Diagnosis and Treatment > Medication
The University of Sydney, Faculty of Medicine and Health, Sydney, New South Wales, Australia
Search for other papers by Albert S Kim in
Google Scholar
PubMed
Search for other papers by Rashida Hakeem in
Google Scholar
PubMed
Search for other papers by Azaliya Abdullah in
Google Scholar
PubMed
Department of Clinical Biochemistry, PathWest Laboratory Medicine WA, Royal Perth Hospital and Fiona Stanley Hospital Network, Perth, Western Australia, Australia
Search for other papers by Amanda J Hooper in
Google Scholar
PubMed
Department of Genetic Medicine, Westmead Hospital, Westmead, New South Wales, Australia
Search for other papers by Michel C Tchan in
Google Scholar
PubMed
Department of Maternal-Fetal Medicine, Westmead Institute for Maternal-Fetal Medicine, Westmead Hospital, Westmead, New South Wales, Australia
Search for other papers by Thushari I Alahakoon in
Google Scholar
PubMed
The University of Sydney, Faculty of Medicine and Health, Sydney, New South Wales, Australia
Department of Diabetes and Endocrinology, Royal North Shore Hospital, St Leonards, New South Wales, Australia
Search for other papers by Christian M Girgis in
Google Scholar
PubMed
Summary
A 19-year-old female presented at 25-weeks gestation with pancreatitis. She was found to have significant hypertriglyceridaemia in context of an unconfirmed history of familial hypertriglyceridaemia. This was initially managed with fasting and insulin infusion and she was commenced on conventional interventions to lower triglycerides, including a fat-restricted diet, heparin, marine oil and gemfibrozil. Despite these measures, the triglyceride levels continued to increase as she progressed through the pregnancy, and it was postulated that she had an underlying lipoprotein lipase defect. Therefore, a multidisciplinary decision was made to commence therapeutic plasma exchange to prevent further episodes of pancreatitis. She underwent a total of 13 sessions of plasma exchange, and labour was induced at 37-weeks gestation in which a healthy female infant was delivered. There was a rapid and significant reduction in triglycerides in the 48 h post-delivery. Subsequent genetic testing of hypertriglyceridaemia genes revealed a missense mutation of the LPL gene. Fenofibrate and rosuvastatin was commenced to manage her hypertriglyceridaemia postpartum and the importance of preconception counselling for future pregnancies was discussed. Hormonal changes in pregnancy lead to an overall increase in plasma lipids to ensure adequate nutrient delivery to the fetus. These physiological changes become problematic, where a genetic abnormality in lipid metabolism exists and severe complications such as pancreatitis can arise. Available therapies for gestational hypertriglyceridaemia rely on augmentation of LPL activity. Where there is an underlying LPL defect, these therapies are ineffective and removal of triglyceride-rich lipoproteins via plasma exchange should be considered.
Learning points:
-
Hormonal changes in pregnancy, mediated by progesterone,oestrogen and human placental lactogen, lead to a two- to three-fold increase in serum triglyceride levels.
-
Pharmacological intervention for management of gestational hypertriglyceridaemia rely on the augmentation of lipoprotein lipase (LPL) activity to enhance catabolism of triglyceride-rich lipoproteins.
-
Genetic mutations affecting the LPL gene can lead to severe hypertriglyceridaemia.
-
Therapeutic plasma exchange (TPE) is an effective intervention for the management of severe gestational hypertriglyceridaemia and should be considered in cases where there is an underlying LPL defect.
-
Preconception counselling and discussion regarding contraception is of paramount importance in women with familial hypertriglyceridaemia.
Search for other papers by Varalaxmi Bhavani Nannaka in
Google Scholar
PubMed
Search for other papers by Dmitry Lvovsky in
Google Scholar
PubMed
Summary
Angina pectoris in pregnancy is unusual and Prinzmetal’s angina is much rarer. It accounts for 2% of all cases of angina. It is caused by vasospasm, but the mechanism of spasm is unknown but has been linked with hyperthyroidism in some studies. Patients with thyrotoxicosis-induced acute myocardial infarction are unusual and almost all reported cases have been associated with Graves’ disease. Human chorionic gonadotropin hormone-induced hyperthyroidism occurs in about 1.4% of pregnant women, mostly when hCG levels are above 70–80 000 IU/L. Gestational transient thyrotoxicosis is transient and generally resolves spontaneously in the latter half of pregnancy, and specific antithyroid treatment is not required. Treatment with calcium channel blockers or nitrates reduces spasm in most of these patients. Overall, the prognosis for hyperthyroidism-associated coronary vasospasm is good. We describe a very rare case of an acute myocardial infarction in a 27-year-old female, at 9 weeks of gestation due to right coronary artery spasm secondary to gestational hyperthyroidism with free thyroxine of 7.7 ng/dL and TSH <0.07 IU/L.
Learning points:
-
AMI and cardiac arrest due to GTT despite optimal medical therapy is extremely rare.
-
Gestational hyperthyroidism should be considered in pregnant patients presenting with ACS-like symptoms especially in the setting of hyperemesis gravidarum.
-
Our case highlights the need for increased awareness of general medical community that GTT can lead to significant cardiac events. Novel methods of controlling GTT as well as medical interventions like ICD need further study.
