However, DBA is characterized by dominant inheritance, and arises from partial loss of ribosomal function, so it is possible that erythroid progenitors are more sensitive to this decreased function, while most other tissues are less affected. Diagnosis
Typically, a diagnosis of DBA is made through a blood count and a bone marrow biopsy. A diagnosis of DBA is made on the basis of anemia, low reticulocyte (immature red blood cells) counts, and diminished erythroid precursors in bone marrow. Features that support a diagnosis of DBA include the presence of congenital abnormalities, macrocytosis, elevated fetal hemoglobin, and elevated adenosine deaminase levels in red blood cells.Most patients are diagnosed in the first two years of life. However, some mildly affected individuals only receive attention after a more severely affected family member is identified.About 20–25% of DBA patients may be identified with a genetic test for mutations in the RPS19 gene. Treatment
Corticosteroids can be used to treat anemia in DBA. In a large study of 225 patients, 82% initially responded to this therapy, although many side effects were noted. Some patients remained responsive to steroids, while efficacy waned in others. Blood transfusions can also be used to treat severe anemia in DBA. Periods of remission may occur, during which transfusions and steroid treatments are not required. Bone marrow transplantation (BMT) can cure hematological aspects of DBA. This option may be considered when patients become transfusion-dependent because frequent transfusions can lead to iron overloading and organ damage. However, adverse events from BMTs may exceed those from iron overloading.
Roths spots, also known as Litten spots or the Litten sign, are non-specific red spots with white or pale centres, seen on the retina and although traditionally associated with infective endocarditis, can occur in a number of other conditions including hypertension, diabetes, collagen vascular disease, extreme hypoxia, leukemia and HIV.Red and white retinal spots were first observed in 1872 by Swiss physician Moritz Roth, and named "Roth spots" six years later by Moritz Litten. They are typically observed via fundoscopy (using an ophthalmoscope to view inside the eye) or slit lamp exam.The original retinal spots identified in 1872 were attributed to nerve-fibres that had burst. Present-day analysis shows that they can be composed of coagulated fibrin including platelets, focal ischaemia, inflammatory infiltrate, infectious organisms, or neoplastic cells. Cause
Roths spots occur in conditions that predispose to endothelial damage of retinal capillaries, that is when there is dysfunction and disruption of the endothelium of retinal capillaries. Looking through the microscope reveals lesions with white centers made mainly of fibrin, depicting a fibrin-platelet plug at the site of vessel damage. Associated conditions
Conditions associated with Roths spots include:

Infective endocarditis
Anaemia/thrombocytopenia
Collagen vascular disease
Leukemia
Hypertensive retinopathy
Diabetic retinopathy
Pre-eclampsia
Human Immunodeficiency Virus (HIV)
Extreme hypoxia
Shaken-baby syndromeand also:
Candida albicans infection
vascular diseases
kala azar

Prevalence
Roths spots occur in only 5% of people with infective endocarditis. Litten, however reported a figure of 80%. See also
Oslers nodes
Janeway lesion
Splinter haemorrhage

References
External links
Image from the New England Journal of Medicine: Endocarditis
Image from the New England Journal of Medicine: CML