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 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 7  |  Issue : 2  |  Page : 104-107

Audit of partial and complete hydatidiform moles in tertiary care hospital in rural inhabitants of India


Department of Pathology, Rural Institute of Medical Science and Research, Safai, Etawah, Uttar Pradesh, India

Date of Web Publication7-Jan-2015

Correspondence Address:
Dr. Seema Dayal
Department of Pathology, Rural Institute of Medical Science and Research, Safai, Etawah, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2349-5006.148810

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  Abstract 

Introduction: The word hydatidiform means drop of water and mole is a shapeless mass. It is an abnormal placenta having enlarged, edematous and vesicular chorionic villi accompanied by variable amount of proliferative trophoblast. It is of two types complete and partial. The diagnosis is based on clinical findings, biochemical markers like human chorionic gonadotropin (HCG) histopathology and genetics. The objective of this study was to determine the frequency, clinical presentation and significance of HCG and histopathology in the diagnosis of hydatidiform mole.
Materials and Methods: Results were measured in terms of age of patients, gestational age, clinical details, investigations specially HCG, histopathology.
Results: Totally 67 specimens were examined and diagnosed, which included 37 cases of complete and 30 cases of partial mole. The common age of patients with complete hydatidiform mole was above 35 years whereas 21-35 years with partial hydatiform mole. Most presenting complaint was bleed/vaginum.
Conclusion: Complete mole was more frequent. Histopathological examination along with clinical findings and HCG is mandatory to differentiate Complete and Partial Mole. The clinical findings may overlap due to earlier removal of hydatiform mole before the clinical symptoms develop even after expulsion of the fetus both of which may result in a false diagnosis. We concluded that there is no single criterion to differentiate Complete from partial mole. P57kip2 expression will complement histopathological evaluation in the diagnosis of difficult cases.

Keywords: Complete hydatidiform mole, human chorionic gonadotropin, hydatidiform mole, partial hydatiform mole, trophoblast hyperplasia


How to cite this article:
Dayal S, Chaturvedi V, Singh A, Negi S. Audit of partial and complete hydatidiform moles in tertiary care hospital in rural inhabitants of India. Indian J Health Sci Biomed Res 2014;7:104-7

How to cite this URL:
Dayal S, Chaturvedi V, Singh A, Negi S. Audit of partial and complete hydatidiform moles in tertiary care hospital in rural inhabitants of India. Indian J Health Sci Biomed Res [serial online] 2014 [cited 2019 May 19];7:104-7. Available from: http://www.ijournalhs.org/text.asp?2014/7/2/104/148810


  Introduction Top


Hydatidiform mole (HM) is an abnormal placenta characterized by enlarged, edematous and vesicular chorionic villi accompanied by a variable amount of proliferative trophoblast. HM also occurs in the  Fallopian tube More Details and ovary even in ectopic pregnancies too. It is subdivided into complete hydatiform mole (CHM) and partial hydatiform mole (PHM) based on morphological, cytogenetic and laboratory investigations. Human chorionic gonadotropin (HCG) is raised in both pregnancies, CHM and PHM. [1] A more ominous behavior associated with no fall of HCG after expulsion of the mole. The diagnosis is based on histopathology and genetic origin. [2] Accurate diagnosis of HM is important, as the risk of persistent gestational trophoblast disease including choriocarcinoma is significantly high. It has been estimated that 1-2% of CHM are followed by a choriocarcinoma. [3] Choriocarcinoma can also be preceded by partial mole, ectopic pregnancy, nonmolar intra uterine abortion or term pregnancy. [4] The incidence rate of HM in United States and Europe is approximately 1 in 1000 to 1 in 2000 pregnancies [5] and in India about 1 in 400 pregnancies. [6] Histopathological examination is the main tool in the diagnosis of molar pregnancy including trophoblastic hyperplasia, villous outline, hydropic swelling, presence of distinct cisterns, nucleated red blood cell (RBC) in fetal vessels. [7] However, there is considerable overlap in the histological features between CHM and PHM resulting in significant inter-observer variability in the diagnosis. [8] Molar pregnancies are being evacuated early in gestation, before the development of well-established classical morphological features, thus adding to difficulties in diagnosis. Thus, this study was planned with the aim to determine the frequency, clinical findings and laboratory investigations including HCG histopathological evaluation of HM from this part of India. However, to our knowledge, such analysis of hydatidiform moles in rural India has not been performed.


  Materials and Methods Top


This is a retrospective study conducted in Department of Pathology at Rural Institute of Medical Science and Research Safai, Etawah, Uttar Pradesh from January 2008 to July 2014. Predesigned proforma was filled at the time of presentation that included patient's detail with molar pregnancy. All the details were analyzed regarding age of patients, gestational age, signs and symptoms, HCG markers, histopathology and other relevant investigations, clinical details such as intake of oral contraceptive, frequency of molar pregnancy, abortion and socioeconomic status of patients were also included.

All patients of molar pregnancies have elevated β-HCG. Histopathological examination was attempted in all cases, even when material was scanty. Gross and section of the sample was done. Sections were taken at 4 μ and additional sections if required were also included. Sections were stained with H and E. Ethical approval was obtained from the institutional ethical committee.


