The gut is sterile at birth and normal gut flora takes time to establish. The bacteria in the adult gut convert conjugated bilirubin to stercobilinogen which is then oxidized to stercobilin and excreted in the stool. In the absence of sufficient bacteria, the bilirubin is de-conjugated by brush border β-glucuronidase and reabsorbed. This process of re-absorption is called enterohepatic circulation. It has been suggested that bilirubin uptake in the gut (enterohepatic circulation) is increased in breast fed babies, possibly as the result of increased levels of epidermal growth factor (EGF) in breast milk. Breast milk also contains glucoronidase which will increase deconjugation and enterohepatic recirculation of bilirubin. The breast-milk of some women contains a metabolite of progesterone called 3-alpha-20-beta pregnanediol. This substance inhibits the action of the enzyme uridine diphosphoglucuronic acid (UDPGA) glucuronyl transferase responsible for conjugation and subsequent excretion of bilirubin. In the newborn liver, activity of glucuronyl transferase is only at 0.1-1% of adult levels, so conjugation of bilirubin is already reduced. Further inhibition of bilirubin conjugation leads to increased levels of bilirubin in the blood. However, these results have not been supported by subsequent studies. An enzyme in breast milk called lipoprotein lipase produces increased concentration of nonesterified free fatty acids that inhibit hepatic glucuronyl transferase, which again leads to decreased conjugation and subsequent excretion of bilirubin. Physiological jaundice
Most infants develop visible jaundice due to elevation of unconjugated bilirubin concentration during their first week. This is called physiological jaundice. This pattern of hyperbilirubinemia has been classified into two functionally distinct periods.
Persistent pupillary membrane (PPM) is a condition of the eye involving remnants of a fetal membrane that persist as strands of tissue crossing the pupil. The pupillary membrane in mammals exists in the fetus as a source of blood supply for the lens. It normally atrophies from the time of birth to the age of four to eight weeks. PPM occurs when this atrophy is incomplete. It generally does not cause any symptoms. The strands can connect to the cornea or lens, but most commonly to other parts of the iris. Attachment to the cornea can cause small corneal opacities, while attachment to the lens can cause small cataracts. Using topical atropine to dilate the pupil may help break down PPMs. In dogs, PPM is inherited in the Basenji but can occur in other breeds such as the Pembroke Welsh Corgi, Chow Chow, Mastiff, and English Cocker Spaniel. It can also be observed in cats, horses, and cattle. References


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