Although limited by its small sample size and retrospective design, this study provides a primary local dataset on a topic that remains under-investigated in Togo. Some incomplete records were excluded, reflecting constraints inherent to retrospective analyses and suboptimal medical record archiving. Furthermore, the absence of neonatal follow-up data precluded assessment of medium-term outcomes.

The mean age of patients with cirrhosis was 29.9 years, ranging from 22 to 44 years. Tchangai et al., in Togo, similarly reported that the majority of cirrhotic women were aged between 25 and 35 years [5]. Likewise, Ndongo et al., in Senegal, observed a high prevalence of cirrhosis among women under 40 years, with a mean age of 31 years, often progressing silently until pregnancy [6]. This predominance of cirrhosis in young and middle-aged women aligns with a well-documented pattern in developing countries, particularly in sub-Saharan Africa, where signs of hepatic decompensation and progression to cirrhosis typically manifest between 20 and 40 years of age. In contrast, in Western countries, the mean age of pregnant women with cirrhosis tends to be higher. For example, Orman et al., in a large US cohort, reported a mean age of 35 years [7]. This discrepancy reflects regional differences in epidemiological dynamics, likely attributable to variations in underlying etiologies. The occurrence of cirrhosis during pregnancy in young women represents a significant public health concern, associated with delayed diagnosis, inadequate screening for chronic viral hepatitis, and the near absence of preconception care. These findings underscore the need to reinforce systematic screening for liver diseases in women of childbearing age, particularly in regions with high viral endemicity, and to ensure long-term follow-up of HBsAg-positive women prior to subsequent pregnancies.

The majority of pregnant women with cirrhosis (70%) resided in rural areas, underscoring both delayed diagnosis and limited access to specialized care in these settings. These patients frequently present with more advanced stages of cirrhosis at the time of consultation, owing to restricted access to referral hospitals and a lack of awareness regarding the early manifestations of liver disease [8]. This observation is corroborated by a 2017 study in Senegal by Ndongo et al., which demonstrated a correlation between rural origin and greater clinical severity at admission, particularly with an increased prevalence of ascites and hepatic encephalopathy [6]. The situation is further exacerbated by the insufficiency of qualified personnel and diagnostic resources in peripheral healthcare facilities [9]. Patients managed at tertiary centres benefit from more comprehensive multidisciplinary care, which significantly improves both obstetric and hepatic outcomes [10]. This geographical disparity in healthcare access largely accounts for the poorer maternal and fetal outcomes observed in rural populations, including preterm delivery, medical termination of pregnancy, and elevated mortality rates. Moreover, limited health education and widespread unawareness of hepatitis B and cirrhosis in rural areas contribute to these diagnostic delays. These findings highlight the urgent need to strengthen community health strategies, particularly through the training of rural healthcare workers in the detection of cirrhosis, alongside the implementation of mandatory viral hepatitis screening during antenatal consultations at primary healthcare facilities.

Fifty percent of the cirrhotic patients were multiparous, with parity ranging from three to four, and presented with a poor prognosis (Child-Pugh Class C). These findings indicate a predominance of cirrhosis among women who have experienced multiple previous pregnancies. Multigravidity has been identified in several studies as a factor that may increase obstetric risk in women with chronic liver disease. According to the literature, women infected with HBV who have undergone several pregnancies are considered at higher risk of progression to cirrhosis due to chronic hormonal fluctuations and repeated immune stimulation during successive gestations [11]. These multiparous cirrhotic patients are also more likely to experience hemorrhagic complications, particularly during labor and delivery, owing to fragile vasculature and altered coagulation parameters [10]. Furthermore, multiparity may delay consultation, especially in rural women who, having previously experienced uncomplicated pregnancies, may underestimate the severity of cirrhosis symptoms. This socio-behavioral factor was highlighted by Balaka et al., who recommended enhanced monitoring of multiparous women with a history of hepatopathy [8].

