Obstet Gynecol Reprod Biol 2006;125:59-65.  Back to cited text no. 13
    
14.
Haram K, Svendsen E, Abildgaard U. The HELLP syndrome: Clinical issues and management. A Review. BMC Pregnancy Childbirth 2009;9:8.  Back to cited text no. 14
    
15.
Parnas M, Sheiner E, Shoham-Vardi I, Burstein E, Yermiahu T, Levi I, et al. Moderate to severe thrombocytopenia during pregnancy. Eur J Obstet Gynecol Reprod Biol 2006;128:163-8.  Back to cited text no. 15
    
16.
Sibai BM. Imitators of severe pre-eclampsia/eclampsia. Clin Perinatol 2004;31:835-52.  Back to cited text no. 16
    
17.
Martin JN Jr, Rinehart BK, May WL, Magann EF, Terrone DA, Blake PG. The spectrum of severe preeclampsia: Comparative analysis by HELLP (hemolysis, elevated liver enzyme levels, and low platelet count) syndrome classification. Am J Obstet Gynecol 1999;180:1373-84.  Back to cited text no. 17
    
18.
Osmanagaoglu MA, Osmanagaoglu S, Ulusoy H, Bozkaya H. Maternal outcome in HELLP syndrome requiring intensive care management in a Turkish hospital. Sao Paulo Med J 2006;124:85-9.  Back to cited text no. 18
    
19.
Svenningsen R, Morken NH, Kahn JA. Corticosteroids in the treatment of HELLP-syndrome? Tidsskr Nor Laegeforen 2006;126:2253-6.  Back to cited text no. 19
    
20.
Aldemir M, Baç B, Taçyildiz I, Yağmur Y, Keleş C. Spontaneous liver hematoma and a hepatic rupture in HELLP syndrome: Report of two cases. Surg Today 2002;32:450-3.  Back to cited text no. 20
    
21.
Giannubilo SR, Tranquilli AL, Santolini C, Prinicipi F, Mancinelli R, Littarru GP. Placental CoQ10 levels in HELLP syndrome. Biofactors 2005;25:159-63.  Back to cited text no. 21
    
22.
Smulian J, Shen-Schwarz S, Scorza WE, Kinzler WL, Vintzileos AM. A clinicohistopathological comparison between HELLP syndrome and severe preeclampsia. J Matern Fetal Neonatal Med 2004;16:287-93.  Back to cited text no. 22
    
23.
Tranquilli AL, Giannubilo SR, Tedeschi E, Bezzeccheri V, Suzuki H, Menegazzi M. Placental expression of nitric oxide synthase during HELLP syndrome: The correlation with maternal-fetal Doppler velocimetry. Acta Obstet Gynecol Scand 2005;84:849-53.  Back to cited text no. 23
    
24.
Abdelazim I, Farghali MM, Elbiaa AA, Abdelrazak KM, Hussain M, Yehia AH, et al. Impact of antenatal oxytocin infusion on neonatal respiratory morbidity associated with elective cesarean section. Arch Med Sci 2017;13:629-34.  Back to cited text no. 24
    
25.
Abdelazim IA, Shikanova S, Kanshaiym S, Karimova B, Sarsembayev M, Starchenko T. Cesarean section scar dehiscence during pregnancy: Case reports. J Family Med Prim Care 2018;7:1561-5. Doi: 10.4103/jfmpc.jfmpc_361_18.  Back to cited text no. 25
  [Full text]  
26.
Haram K, Søfteland E, Hervig T, Pirhonen J. Thrombocytopaenia in pregnancy. Tidsskr Nor Laegeforen 2003;123:2250-2.  Back to cited text no. 26
    
27.
Sukenik-Halevy R, Ellis MH, Fejgin MD. Management of immune thrombocytopenic purpura in pregnancy. Obstet Gynecol Surv 2008;63:182-8.  Back to cited text no. 27
    
28.
Groot E, de Groot PG, Fijnheer R, Lenting PJ. The presence of active von Willebrand factor under various pathological conditions. Curr Opin Hematol 2007;14:284-9.  Back to cited text no. 28
    
