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HYPOTHYROIDISM MASQUERADING
AS OVARIAN MALIGNANCY
Introduction
• Primary hypothyroidism is a common endocrine
abnormality leading to multiple system impairment.
• Hypothyroidism may cause reproductive endocrinology
disorders as well
• Van Wyk Grumbach syndrome (VWGS)- Juvenile
primary hypothyroidism causing cystic ovaries and
pseudoprecocious puberty is well documented in
literature.
• There are only a few reports of primary hypothyroidism
presenting as ovarian cysts in adults.
• Bilateral ovarian enlargement seen in
hypothyroidism resolves with levothyroxine
replacement.
• The devastating complication of ovarian
torsion leading to infarction is rare.
Case report
• 22yrs, unmarried, female
• c/c-Pain lower abdomen x 3months
-Distension abdomen x 1months
• HPI- pain sudden in onset, severe in intensity,
spasmodic in nature, radiating to thighs and relives on
medication. Associated with distension of abdomen gradual in
onset, progressive in nature causing early satiety & fullness
after meal. There was h/o chronic constipation, cold
intolerance and easy fatiguability.
No H/O nausea, vomiting, haematemesis, jaundice,
malaena, loss of apetite weight loss, evening rise of
temperature, respiratory distress, burning micturition,
discharge P/V.
• Menstruation H/O
 menarche -14yrs
LMP 28/2/17
 cycles – irregular
 increase flow
 Family H/O- Father is a k/c/o hypothyroidism
on regular medication
• Examination
 Height -125cm
 Weight – 45kg
 Pulse -86/min
 B.P. -124/84 mm Hg
 Pallor +
 Coarse skin
 Pedal Oedema +
 Thyroid not palpable
 Breast/Respiratory/CVS/ CNS- WNL
• P/A-
 free fluid present
A tense cystic mass, 15x10 cm palpable on Rt.
Illiac and hypogastrium, non tender, well defined
margin, smooth surface, with restricted mobility
No organomegaly
P/R – no nodularity felt, rectal mucosa free
Investigations
• UPT –ve
• Hb – 5mg/dl
• CA- 235
• TSH ->150 , FT3 -14.41, FT4- 1.4
• Prolactin – 122.3
• CEA- 3.64
• FSH- 7.8
• LH- < .07
• Testosterone 5.45
• LDH – 226
• B- HCG - <2
• DHEA- 67
• USG-
– free fluid seen in POD
– Large solid cystic thick septated mass
(12.6x5.6cm) mass in Lt. adnexa crossing midline
– Rt. Ovary was enlarged to approx. 270 cc
– Uterus normal
• CEMR Pelvis
– Multiloculated cystic lesion with thick
septationscm in Lt. ovary (10.6x 8.4x4.9 cm)
– 9.2x9.6x
Management
• 4 units of PCV was transfused after consent
• Patient was prepared for laparotomy but
anaesthesiologist advised Endo opinion for
hypothyroidism
• Endocrinology opinion was taken and surgery
withold and patient kept on follow up with
thyroxine 150 ug OD.
• After one month patient was readmitted with
similar episode of pain abdomen but mass
decreased in size P/A
• Usg showed features s/o torsion ovary in left side
• TSH level decreased to 1.1
• Patient was taken up for laparotomy.
• Per-op examination revealed
– b/l ovarian cyst 8x8 cm
– Lt. Cyst torsion present (two twist & torsion in fallopian
tube)
– Multiple cystic ovaries in Rt. side
– Uterus normal
– omentum adhered to Rt. Ovary and uterus
– Adhesiolysis, detortion f/b b/l ovarian cystectomy done.
– Specimen sent for HPE
Histopathology
A B
• Revealed cyst containing extensive areas of haemorrhagic
infarction and a few foci of dystrophic calcification.
• Post op peroid was uneventful
• Patient was discharged and advised to
continue throxine (150 ug OD)
• On follow up after 3 months
– patient was symptom free
– USG revealed no adnexal mass b/l
Discussion
• Ovarian cysts are a common cause for gynecological
surgery.
• Etiology can vary due to complex composition and
function of ovary
• Some only result from reproductive endocrine
dysfunction and resolve without surgery after
endocrine correction
• ovarian hyperstimulation syndrome (OHSS) is such a
disorder.
• With multiple follicles developing, the ultrasound
images of the ovaries appear similar to multilocular
cystadenoma with multiple septa.
• Without h/o or c/f of precocious puberty (Van
Wyk and Grumbach syndrome) in young girls,
reproductive organ ultrasound evaluations in
hypothyroid adults is ignored.