Overall, these data support the integration of systematic hepatic monitoring into the antenatal care of at-risk multiparous women, particularly in resource-limited settings such as the Kara region. In 70% of cases, cirrhosis was diagnosed during the second trimester. Severe complications-including massive ascites, hepatic encephalopathy, and gastrointestinal bleeding-predominantly arose from 28 weeks of amenorrhea, consistent with Riely et al., who reported that hepatic decompensation most frequently occurs during the third trimester, when hemodynamic load is maximal [12]. Early screening for cirrhosis in pregnant women would substantially improve obstetric and neonatal outcomes, particularly by facilitating multidisciplinary management from the first trimester [13]. Conversely, diagnosis during the third trimester, as observed in 30% of our patients, was associated with frequent obstetric complications, notably prematurity. These findings are consistent with those of Orman et al., who reported a prematurity rate of up to 35% in pregnant women with cirrhosis, predominantly in cases of delayed diagnosis [7].

The predominant functional symptoms observed were asthenia (profound fatigue) and pallor, affecting 60% of patients, followed by abdominal pain (50%), headaches, and dizziness. Although these manifestations are not specific to hepatic decompensation, they should prompt clinical vigilance in the context of pregnancy. Sarin et al., in India, similarly reported such non-specific signs in the early stages of cirrhosis in pregnant women, particularly asthenia and epigastric pain [14]. Hematemesis and melaena, although less frequent in our series (20%), represent severe indicators of portal hypertension with variceal rupture, constituting both obstetric and hepatological emergencies.

Pallor and headaches are generally attributable to anemia, a common complication of cirrhosis, as confirmed by biological parameters showing anemia in 70% of cases. According to Nguyen et al. (2016), these signs must be interpreted within a comprehensive clinical context, as they may mimic other obstetric pathologies, including preeclampsia or hemolytic syndromes [13].

All patients (100%) presented with ascites, which represents the most specific and consistent clinical sign of advanced cirrhosis, a stage where therapeutic options are particularly limited in our setting. Ascitic decompensation constitutes the primary complication of cirrhosis. In the series reported by Runyon et al. (2013), ascites was present in 50% to 85% of cases of decompensated cirrhosis and is considered a marker of poor prognosis [15]. In pregnant women, its detection is often obscured by the physiological increase in abdominal volume, which may be mistaken for uterine enlargement. The presence of ascites in all patients in our series reflects delayed diagnosis in routine clinical practice.

Splenomegaly was observed in 50% of patients, consistent with the pathophysiology of decompensated cirrhosis, in which portal hypertension induces splenic congestion and increased splenic volume. This prevalence is lower than that reported by Sarin et al. in India, who observed splenomegaly in 75% of cases [14]. A thorough clinical examination, even within an obstetric context, combined with systematic abdominal ultrasonography, is essential for prompt diagnosis and early detection of complications.

Paraclinically, several biochemical abnormalities were identified in the pregnant cirrhotic patients, reflecting the severity of hepatic involvement and its systemic consequences. Ninety percent of patients exhibited cytolysis, indicative of hepatocellular necrosis. These findings are consistent with those of Nguyen et al., who reported moderate to severe cytolysis in 85% of pregnant women with cirrhosis [13]. All patients (100%) demonstrated a low prothrombin ratio (PR) below 50%. In the series by Terrault et al., a PR below 50% was observed in more than half of the pregnant cohort [11]. A reduced prothrombin ratio is significantly associated with an increased risk of complications, such as gastrointestinal bleeding. This hemorrhagic risk is further compounded by thrombocytopenia, present in 40% of these patients, particularly during the perinatal period.

Morphologically, ultrasonography is an indispensable investigation for the diagnosis of cirrhosis. It confirmed the diagnosis by demonstrating a dysmorphic liver, ascites, and, in some cases, splenomegaly. Ascites is detected by ultrasound in over 80% of cases of decompensated cirrhosis [11], while splenomegaly, a classic indicator of portal hypertension, is reported in 60% to 80% of cases according to Sarin et al. [14]. Abdominal ultrasonography should therefore be performed systematically in the presence of any non-specific signs during pregnancy.