29.
Franchini M. Thrombotic microangiopathies: An update. Hematology 2006;11:139-46.  Back to cited text no. 29
    
30.
Mayer SA, Aledort LM. Thrombotic microangiopathy: Differential diagnosis, pathophysiology and therapeutic strategies. Mt Sinai J Med 2005;72:166-75.  Back to cited text no. 30
    
31.
Le Thi TD, Tieulie N, Costedoat N, Andreu MR, Wechsler B, Vauthier-Brouzes D, et al. The HELLP syndrome in the antiphospholipid syndrome: Retrospective study of 16 cases in 15 women. Ann Rheum Dis 2005;64:273-8.  Back to cited text no. 31
    
32.
Cavkaytar S, Ugurlu EN, Karaer A, Tapisiz OL, Danisman N. Are clinical symptoms more predictive than laboratory parameters for adverse maternal outcome in HELLP syndrome? Acta Obstet Gynecol Scand 2007;86:648-51.  Back to cited text no. 32
    
33.
Wicke C, Pereira PL, Neeser E, Flesch I, Rodegerdts EA, Becker HD. Sub-capsular liver hematoma in HELLP syndrome: Evaluation of diagnostic and therapeutic options-a unicenter study. Am J Obstet Gynecol 2004;190:106-12.  Back to cited text no. 33
    
34.
Stewart MW, Brazis PW, Guier CP, Thota SH, Wilson SD. Purtscher-like retinopathy in a patient with HELLP syndrome. Am J Ophthalmol 2007;143:886-7.  Back to cited text no. 34
    
35.
Altamura C, Vasapollo B, Tibuzzi F, Novelli GP, Valensise H, Rossini PM, et al. Postpartum cerebellar infarction and haemolysis, elevated liver enzymes, low platelet (HELLP) syndrome. Neurol Sci 2005;26:40-2.  Back to cited text no. 35
    
36.
Zeidman LA, Videnovic A, Bernstein LP, Pellar CA. Lethal pontine hemorrhage in postpartum syndrome of hemolysis, elevated liver enzyme levels, and low platelet count. Arch Neurol 2005;62:1150-3.  Back to cited text no. 36
    
37.
Curtin WM, Weinstein L. A review of HELLP syndrome. J Perinatol 1999;19:138-43.  Back to cited text no. 37
    
38.
Drakeley AJ, Le Roux PA, Anthony J, Penny J. Acute renal failure complicating severe preeclampsia requiring admission to an obstetric intensive care unit. Am J Obstet Gynecol 2002;186:253-6.  Back to cited text no. 38
    
39.
Osmanağaoğlu MA, Erdoğan I, Zengin U, Bozkaya H. Comparison between HELLP syndrome, chronic hypertension, and superimposed preeclampsia on chronic hypertension without HELLP syndrome. J Perinat Med 2004;32:481-5.  Back to cited text no. 39
    
40.
Gul A, Cebeci A, Aslan H, Polat I, Ozdemir A, Ceylan Y. Perinatal outcomes in severe preeclampsia-eclampsia with and without HELLP syndrome. Gynecol Obstet Invest 2005;59:113-8.  Back to cited text no. 40
    
41.
Chhabra S, Qureshi A, Datta N. Perinatal outcome with HELLP/partial HELLP complicating hypertensive disorders of pregnancy. An Indian rural experience. J Obstet Gynaecol 2006;26:531-3.  Back to cited text no. 41
    
42.
Roelofsen AC, van Pampus MG, Aarnoudse JG. The HELLP-syndrome; maternal-fetal outcome and follow up of infants. J Perinat Med 2003;31:201-8.  Back to cited text no. 42
    
43.
Geary M. The HELLP syndrome. Br J Obstet Gynaecol 1997;104:887-91.  Back to cited text no. 43
    
44.
Sibai BM, Taslimi MM, el-Nazer A, Amon E, Mabie BC, Ryan GM. Maternal-perinatal outcome associated with the syndrome of hemolysis, elevated liver enzymes, and low platelets in severe preeclampsia-eclampsia. Am J Obstet Gynecol 1986;155:501-9.  Back to cited text no. 44
    




 

Top
   
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
   Abstract
  Introduction
  Case Reports
  Discussion
  Conclusion
   References

 Article Access Statistics
    Viewed37    
    Printed2    
    Emailed0    
    PDF Downloaded9    
    Comments [Add]    

Recommend this journal