Therefore, treatment with phenobarbital is effective, generally with a decrease of at least 25% in serum bilirubin. In fact, this can be used, along with these other factors, to differentiate type I and II. Differential diagnosis
Neonatal jaundice may develop in the presence of sepsis, hypoxia, hypoglycemia, hypothyroidism, hypertrophic pyloric stenosis, galactosemia, fructosemia, etc. Hyperbilirubinemia of the unconjugated type may be caused by:

increased production
hemolysis (e.g., hemolytic disease of the newborn, hereditary spherocytosis, sickle cell disease)
ineffective erythropoiesis
massive tissue necrosis or large hematomas
decreased clearance
drug-induced
physiological neonatal jaundice and prematurity
liver diseases such as advanced hepatitis or cirrhosis
breast milk jaundice and Lucey–Driscoll syndrome
Crigler–Najjar syndrome and Gilbert syndromeIn Crigler–Najjar syndrome and Gilbert syndrome, routine liver function tests are normal, and hepatic histology usually is normal, too. No evidence for hemolysis is seen. Drug-induced cases typically regress after discontinuation of the substance. Physiological neonatal jaundice may peak at 85–170 μmol/L and decline to normal adult concentrations within two weeks. Prematurity results in higher levels. Treatment
Plasmapheresis and phototherapy are used for treatment. Liver transplant is curative. Research
A San Francisco-based company named Audentes Therapeutics is currently investigating the treatment of Crigler–Najjar syndrome with one of their gene replacement therapy products, AT342. Preliminary success has been found in early stages of a phase 1/2 clinical trial.One 10-year-old girl with Crigler–Najjar syndrome type I was successfully treated by liver cell transplantation.The homozygous Gunn rat, which lacks the enzyme uridine diphosphate glucuronyltransferase (UDPGT), is an animal model for the study of Crigler–Najjar syndrome.
A lentigo () (plural lentigines, ) is a small pigmented spot on the skin with a clearly defined edge, surrounded by normal-appearing skin. It is a harmless (benign) hyperplasia of melanocytes which is linear in its spread. This means the hyperplasia of melanocytes is restricted to the cell layer directly above the basement membrane of the epidermis where melanocytes normally reside. This is in contrast to the "nests" of multi-layer melanocytes found in moles (melanocytic nevi). Because of this characteristic feature, the adjective "lentiginous" is used to describe other skin lesions that similarly proliferate linearly within the basal cell layer. Diagnosis
Conditions characterized by lentigines include:
Lentigo simplex
Solar lentigo (Liver spots)
PUVA lentigines
Ink spot lentigo
LEOPARD syndrome
Mucosal lentigines
Multiple lentigines syndrome
Moynahan syndrome
Generalized lentiginosis
Centrofacial lentiginosis
Carney complex
Inherited patterned lentiginosis in black persons
Partial unilateral lentiginosis
Peutz–Jeghers syndrome
Lentigo maligna
Lentigo maligna melanoma
Acral lentiginous melanoma

Differential diagnosis
Lentigines are distinguished from freckles (ephelis) based on the proliferation of melanocytes. Freckles have a relatively normal number of melanocytes but an increased amount of melanin. A lentigo has an increased number of melanocytes. Freckles will increase in number and darkness with sunlight exposure, whereas lentigines will stay stable in their color regardless of sunlight exposure. Treatment
Lentigines by themselves are benign, however one might desire the removal or treatment of some of them for cosmetic purposes. In this case they can be removed surgically, or lightened with the use of topical depigmentation agents.