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Adenomyosis.
Adenomyosis is infrequently diagnosed and its symptomatology is not clearly understood. In spite of long cognizance and many publications,[3], [6], [7], [9] there is still a widespread disagreement as to its incidence, theories of origin, symptomatology and associated pathology. In a bid to unsolve this enigma, the present study was undertaken to determine (1) the incidence of. adenomyosis in surgically removed uteri (2) the functional status of the surface and ectopic endometrium (3) relation to symptomatology and (4) the possible factors causing adenomyosis.
The material for study consisted of surgically removed uteri during a five year period from July 1974 to June 1979 at the B. Y. L. Nair Charitable Hospital, Bombay. Histological sections were prepared by routine paraffin processing and stained by haematoxylin and eosin. In this study, adenomyosis was diagnosed by the presence of normal appearing endometrial glands and stroma, one or more low power fields away from the endometrial myometrial junction. Applying Molitor's[10] criteria, the depth of penetration was graded as follows: Grade I: Penetration of ectopic endometrium into the inner third of the myometrium Grade II: Penetration of ectopic endometrium into the middle third of myometrium. Grade III: Penetration of ectopic endometrium into the outer third of myometrium. Following Bird et al,[4] the degree of involvement was judged according to the number of ectopic glands per low power field (L.P.F.). Mild-1 to 3 glands/L.P.F. Moderate- 4 to 9 glands/L.P.F. Severe-10 or more glands/L.P.F. Relevant clinical findings, status of surface and ectopic endometrium and associated pathological lesions were noted.
In the present series, out of 1,070 uteri studied, adenomyosis was detected in 105 uteri thus giving an incidence of 9.81%. [Table 1] shows the age, parity and number of years after last delivery in 105 cases of adenomyosis. Majority of the patients (50.5%) were between the 4th and 5th decade of life. 54.3% of patients had history of more than four deliveries and 56.2% of cases had their last delivery more than 10 years back. Dysfunctional uterine bleeding was present in 76 out of 105 cases. Prolapse was seen in 28 cases; 14 patients complained of pain in abdomen. Leucorrhea and dysmenorrhea were present in 11 and 10 patients respectively. Post-menopausal P.V. bleeding was present only in 2 cases. 89.5%; of uteri were bulky, 6.7% were normal in size and 3.8 were atrophied. [Table 2] shows the histopathological findings in 105 cases of adenomyosis. [Table 3] shows the clinico-pathological correlation of the patients with menstrual disturbances according to Grade and degree of involvement of the uterus. [Table 4] shows the associated pathological lesions.
The reported incidence of adenomyosis based on unselected hysterectomies and by giving essential routine sections, varies from 16 to 39%[3], [9] ,[10] Such wide variation along with our incidence of 9.8% reflects the incidence in surgical pathology without giving any extra sections. According to Bird et al,[4] the incidence almost doubles if extra sections are studied from various uterine walls. Majority of our patients were between the 4th and the 5th decade of life. The peak incidence reported by others[3], [4], [9] is also between the 4th and 5th decades. The incidence of adenomyosis was also found to be snore in multiparous women which tallies with a similar finding of many workers.[2], [3], [12] According to Israel et al,[8] every pregnancy increases the chances of endometrial penetration into myometrium. This could be explained on anatomical basis that because of lack of submucosa in the uterus, endometrial glands penetrate into the myometrium easily and get caught as infoldings into the hypertrophied myometrium when it contracts after delivery. 61.9% of the patients had history of last delivery more than 10 years back. Bhatt[2] had 42% of patients and Rosario[12] had 70.5% of the patients with their last delivery 10, years back in their series. This indicates prolonged action of estrogens uninterrupted by progesterone which may be responsible for the development of adenomyosis. Out of various presenting symptoms, dysfunctional uterine bleeding including menorrhagia and any other type of irregular bleeding was the commonest symptom. Spatt,[13] Baylay and Yates[1] and Bensen and Sneeden[2] have also noted the same. According to Bhatt,[3] menorrhagia is a common symptom after 40 years of age and dysmenorrhoea before 40 years of age. Some of the symptoms may be due to associated lesions, but Hunter and coworkers, believe that adenomyosis without associated lesions can also cause symptoms. Majority of the uteri in our series were bulky. It is not necessary to get bulky uterus in all cases of adenomyosis.[3] Atrophied uteri initially may be bulky, but are gradually atrophied with age.[9] Symptoms of menstrual disturbances, correlated with bulky uterus, may help in clinical diagnosis of adenomyosis. In our series, 6 cases were diagnosed clinically as adenomyosis. Functional response was present in 17 ectopic endometria out of 22 surface endometria showing secretory activity, giving a discrepancy of 22.7%. The ectopic endometrium is believed to be sllightly different from the normally situated endometrium and resembles the glands found in stratum basalis of normal endometrium. Hence, the adenomyosic glands do not participate, to a greater extent, in cyclic hormonal changes and do not respond to progesterone stimulus.[3] However, Novak and Delima[12] believe that occasionally ectopic endometrium exhibits the cyclic functional responsiveness of normal endometrium, but more often it is of an immature, unripe variety. According to Dreyfuss[5] and Hunter[7] ectopic endometrium shows normal picture corresponding to that period of menstrual cycle. Spatt[13] has noted anovulatory endometrium in majority of the cases. Theory of hyperoestrinism uninterrupted by progesterone is again supported by the histological findings of myometrial hyperplasia and oestrogenic response in the glands showing a proliferative phase or cystic hyperplasia. Mathur et al[9] have stressed a lot on cellular infiltration. We have also noted lymphocytic, eosinophilic or mixed infiltration in 23.8% of cases, indicating chronicity of the disease. Fresh haemorrhage or haemosiderin pigment indicating extravasation of blood was seen in 30.5% of cases. [Table 3] shows clinico-pathological correlation between menstrual disturbances and the grade and degree of involvement of adenomyosis. Majority of the patients with menstrual disturbances had Grade II or III penetration and moderate degree of adenomyosis. Menorrhagia was proportional to the degree of involvement i.e. the number of ectopic glands; whereas dysmenorrhoea was proportional to the depth of penetration. 60`x, of cases were seen in Grade III penetration. So, it can be considered that higher the degree and grade of involvement the greater are the menstrual disturbances. Molitor[10] and Bird el al[4] have strongly recommended these criteria and according to Bensen and Sneeden[2] more the menstrual disturbances, larger is the uterus. Israel and Woultersz[8] combine all the three and this also tallies with our observations that menorrhagia, increasing dysmenorrhoea and bulky uterus lead to the clinical diagnosis of adenomyosis. It is impossible to assess the exact incidence of associated pathology. In our series, leiomyomas were the commonest associated lesions [Table 4]. Other workers[2], [5], [9], [13] have also reported the same association. This again explains hyperestrinism causing higher incidence of leiomyoma along with adenomyosis.
We are thankful to the Dean-Dr. M. S. Kekre, Head of the Department of Pathology and Head of the Department of Obstetrics and Gynaecology, for allowing us to present hospital record.
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