Letters to the Editor—Brief Communications / European Journal of Obstetrics & Gynecology and Reproductive Biology 187 (2015) 72–77
74
References [1] Spellacy WN, Gravem H, Fisch RO. The umbilical cord complications of true knots, nuchal coils, and cords around the body. Report from the collaborative study of cerebral palsy. Am J Obstet Gynecol 1966;94:1136–42. [2] Ramo´n Y, Cajal CL, Martı´nez RO. Prenatal diagnosis of true knot of the umbilical cord. Ultrasound Obstet Gynecol 2004;23:99–100. [3] Hershkovitz R, Silberstein T, Sheiner E, et al. Risk factors associated with true knot of the umbilical cord. Eur J Obstet Gynecol Reprod Biol 2001;98:36–9. [4] Sørnes T. Umbilical cord knots. Acta Obstet Gynecol Scand 2000;79:157–9.
O. Vasilj* R. Matijevic V. Blagaic B. Miskovic Department of Obstetrics and Gynaecology, Clinical Hospital Sveti Duh, Zagreb, Croatia *Corresponding author at: Department of Obstetrics and Gynaecology, Clinical Hospital Sveti Duh, Sveti Duh 64, 10000 Zagreb, Croatia. Tel.: +385 91 3712 262; fax: +385 1 3712 293 E-mail address: [email protected] (O. Vasilj). 1 January 2015 http://dx.doi.org/10.1016/j.ejogrb.2015.02.023
Severe hyperemesis gravidarum associated with gestational thyrotoxicosis and acute biliary pancreatitis Dear Editors, Hyperemesis gravidarum (HG) is a severe form of first trimester nausea and vomiting, most likely due to a self-limited beta-hCGdriven hyperthyroidism [1]. HG is well known from endocrinologists for its presentation with transient gestational hyperthyroidism while obstetricians are more familiar with metabolic imbalance or gastro-intestinal symptoms. We report here the case of severe HG in a 32-year-old Guinean woman who cumulated endocrine and rare digestive complications. This G3P1 patient (one singleton pregnancy, one miscarriage) was referred to our endocrine ward for major vomiting, weight loss ( 8 kg; anterior weight 63 kg) and moderate signs of hyperthyroidism at 5 weeks of amenorrhea (WA) of a dichorionic twin
pregnancy, suggestive of HG. She had a history of severe HG (32% weight loss) with gestational hyperthyroidism during her previous pregnancy 4 years earlier, which required transient propylthiouracyl (PTU) treatment until 21 WA. She had no other risk factor of HG. Graves’ disease, which is the main differential diagnosis of hyperthyroidism, was ruled out, as anti-TSH-receptor and antiTPO antibodies were negative. She was started on intravenous rehydration associated with food withdrawal and use of antivomiting drugs. However, as hyperthyroidism increased markedly (Table 1) with a worsening of weight loss ( 13 kg; 21% of body weight), we decided to introduce PTU treatment. Due to an increase of lipase and liver enzymes levels, we used low doses of PTU with a rigorous monitoring of hepatic function. One week after the beginning of the PTU treatment, the patient displayed jaundice and abdominal pain, concomitantly with an increase of lipase levels, suggestive of a pancreatitis, which was confirmed by ultrasound imaging and MRCP (Balthazar C). Using a conservative care including IV rehydratation and food administration via parenteral route, the patient improved both clinically and biochemically. PTU was stopped at 13 WA as fT4 level was normalized and the patient was discharged from the hospital at 14 WA. She remained euthyroid until delivery. She gave birth prematurely (35 WA), without fetal complications (boy and girl, respectively 2140 g [12th cent.] and 2150 g [22th cent.]). HG is a self-limited pregnancy disorder of the first trimester, characterized by excessive nausea and vomiting (with more than three episodes of vomiting per day) associated with ketonuria and more than 3 kg or 5% weight loss [1]. This disorder has an estimated incidence of 0.5–2% of all live births. Dietary advice and low dose anti-emetics are often sufficient to improve symptoms and quality of life until the natural resolving around 20 WA. The exact etiology of HG remains unknown but HG is usually associated with hyperthyroidism [2], due to structural homology of hCG with TSH, enabling hCG to act like TSH and hyperstimulate the thyroid function. Our patient with three risk factors for HG (twin pregnancy, previous history of HG and ethnicity) had a severe form of HG likely due to the extremely high levels of hCG. HG is often associated with hepatic disturbances [3], though physiopathology is poorly understood. Acute pancreatitis is very rare in pregnancy and is usually linked to gallstones or hyperlipidemia [4]. Weng et al. [5] reported one case of HG associated with jaundice and secondary pancreatitis. However, in their case, pancreatitis occurred after HG was resolved, with no evident patho-physiological mechanism. In our patient, the increase of pancreatic enzymes occurred concomitantly with hyperthyroidism, before the introduction of PTU. We assume that
Table 1 Evolution of hormonal, liver and pancreatic tests during the first trimester of the pregnancy. Term (weeks of amenorrhea + days)
5 WA + 1
6 WA + 1
7 WA + 5
9 WA
9 WA + 6
10 WA + 5
12 WA + 1
12 WA + 6
14 WA
Daily dose of PTU administrated (mg) TSH (mUI/L; N: 0.053–3.23) fT4 (pmol/L; N: 11.47–19.23) fT3 (pmol/L; N: 3.8–6.7) b-hCG (UI/L) SGPT (U/L; N: 10–31) SGOT (U/L; N: 10–31) Gamma-GT (U/L; N: 5–36) Alkaline phosphatase (U/L; N: 39–105) Total bilirubin (mmol/L; N: 3–22) Conjugated bilirubin (mmol/L; N: 0–4) Lipase (U/L; N: 5–55)
– 0.028 21.5 4.52 173,446 16 23 31 62 16 5 28
–
74
References [1] Spellacy WN, Gravem H, Fisch RO. The umbilical cord complications of true knots, nuchal coils, and cords around the body. Report from the collaborative study of cerebral palsy. Am J Obstet Gynecol 1966;94:1136–42. [2] Ramo´n Y, Cajal CL, Martı´nez RO. Prenatal diagnosis of true knot of the umbilical cord. Ultrasound Obstet Gynecol 2004;23:99–100. [3] Hershkovitz R, Silberstein T, Sheiner E, et al. Risk factors associated with true knot of the umbilical cord. Eur J Obstet Gynecol Reprod Biol 2001;98:36–9. [4] Sørnes T. Umbilical cord knots. Acta Obstet Gynecol Scand 2000;79:157–9.
