2 Day after admission ALAT IU/L ASAT IU/L PAL IU/L BIL T µmol/L BIL D µmol/L Creatinine µmol/L Uric acid mmol/L Hemoglobin g/dL Platelets/mm3 WBC PT % Glucose mmol/L WBC: white blood cell. PT: prothrombin time. ASAT: aspartate aminotransferase. ALAT: alanine aminotransferase. 1 104 108 138 14 8,5 64 144 12,2 213000 7600 96% 3,6 Case Reports in Obstetrics and Gynecology 3 248 122 118 23,2 17,4 78 138 12,3 178000 7800 76% 4 Table 1: Biologic analysis evolution. 7 213 104 123 18,4 12,6 67 145 11,9 198000 8500 78% 4,9 21 165 106 121 16,7 11,2 56 164 12 187000 9200 81% 5,1 42 172 110 142 14,5 10,4 64 154 11,5 201000 7400 92% 4,4 63 146 96 134 16 12,1 61 151 11,7 221000 10100 84% 5,3 84 134 98 129 15,8 11,3 73 167 11,4 197000 10700 79% 4,8 91 145 102 119 17,3 12,9 57 173 11,8 184000 12000 85% 5,5 Figure 1 Furthermore, modern advances in diagnostic capabilities have given us a better understanding of the pathological pro- cess, and many cases with a milder clinical course as well as subclinical cases have been reported [4–6]. Our observation is unusual by its clinical evolution until term and time of aris- ing (second trimester). Indeed, Monga and katz [2] reported a case of AFLP arising at 22 weeks’ gestation in 35 years women. However, in this case evolution was interrupted because of a disseminated intravascular coagulation. Also, Suzuki et al. [3] reported a case arising at 23 weeks of gestation for which the interval between symptom occur- rence and fetal demise was only one week and pregnancy was quickly interrupted. Curiously, biological ﬁndings in our observation were constant during evolution of pregnancy, particularly, pro- thrombin test and platelet counts. These ﬁndings may conﬁrm the cases with subclinical or milder clinical course already reported. Usually, there is no speciﬁc treatment for acute fatty liver of pregnancy except prompt termination of pregnancy and pathological changes as a rule improve rapidly after delivery. Liver biopsy is the best way to conﬁrm the diagnosis, but because it is invasive, it is not always performed. Further- more, today we can take advantage of noninvasive procedures to demonstrate fat in the liver and to exclude other liver diseases such as viral hepatitis [7]. Histopathological ﬁnding in liver biopsies is small and midsized intracellular vacuoles, without displacement of the nucleus and ballooning hepato- cytes. Recently, an association between AFLP and a deﬁciency of the enzyme long-chain 3-hydroxyacyl-CoA dehydrogenase was suggested. This enzyme is one of the four enzymes, which break down long-chain fatty acids in the liver. Deﬁciency of this enzyme results in the increased accu- mulation of long-chain fatty acids [8]. However, the exact mechanism that explains these mild clinical presentations remains unknown. This case, one of few reported cases, shows that even in the second trimester, the diagnosis of acute fatty liver should be considered when a woman presents with deteriorating liver function, jaundice, and coagulopathy. The particularity of this case is the unusual evolution; with a stable clinical and biological perturbations for 13 weeks after diagnosis of AFLP. Finally, the diagnosis of AFLP must be suspected in front of all digestive symptomatology in the second or the third trimester of pregnancy. References [1] M. Knight, C. Nelson-Piercy, J. J. Kurinczuk, P. Spark, and P. Brocklehurst, “A prospective national study of acute fatty liver of pregnancy in the UK,” Gut, vol. 57, no. 7, pp. 951–956, 2008. [2] M. Monga and A. R. Katz, “Acute fatty liver in the second trimester,” Obstetrics and Gynecology, vol. 93, no. 5, pp. 811– 813, 1999. [3] S. Suzuki, S. Watanabe, and A. Tsutomu, “Acute fatty liver of pregnancy at 23 weeks of gestation,” British Journal of Obstetrics and Gynaecology, vol. 108, no. 2, pp. 223–224, 2001.