Seventy percent of cirrhosis cases in pregnant women were attributable to chronic hepatitis B virus (HBV) infection. The predominance of HBV as a cause of cirrhosis in predominantly young pregnant women is well established in sub-Saharan Africa and aligns with trends reported in multiple African studies, in which HBV infection is frequently acquired during childhood, but hepatic decompensation and progression to cirrhosis typically manifest between 20 and 40 years of age [6]. In contrast, in developed countries, the most common etiologies of cirrhosis include alcohol-related liver disease, hepatitis C virus (HCV) infection, and metabolic dysfunction-associated steatohepatitis (MASH) [16]. The high prevalence of mother-to-child transmission of HBV, coupled with delayed screening, accounts for the elevated incidence observed in our setting. Metabolic and autoimmune causes are often underdiagnosed owing to the limited availability of specific diagnostic tests.

Several complications of cirrhosis were observed in the pregnant women, most notably hepatic encephalopathy (HE) in 40% of cases. This frequency is somewhat higher than that reported by Sarin et al., who estimated it at approximately 15% - 20% [14], a discrepancy likely attributable to delayed patient management in our setting. Two patients (10%) experienced upper gastrointestinal bleeding (UGIB) due to ruptured esophageal varices secondary to portal hypertension. Upper gastrointestinal endoscopy in these patients revealed large Grade 3 esophageal varices with red signs. However, the lack of routine endoscopic screening constitutes a significant limitation, exacerbated by increased uterine height during pregnancy. In a United States cohort, Orman et al. reported a bleeding rate of 30% among pregnant women with cirrhosis [7]. Hepatocellular carcinoma (HCC), the ultimate complication of cirrhosis, was diagnosed in 30% of patients, a prevalence higher than that reported in the literature. Indeed, some studies indicate that HCC is rare during pregnancy, accounting for fewer than 5% of cases [11][12]. HCC is notably more common in our context of HBV endemicity, where infection likely occurred during the neonatal period, compounded by delayed diagnosis. Spontaneous infection of the ascitic fluid was observed in one patient, representing a frequent and serious complication in decompensated cirrhotic patients. Analysis of ascitic fluid was not routinely performed by the gynecologists and obstetricians. Cirrhosis constitutes a vulnerable physiological state that predisposes patients to various spontaneous infections, including those of the ascitic fluid, urinary tract, lungs, and skin.

We observed an alarming maternal mortality rate of 60%. This high rate is, unfortunately, consistent with several contributing factors, notably delayed diagnosis, limited access to specialized care, and poorly controlled acute complications that exacerbate prognosis. This rate exceeds that reported by Faye et al. in Senegal, who documented a maternal mortality of 30% among pregnant women with cirrhosis, often associated with severe complications [17]. In contrast, Orman et al. reported a maternal mortality of 0.45% in the United States, rising to 15% - 20% in cases of decompensated cirrhosis with multiple complications [7]. These figures reflect the benefits of multidisciplinary management in countries with more structured healthcare systems. Recent data indicate that pregnant women with cirrhosis face a 40-fold higher risk of maternal mortality compared with the general obstetric population (0.46% vs 0.01%) [18]. In our study, women who continued their pregnancy into the third trimester predominantly exhibited severe hepatic decompensation, with two maternal deaths recorded. In contrast, patients who underwent early medical termination of pregnancy experienced partial or transient stabilization of their hepatic status, likely attributable to the reduction in hemodynamic and hormonal stress following pregnancy termination. The third trimester represents a particularly critical period for cirrhotic women, with peaks in maternal mortality and hepatic complications [13]. Future studies could assess the potential benefits of early medical termination on maternal health in cirrhotic pregnancies within our context.

Regarding pregnancy outcomes and neonatal status, 40% of pregnancies were medically terminated, 30% resulted in stillbirths, and 20% ended in preterm delivery. These unfavorable outcomes are consistent with the findings of Riely, who reported that fewer than 25% of pregnancies in women with cirrhosis reach term without major complications [12]. Chronic fetal distress is likely attributable to placental hypoperfusion secondary to maternal hepatic decompensation [13]. Close monitoring from the onset of pregnancy is therefore essential to guide and optimize multidisciplinary management.