O. Vasilj* R. Matijevic V. Blagaic B. Miskovic Department of Obstetrics and Gynaecology, Clinical Hospital Sveti Duh, Zagreb, Croatia *Corresponding author at: Department of Obstetrics and Gynaecology, Clinical Hospital Sveti Duh, Sveti Duh 64, 10000 Zagreb, Croatia. Tel.: +385 91 3712 262; fax: +385 1 3712 293 E-mail address: [email protected] (O. Vasilj). 1 January 2015 http://dx.doi.org/10.1016/j.ejogrb.2015.02.023
Severe hyperemesis gravidarum associated with gestational thyrotoxicosis and acute biliary pancreatitis Dear Editors, Hyperemesis gravidarum (HG) is a severe form of first trimester nausea and vomiting, most likely due to a self-limited beta-hCGdriven hyperthyroidism [1]. HG is well known from endocrinologists for its presentation with transient gestational hyperthyroidism while obstetricians are more familiar with metabolic imbalance or gastro-intestinal symptoms. We report here the case of severe HG in a 32-year-old Guinean woman who cumulated endocrine and rare digestive complications. This G3P1 patient (one singleton pregnancy, one miscarriage) was referred to our endocrine ward for major vomiting, weight loss ( 8 kg; anterior weight 63 kg) and moderate signs of hyperthyroidism at 5 weeks of amenorrhea (WA) of a dichorionic twin
pregnancy, suggestive of HG. She had a history of severe HG (32% weight loss) with gestational hyperthyroidism during her previous pregnancy 4 years earlier, which required transient propylthiouracyl (PTU) treatment until 21 WA. She had no other risk factor of HG. Graves’ disease, which is the main differential diagnosis of hyperthyroidism, was ruled out, as anti-TSH-receptor and antiTPO antibodies were negative. She was started on intravenous rehydration associated with food withdrawal and use of antivomiting drugs. However, as hyperthyroidism increased markedly (Table 1) with a worsening of weight loss ( 13 kg; 21% of body weight), we decided to introduce PTU treatment. Due to an increase of lipase and liver enzymes levels, we used low doses of PTU with a rigorous monitoring of hepatic function. One week after the beginning of the PTU treatment, the patient displayed jaundice and abdominal pain, concomitantly with an increase of lipase levels, suggestive of a pancreatitis, which was confirmed by ultrasound imaging and MRCP (Balthazar C). Using a conservative care including IV rehydratation and food administration via parenteral route, the patient improved both clinically and biochemically. PTU was stopped at 13 WA as fT4 level was normalized and the patient was discharged from the hospital at 14 WA. She remained euthyroid until delivery. She gave birth prematurely (35 WA), without fetal complications (boy and girl, respectively 2140 g [12th cent.] and 2150 g [22th cent.]). HG is a self-limited pregnancy disorder of the first trimester, characterized by excessive nausea and vomiting (with more than three episodes of vomiting per day) associated with ketonuria and more than 3 kg or 5% weight loss [1]. This disorder has an estimated incidence of 0.5–2% of all live births. Dietary advice and low dose anti-emetics are often sufficient to improve symptoms and quality of life until the natural resolving around 20 WA. The exact etiology of HG remains unknown but HG is usually associated with hyperthyroidism [2], due to structural homology of hCG with TSH, enabling hCG to act like TSH and hyperstimulate the thyroid function. Our patient with three risk factors for HG (twin pregnancy, previous history of HG and ethnicity) had a severe form of HG likely due to the extremely high levels of hCG. HG is often associated with hepatic disturbances [3], though physiopathology is poorly understood. Acute pancreatitis is very rare in pregnancy and is usually linked to gallstones or hyperlipidemia [4]. Weng et al. [5] reported one case of HG associated with jaundice and secondary pancreatitis. However, in their case, pancreatitis occurred after HG was resolved, with no evident patho-physiological mechanism. In our patient, the increase of pancreatic enzymes occurred concomitantly with hyperthyroidism, before the introduction of PTU. We assume that
Table 1 Evolution of hormonal, liver and pancreatic tests during the first trimester of the pregnancy. Term (weeks of amenorrhea + days)
5 WA + 1
6 WA + 1
7 WA + 5
9 WA
9 WA + 6
10 WA + 5
12 WA + 1
12 WA + 6
14 WA
Daily dose of PTU administrated (mg) TSH (mUI/L; N: 0.053–3.23) fT4 (pmol/L; N: 11.47–19.23) fT3 (pmol/L; N: 3.8–6.7) b-hCG (UI/L) SGPT (U/L; N: 10–31) SGOT (U/L; N: 10–31) Gamma-GT (U/L; N: 5–36) Alkaline phosphatase (U/L; N: 39–105) Total bilirubin (mmol/L; N: 3–22) Conjugated bilirubin (mmol/L; N: 0–4) Lipase (U/L; N: 5–55)
– 0.028 21.5 4.52 173,446 16 23 31 62 16 5 28
–
