Intrahepatic cholestasis of pregnancy | |
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Classification and external resources | |
Specialty | obstetrics |
ICD-10 | O26.6 |
ICD-9-CM | 646.73 |
DiseasesDB | 6884 |
Patient UK | Intrahepatic cholestasis of pregnancy |
Intrahepatic cholestasis of pregnancy (ICP), also known as obstetric cholestasis, cholestasis of pregnancy, jaundice of pregnancy, and prurigo gravidarum, is a medical condition in which cholestasis occurs during pregnancy. It typically presents with troublesome itching and can lead to complications for both mother and fetus.
Pruritus (itching) has long been considered to be a common symptom of pregnancy. The vast majority of times, itching is a minor annoyance caused by changes to the skin, especially that of the abdomen. However, there are instances when itching is a symptom of ICP. This is usually most intense on the palms of the hands, and the soles of the feet, but can be widespread.
ICP occurs most commonly in the third trimester, but can begin at any time during the pregnancy.
Most women with this condition present in third trimester with itching without a rash. Typically, the itching is localized to the palms of the hands and soles of the feet but can be anywhere on the body.
Hallmarks of ICP include the following symptoms:
Most common:
Less common:
It is important to note that not all ICP sufferers have all of the above symptoms. For example, Jaundice only occurs in relatively small subset of cases, and in some cases abnormal lab results were not seen until 15 weeks or more after the onset of symptoms.
The causes of intrahepatic cholestasis of pregnancy are still not fully understood.Hormones and genetic factors are likely to be important in the pathogenesis of the disease. A number of features of the disease suggest a link to hormones:
Estrogens, and particularly glucuronides such as estradiol-17β-D-glucuronide, have been shown to cause cholestasis in animal studies, by reducing bile acid uptake by .
Treatment with progesterone in the third trimester of pregnancy has been shown to be associated with the development of ICP, and levels of metabolites of progesterone, particularly sulfated progesterone, are higher in patients with ICP than unaffected women, suggesting that progesterone also has a role in ICP.
Clustering of cases of ICP in families, geographic variation in rates of ICP, and recurrence of ICP in 45-70% of subsequent pregnancies all suggest a genetic component to the disease. Genetic mutations in the hepatocellular transport protein ABCB4 (MDR3), which controls secretion of phosphatidylcholine into bile, have been found in 15% of cases of ICP.