Unfortunately, having chronic erythrocyte transfusions, it can be extremely harmful to the body and can cause severe complications.To help with dry eye symptoms and visual function, topical lubrication can be used. A more invasive way to help treat Gunthers disease would be to have surgery. There have been numerous studies that have stated that bone marrow transplantation is successful. This is a recently new development for Gunthers disease so the long-term effects are still unresourced. If a patient has a life-threatening infectious complication then bone marrow transplantation is no longer relevant for them. There are also reports that stem cell transplantation is successful in a limited number of participants

Eponym
The disorder is named after the German physician who discovered it, Hans Günther (1884-1956). See also
Porphyria cutanea tarda
List of cutaneous conditions
List of dental abnormalities associated with cutaneous conditions

References
External links
Porphyria, congenital erythropoietic at NIHs Office of Rare Diseases
People who have been treated with fludarabine will usually be asked to take co-trimoxazole or to use monthly nebulised pentamidine to prevent Pneumocystis jiroveci pneumonia. The profound lymphopenia caused by fludarabine renders patients susceptible to transfusion-associated graft versus host disease, an oftentimes fatal complication of blood transfusion. For this reason, all patients who have ever received fludarabine should only be given irradiated blood components. Fludarabine causes anemia, thrombocytopenia and neutropenia, requiring regular blood count monitoring. Some patients require blood and platelet transfusion, or G-CSF injections to boost neutrophil counts. Fludarabine is associated with the development of severe autoimmune hemolytic anemia in a proportion of patients.Difficulties are often encountered when harvesting peripheral blood stem cells from patients previously treated with fludarabine. Pharmacology
Fludarabine is a purine analog, and can be given both orally and intravenously. Fludarabine inhibits DNA synthesis by interfering with ribonucleotide reductase and DNA polymerase. It is active against both dividing and resting cells. Being phosphorylated, fludarabine is ionized at physiologic pH and is effectually trapped in blood. This provides some level of specificity for blood cells, both cancerous and healthy. History
Fludarabine was produced by John Montgomery and Kathleen Hewson of the Southern Research Institute in 1968. Names
Fludarabine is generally administered as its 5-O-phosphorylated form known as fludarabine phosphate, which is rapidly dephosphorylated to fludarabine in the plasma. References
External links
"Fludarabine". Drug Information Portal. U.S. National Library of Medicine.