• Without hCG triggering the release of certain
ovarian vasoactive substances , typical
complications of OHSS, such as severe
abdominal distention, serious
hemoconcentration, massive ascites or pleural
effusion may be lacking.
Pathophysiology
• Hypothyroidism though common, concomitant ovarian
hyperstimulation is rare
• Exact mechanism not clear though multiple
hypotheses formulated
• First - TSH, FSH and their receptors have related
structures. Extremely high concentrations of TSH in
hypothyroidism may be sufficient to cause the
activation of FSHR
• Second - the patients of hypothyroidism with
multilocular ovaries reported by most of the authors
showed relatively high FSH and low LH levels.
hypothyroidism ↑prolactin
↑TRH low GnRH pulse ↓ LH
↓ estrogen
↑ TSH ↑FSH
• Third - TSH may sensitize the ovaries to
gonadotropin stimulation by stimulating
nuclear thyroid receptors in the granulosa
cells, thereby exacerbating ovarian
hyperstimulation.
• Myxedematous-type infiltration might also
account for the interference of
steroidogenesis in the ovary and contribute to
ovarian cystic changes
• Although etiopathology is speculative, treatment
approach for ovarian hyperstimulation due to
hypothyroidism is clear.
• Evidence exists that supplementation with
thyroid hormone can lead to the complete
regression of the multicystic ovarian
enlargement, even in patients with high CA-125
levels.
• Surgical exploration should be reserved only for
ovarian torsion or rupture.
• Intraop suspicion of malignancy- frozen
sectioning should be performed prior to
oophorectomy.
• Panico et al did ovarian wedge resection for
persistent ovarian enlargement after adequate
thyroid replacement therapy for 14 months.
The histological section in their case showed a
benign ovarian cyst with extensive
hemorrhage and myxedematous infiltration.
• Other treatments, such as aspiration, may be
considered as well for persistent cysts.
• When adequate thyroid replacement therapy
fails,surgical excision should be considered.
Conclusion
• Although very rare, profound hypothyroidism can
cause multicystic ovaries in an adult.
• They may mimic ovarian carcinoma in the
presence of elevated CA-125 levels.
• hypothyroidism and other endocrine disorders
should be considered in the differential diagnosis
of adult females presenting with multicystic
ovarian tumors to avoid unnecessary and
catastrophic ovarian resection.
Referrences

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Hypothyroidism masquerading as ovarian malignancy

  • 2. Introduction • Primary hypothyroidism is a common endocrine abnormality leading to multiple system impairment. • Hypothyroidism may cause reproductive endocrinology disorders as well • Van Wyk Grumbach syndrome (VWGS)- Juvenile primary hypothyroidism causing cystic ovaries and pseudoprecocious puberty is well documented in literature. • There are only a few reports of primary hypothyroidism presenting as ovarian cysts in adults.
  • 3. • Bilateral ovarian enlargement seen in hypothyroidism resolves with levothyroxine replacement. • The devastating complication of ovarian torsion leading to infarction is rare.
  • 4. Case report • 22yrs, unmarried, female • c/c-Pain lower abdomen x 3months -Distension abdomen x 1months • HPI- pain sudden in onset, severe in intensity, spasmodic in nature, radiating to thighs and relives on medication. Associated with distension of abdomen gradual in onset, progressive in nature causing early satiety & fullness after meal. There was h/o chronic constipation, cold intolerance and easy fatiguability. No H/O nausea, vomiting, haematemesis, jaundice, malaena, loss of apetite weight loss, evening rise of temperature, respiratory distress, burning micturition, discharge P/V.
  • 5. • Menstruation H/O  menarche -14yrs LMP 28/2/17  cycles – irregular  increase flow  Family H/O- Father is a k/c/o hypothyroidism on regular medication
  • 6. • Examination  Height -125cm  Weight – 45kg  Pulse -86/min  B.P. -124/84 mm Hg  Pallor +  Coarse skin  Pedal Oedema +  Thyroid not palpable  Breast/Respiratory/CVS/ CNS- WNL
  • 7. • P/A-  free fluid present A tense cystic mass, 15x10 cm palpable on Rt. Illiac and hypogastrium, non tender, well defined margin, smooth surface, with restricted mobility No organomegaly P/R – no nodularity felt, rectal mucosa free
  • 8. Investigations • UPT –ve • Hb – 5mg/dl • CA- 235 • TSH ->150 , FT3 -14.41, FT4- 1.4 • Prolactin – 122.3 • CEA- 3.64 • FSH- 7.8 • LH- < .07 • Testosterone 5.45 • LDH – 226 • B- HCG - <2 • DHEA- 67
  • 9. • USG- – free fluid seen in POD – Large solid cystic thick septated mass (12.6x5.6cm) mass in Lt. adnexa crossing midline – Rt. Ovary was enlarged to approx. 270 cc – Uterus normal • CEMR Pelvis – Multiloculated cystic lesion with thick septationscm in Lt. ovary (10.6x 8.4x4.9 cm) – 9.2x9.6x
  • 10.
