Pre-labour premature rupture of membranes (PPROM) is defined as rupture of membranes more than 1 hour prior to the onset of labour at <37 weeks gestation. PPROM occurs in approximately 3% of pregnancies and is responsible for a third of all preterm births. Once membranes are ruptured prolonging the pregnancy has no maternal physical advantage but fetal morbidity and mortality are improved daily at early gestations: 19% of those infants born <25 weeks develop cerebral palsy (CP) and 28% have severe motor disability. Those infants born extremely pre term (<28 weeks) cost the public sector £75835 (95% CI £27906–145508) per live birth not to mention the emotional cost to the family. To prolong gestation is therefore the suggested goal: however how and why might we delay birth in those at risk?

Hepatitis B and its complications are one of the major global health problems. Around 2 billion individuals are infected by hepatitis B virus (HBV) worldwide, more than 350 million are chronically infected, and approximately 15 to 40 percents of them will develop serious complications such as liver cirrhosis, hepatic failure, or hepatocellular carcinoma (HCC). The worldwide prevalence of chronic HBV infection ranges from 0.1 to 20 percent and varies widely in different geographic areas. According to the prevalence rate, WHO has classified countries into 3 levels: high areas (>8%) such as Africa, Asia, Western Pacific and Middle East; intermediate areas (2–8%) such as South America and Eastern Europe, and low areas (<2%) such as Western Europe, North America, and Australia.

Approximately 12%–27% of cerebrovascular disease in women of childbearing age is associated with pregnancy. The reported incidence of stroke in pregnancy ranges from 0.01%–0.05%. While these events are uncommon, they are often clinically devastating. The Center for Disease Control's (CDC) review of death certificates in all 50 states and the District of Columbia found that neurologic or neurovascular problems are one of the leading causes of mortality in pregnancy.

Glomerulonephritis (GN) may be manifest clinically in several ways. It may be asymptomatic and associated with only minor urinary dipstick abnormalities, GN may present with one of the classic renal nephritic or nephrotic syndromes, or may be associated with progressive chronic kidney disease with hypertension and the gradual development of uraemia, or it may present with fulminating life threatening illness with severe acute kidney injury. The development of GN may indicate a primary renal limited disease, or may be secondary in association with systemic diseases such as systemic lupus erythematosus (SLE), myeloma, infections or diabetes. Although immunological abnormalities underlie the development of many forms of GN, precise pathogenic mechanisms remain unclear and diagnostic labels may simply reflect a description of the glomerular histological changes observed (Table 1).