In the tumorous stage a dense infiltrate of medium-sized lymphocytes with cerebriform nuclei expands the dermis. Accurate staging of mycosis fungoides is essential to determine appropriate treatment and prognosis. Staging is based on the tumor, node, metastasis, blood (TNMB) classification proposed by the Mycosis Fungoides Cooperative Group and revised by the International Society for Cutaneous Lymphomas/European Organization of Research and Treatment of Cancer. This staging system examines the extent of skin involvement (T), presence of lymph node (N), visceral disease (M), and presence of Sezary cells in the peripheral blood (B).Most patients with mycosis fungoides have early-stage disease (Stage IA-IIA) at the time of their initial diagnosis. People with early stage disease that is primarily confined to the skin have a favorable prognosis. People with advanced stage (Stage IIB-IVB) are often refractory to treatment and have an unfavorable prognosis. Treatment options for people with advanced stage disease are designed to reduce tumor burden, delay disease progression, and preserve quality of life. Treatment
The most commonly recommended first-line treatment for mycosis fungoides is psoralen plus ultraviolet A (PUVA therapy). PUVA is a photochemotherapy that involves topical or oral administration of the photosensitizing drug psoralen followed by skin exposure to ultraviolet radiation. Systemic treatments of mycosis fungoides often lead to resistance; as such, additional treatment options are often necessary in advanced disease.Other treatments that have been suggested, however, larger and more extensive research is needed to identify effective treatment strategies for this disease.
Crigler–Najjar syndrome is a rare inherited disorder affecting the metabolism of bilirubin, a chemical formed from the breakdown of the heme in red blood cells. The disorder results in a form of nonhemolytic jaundice, which results in high levels of unconjugated bilirubin and often leads to brain damage in infants. The disorder is inherited in an autosomal recessive manner. The annual incidence is estimated at 1 in 1,000,000.This syndrome is divided into types I and II, with the latter sometimes called Arias syndrome. These two types, along with Gilberts syndrome, Dubin–Johnson syndrome, and Rotor syndrome, make up the five known hereditary defects in bilirubin metabolism. Unlike Gilberts syndrome, only a few causes of Crigler–Najjar syndrome are known. Signs and symptoms
Jaundice 
Diarrhea
Vomiting
Fever
Confusion
Slurred speech
Difficulty swallowing
Change in gait, staggering frequent falling
Seizures

Cause
It is caused by abnormalities in the gene coding for uridine diphosphoglucuronate glucuronosyltransferase (UGT1A1). UGT1A1 normally catalyzes the conjugation of bilirubin and glucuronic acid within hepatocytes. Conjugated bilirubin is more water-soluble and is excreted in bile. Diagnosis
Type I
This is a very rare disease (estimated at 0.6–1.0 per million live births), and consanguinity increases the risk of this condition (other rare diseases may be present). Inheritance is autosomal recessive. Intense jaundice appears in the first days of life and persists thereafter. Type 1 is characterised by a serum bilirubin usually above 345 μmol/L [20 mg/dL] (range 310–755 μmol/L [18–44 mg/dL]) (whereas the reference range for total bilirubin is 2–14 μmol/L [0.1–0.8 mg/dL]). No UDP glucuronosyltransferase 1-A1 expression can be detected in the liver tissue.