  • 11. Management • 4 units of PCV was transfused after consent • Patient was prepared for laparotomy but anaesthesiologist advised Endo opinion for hypothyroidism • Endocrinology opinion was taken and surgery withold and patient kept on follow up with thyroxine 150 ug OD. • After one month patient was readmitted with similar episode of pain abdomen but mass decreased in size P/A
  • 12. • Usg showed features s/o torsion ovary in left side • TSH level decreased to 1.1 • Patient was taken up for laparotomy. • Per-op examination revealed – b/l ovarian cyst 8x8 cm – Lt. Cyst torsion present (two twist & torsion in fallopian tube) – Multiple cystic ovaries in Rt. side – Uterus normal – omentum adhered to Rt. Ovary and uterus – Adhesiolysis, detortion f/b b/l ovarian cystectomy done. – Specimen sent for HPE
  • 13. Histopathology A B • Revealed cyst containing extensive areas of haemorrhagic infarction and a few foci of dystrophic calcification.
  • 14. • Post op peroid was uneventful • Patient was discharged and advised to continue throxine (150 ug OD) • On follow up after 3 months – patient was symptom free – USG revealed no adnexal mass b/l
  • 15. Discussion • Ovarian cysts are a common cause for gynecological surgery. • Etiology can vary due to complex composition and function of ovary • Some only result from reproductive endocrine dysfunction and resolve without surgery after endocrine correction • ovarian hyperstimulation syndrome (OHSS) is such a disorder. • With multiple follicles developing, the ultrasound images of the ovaries appear similar to multilocular cystadenoma with multiple septa.
  • 16. • Without h/o or c/f of precocious puberty (Van Wyk and Grumbach syndrome) in young girls, reproductive organ ultrasound evaluations in hypothyroid adults is ignored. • Without hCG triggering the release of certain ovarian vasoactive substances , typical complications of OHSS, such as severe abdominal distention, serious hemoconcentration, massive ascites or pleural effusion may be lacking.
  • 17. Pathophysiology • Hypothyroidism though common, concomitant ovarian hyperstimulation is rare • Exact mechanism not clear though multiple hypotheses formulated • First - TSH, FSH and their receptors have related structures. Extremely high concentrations of TSH in hypothyroidism may be sufficient to cause the activation of FSHR • Second - the patients of hypothyroidism with multilocular ovaries reported by most of the authors showed relatively high FSH and low LH levels.
  • 18. hypothyroidism ↑prolactin ↑TRH low GnRH pulse ↓ LH ↓ estrogen ↑ TSH ↑FSH
  • 19. • Third - TSH may sensitize the ovaries to gonadotropin stimulation by stimulating nuclear thyroid receptors in the granulosa cells, thereby exacerbating ovarian hyperstimulation. • Myxedematous-type infiltration might also account for the interference of steroidogenesis in the ovary and contribute to ovarian cystic changes
  • 20. • Although etiopathology is speculative, treatment approach for ovarian hyperstimulation due to hypothyroidism is clear. • Evidence exists that supplementation with thyroid hormone can lead to the complete regression of the multicystic ovarian enlargement, even in patients with high CA-125 levels. • Surgical exploration should be reserved only for ovarian torsion or rupture. • Intraop suspicion of malignancy- frozen sectioning should be performed prior to oophorectomy.
  • 21. • Panico et al did ovarian wedge resection for persistent ovarian enlargement after adequate thyroid replacement therapy for 14 months. The histological section in their case showed a benign ovarian cyst with extensive hemorrhage and myxedematous infiltration. • Other treatments, such as aspiration, may be considered as well for persistent cysts. • When adequate thyroid replacement therapy fails,surgical excision should be considered.
  • 22. Conclusion • Although very rare, profound hypothyroidism can cause multicystic ovaries in an adult. • They may mimic ovarian carcinoma in the presence of elevated CA-125 levels. • hypothyroidism and other endocrine disorders should be considered in the differential diagnosis of adult females presenting with multicystic ovarian tumors to avoid unnecessary and catastrophic ovarian resection.