  Results Top


There were 67 cases of molar pregnancies in which definite diagnosis were made and included in this study. Among the 67 molar pregnancies, 37 were diagnosed as the case of CHM whereas 30 were diagnosed as PHM. The study period was from 1 st January to July 2014. Patients with CHM were aged above 35 years. 30 (81.08%) patients were above 35 years of age 6 (16.21%) were of 21-35 years 1 (2.70%) of below 20 years of age. With PHM majority of patients aged between 21 and 35 years 22 (73.33%), 4 (13.33%) each of 20 years and above 35 years [Table 1]. The socioeconomic status of patients in both the groups were low CHM 31 (62%), PHM 19 (38%), followed by middle class CHM 7 (63.63%) and PHM 4 (36.36%). High socioeconomic status was found in least number of cases 4 (66.66%) in CHM and PHM 2 (33.33%) [Table 2]. Gestational age of 10-18 weeks was most common in both CHM 26 (70.27%) and PHM 18 (60%) followed by 19-25 weeks, which was found 7 (18.91%) in CHM, 9 (30%) in PHM, only 4 (10.81%) cases were above 25 weeks of gestation, which was among CHM and in PHM 3 (10%) [Table 3]. The most common presenting clinical symptom was bleeding per vaginum. The other findings such as heavy bleeding, toxiemia of pregnancy, uterus size for dates, hyperthyroidism was found less likely in PHM [Table 4]. Histopathological findings of HM were villous contour, cisterns, trophoblast proliferation and presence of nucleated RBC in fetal vessels [Figure 1] and [Figure 2]. These findings were found more prominent in CHM in comparison with PHM [Table 5].
Figure 1: H&E stained (10x) section showing hydropic degeneration of chorionic villi and trophoblast proliferation but less prominent

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Figure 2: Caption: H&E stained (10x)section showing hydropic degeneration of chorionic villi and marked trophoblast proliferation

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Table 1: Hydatiform mole patient's age of presentation

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Table 2: The socioecnomic status of HM patients

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Table 3: Gestational age of presentation

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Table 4: Clinical findings of HM patients

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Table 5: H/P findings in HM

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  Discussion Top


Swollen, edematous, grape like chorionic villi with trophoblastic hyperplasia is termed as HM. [9] It is also described as degenerative lesion though capable of neoplastic change. [10] All molar pregnancies result from abnormal fertilization. HM may also occur in the fallopian tube and ovary. It is subdivided into complete HM and partial HM based on the morphologic, cytogenetic and clinicopathologic features. Most of molar pregnancies are complete. [11] Our results are also in favor, as we have diagnosed (55.22%) molar pregnancies as complete. Partial molar pregnancies are approximately 25-43%. [12] Our results are quite similar as we have diagnosed 44.77% molar pregnancies as partial mole. Women who are sexually active are at risk for developing gestational trophoblastic disease, but the incidence is substantially higher in women before 20 and after 40 years. [9] In present study among CHM, 30 (81.08%) patients were above 35 years of age and only one patient below and of 20 years age whereas as in patients of partial mole, the age of most common presentation was 21-35 years in that 22 (73.33%) and 4 (13.33%) at 20 years, and 4 (13.33%) above 35 respectively [Table 1]. The low socioeconomic conditions or dietary factors may contribute to the development of gestational trophoblastic disease. [13] The high incidence in Asia is generally attributed to low socioeconomic status and malnutrition. Dietary deficiency in protein, folic acid, iron and environmental factors are incriminated in etiology. Decrease of folic acid in diet predisposes to abnormal trophoblastic proliferation. Majority of our patients 50 (74.62%) that is, 31 (62%) in CHM and 19 (38%) in PHM had low socioeconomic status [Table 2]. In the rural population of developing country like India, living condition and social status are miserable and women are neglected members of family in villages. PHM usually present between 18 and 20 weeks of gestation whereas CHM present between 11 and 25 weeks of pregnancy with vaginal leaking. [14] In this study, molar pregnancy mostly presented at 10-18 weeks of pregnancy CHM 26 (70.27%) and PHM 18 (60%) [Table 3]. The severity of symptoms such as heavy bleeding, toxemia of pregnancy, uterine size for dates, hyperthyroid were more prominent in complete mole than partial. [15] Similar results were found in this study [Table 4]. The single most significant investigation is the serial determination of HCG, which is increased in blood and urine when compared with normal pregnancy. However, more ominous behavior is associated with no fall in HCG after expulsion of the mole. Now a days molar pregnancies are diagnosed earlier because of the routine use of ultrasound. Moreover, molar pregnancies are being evacuated early in gestation, before the development of well-established classical morphological features, causing overlap of symptoms thus adding to the difficulties in diagnosis. The differential diagnosis between CHM and PHM is primarily based on histological features. Up to 80% of cases are first diagnosed by histologic study of spontaneously passed or curetted tissue. Histopathological examination is the main tool in the diagnosis of molar pregnancy including degree of trophoblast hyperplasia, villous outline, hydropic swelling, cistern and fetal vessels in villous outline [Table 5]. Some time there is much overlap in the histologic appearance of CHM and PHM and even experienced pathologist may have difficulty in differentiating between them. Immunohistochemical stain with the P57kip2 antibody can be helpful in the differential diagnosis of CHM. Expression of P57kip2, a maternally imprinted gene is either absent or low in intermediate trophoblast in cases of CHM in contrast to diffuse staining in PHM and nonmolar placentas. [16] It was shown to be a highly specific and sensitive marker. Molecular genetic analysis including Polymorphic markers, fluorescence in situ hybridization and flow cytometry from paraffin embedded tissue may be helpful in classifying cases that do not clearly fall into the category of CHM, PHM or nonmolar hydropic abortion based on morphologic feature alone. Chromosomal analysis and flow cytometric studies of ploidy in molar gestations indicate that cytogenetic distinctions between CHM and PHM are not always clear cut. There are lots of parameters which can used be to differentiate CHM and PHM but clinical findings with histopathology are the main diagnostic tools, whereas P57kip2 being the most specific can complement the difficult undiagnosed cases.


