• Muhammad Ashfaq
  • Muhammad Zahoor Janjua
  • Muhammad Aslam Channa


Background: Gestational diabetes is much more common than pre-existing diabetes i.e. it complicates 2% to 5% of pregnancies. When metabolic control is good, perinatal mortality should be no higher than in general population. However, macrosomia continuous to be a problem in higher than average proportions of such cases. Macrosomia also involves placenta within the chronic hypertensive disease, the most common diagnosis is essential vascular hypertension. Methods: Total 60 full term placenta, 20 from normal and 20 each from gestational diabetics and chronic hypertensive mothers were studied grossly. Shape, attachment of umbilical cord, weight, diameter and central thickness of all placentas were noted. Results: The study demonstrates that there is change of shape i.e. two lobes in one placenta from diabetic group. All other placentae were singly lobed and discoidal shape with central attachment of umbilical cord to the foetal surface of placenta. Weight central thickness and diameter were significantly greater in diabetic group as compared to normal and hypertensive group. Hypertensive group shows non significant decrease in weight of placentae while there was no change in central thickness and diameter of placenta in hypertensive than the normal group. Conclusions: On the basis of results of present study, it is concluded that diabetic’s placentae showed increase in weight, central thickness and diameter. One out of 20 placentae in diabetic group also showed change of shape and attachment of umbilical cord to one love. Hypertensive’s placentae showed no significant change in weight, shape central thickness and attachment of umbilical cord when compared with normal group.Key words: Placenta, Gestational diabetes, Maternal Hypertension.


William PL, Banister LH, Berry MM. Gray’s Anatomy, 37 ed; Edinburgh, Churchill Livingstone 1989;153-6.

Berstein R, Blumenthal HT, Soule SD. Histogenesis of Physiological process in placentae of metabolic disease in pregnancy. Am J Obstet Gynec 1957;74:85-95.

Moore KL. The developing human. 3rd ed; Philadelphia; WB Saunders, 1983; 65-66, 111-118.

Hamilton WJ, Boyd JD. Observation on the human placenta. Proc R Soc Med 1951;44:489-96.

Pinker GD, Robert DWT. A short text book of Gynecology and obstetrics, 8th ed.; Sydney; Hodder & Stoughton, 1976; 106-7.

Kumar V, Cotran S, Robin SL. Basic pathology, 6th ed; Pennsylvania; WB Saunders, 2000; 4–10, 1082-1084.

Queenan JT. Management of high risk pregnancy, 4th ed., England; Blackwell science 1999; 261-70.

Arey LB. Developmental anatomy. 7th ed; Philadelphia; WB Saunders 1974;131-6.

Laga EM, Dirscoll SG, Munro H N. Quantitative studies of human placenta. Biol Neonate 1973;23:260-83.

Teasudale F. Gestational changes in the function structure of human placenta in relation to fetal growth. Am J Obstet Gynec 1980;137:560-8.

Winick M, Coscia A, Noble A. Cellular growth in normal placenta. Pediatr 1967;39:248-51.

Murthy LS, Agarwal KN, Sushila K. Placental morphometric and morphologic alterations in maternal undernutrition. Am J Obstet Gynae 1976;124:641-6.

Laga EM, Driscoll SG, Munro HN. Placental alterations in maternal undernutrition. Pediatr 1972;50:24-6.

Coustan DR. Gestational diabetes. In: Management of high risk pregnancy, 4th ed., England; Blackwell science, 1999; 261-9.

Berstein R, Blumenthal HT, Soule SD Histogenesis of physiological process in placentae of metabolic disease in pregnancy. Am J Obstet Gynec 1957;74:85-95.

Feczko JD, Kluber KM. Cytoarchitecture of muscle in genetic model of murine diabetes. Am J Anat 1988; 182:224-40.

Salvatore AC. The placenta in acute toxemia. Am J Obstet. Gynecol 1968;102:347-53.

Karlsson K, Ljunglslad ULF, Lundgren Y. Blood flow of reproductive system in renal hypertensive rats during pregnancy. Am J Obstet Gynec 1982; 142:1039-44.

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