  Conclusion Top


Clinical findings may overlap because of early evacuation of molar pregnancy before the development of well-established clinical symptoms and even no fall in HCG is also seen even after expulsion of mole. Histopathological examination is diagnostic tool to differentiate CHM and PHM. Sometime features are less striking and overlap. P57kip2 being the highly specific and sensitive marker. P57kip2 expression will complement histopathologic evaluation in the diagnosis of difficult cases.

 
  References Top

1.
Chistopher CP. The female genital tract. Robbins and Cotran Pathologic Basis of Disease. 7 th ed. New Delhi, India: Saunders Elsevier; 2007.  Back to cited text no. 1
    
2.
Fisher RA, Hodges MD, Rees HC, Sebire NJ, Seckl MJ, Newlands ES, et al. The maternally transcribed gene p57(KIP2) (CDNK1C) is abnormally expressed in both androgenetic and biparental complete hydatidiform moles. Hum Mol Genet 2002;11:3267-72.  Back to cited text no. 2
    
3.
Benirscheke K, Kaufmann P. Pathology of the Human Placenta. 4 th ed. New York: Springer; 2002.  Back to cited text no. 3
    
4.
Olive DL, Lurain JR, Brewer JI. Choriocarcinoma associated with term gestation. Am J Obstet Gynecol 1984;148:711-6.  Back to cited text no. 4
    
5.
Craighill MC, Cramer DW. Epidemiology of complete molar pregnancy. J Reprod Med 1984;29:784-7.  Back to cited text no. 5
    
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Dutta DC. Text Book of Obstetrics. 4 th ed. Calcutta: New Central Book Agency; 1998.  Back to cited text no. 6
    
7.
Hoffner L, Dunn J, Esposito N, Macpherson T, Surti U. P57KIP2 immunostaining and molecular cytogenetics: Combined approach aids in diagnosis of morphologically challenging cases with molar phenotype and in detecting androgenetic cell lines in mosaic/chimeric conceptions. Hum Pathol 2008;39:63-72.  Back to cited text no. 7
    
8.
Jaffar R, Kalsoom R, Quershi A. Histopathological review of partial and complete hydatidiform moles in a tertiary care hospital. Biomedica 2011;27:76-80.  Back to cited text no. 8
    
9.
LeGallo RD, Stelow EB, Ramirez NC, Atkins KA. Diagnosis of hydatidiform moles using p57 immunohistochemistry and HER2 fluorescent in situ hybridization. Am J Clin Pathol 2008;129:749-55.  Back to cited text no. 9
    
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Mandal AK, Shramana C. Textbook of Pathology. 1 st ed. New Delhi: Avichal Publication; 2010.  Back to cited text no. 10
    
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Jaun R. Rosai and Ackerman's Pathology. 9 th ed. St. Louis: Mosby; 2004.  Back to cited text no. 11
    
12.
Szulman AE, Surti U. The clinicopathologic profile of the partial hydatidiform mole. Obstet Gynecol 1982;59:597-602.  Back to cited text no. 12
    
13.
Berkowitz RS, Cramer DW, Bernstein MR, Cassells S, Driscoll SG, Goldstein DP. Risk factors for complete molar pregnancy from a case-control study. Am J Obstet Gynecol 1985;152:1016-20.  Back to cited text no. 13
    
14.
Baergen RN, Benirschke K. Silverbergs Principles and Practice of Surgical Pathology and Cytopathology. 4 th ed. Philadelphia: Churchill Living Stone Elsevier; 2006.  Back to cited text no. 14
    
15.
Ming IE, Micheal TM, Robert K. Sternberg's Diagnostic Surgical Pathology. 4 th ed. Philadelphia: Lippincott Williams and Wilkins; 2004.  Back to cited text no. 15
    
16.
Chilosi M, Piazzola E, Lestani M, Benedetti A, Guasparri I, Granchelli G, et al. Differential expression of p57kip2, a maternally imprinted cdk inhibitor, in normal human placenta and gestational trophoblastic disease. Lab Invest 1998;78:269-76.  Back to cited text no. 16
    


    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

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