Most individuals with<unk>  deficiency are asymptomatic. Most people who develop symptoms are male, due to the X-linked pattern of inheritance, but female carriers can be affected due to unfavorable lyonization or skewed X-inactivation, where random inactivation of an X-chromosome in certain cells creates a population of<unk> -deficient red blood cells coexisting with unaffected red blood cells. A female with one affected X chromosome will show the deficiency in approximately half of their red blood cells. However, in some cases, including double X-deficiency, the ratio can be much more than half, making the individual almost as sensitive as males. Red blood cell breakdown (also known as hemolysis) in<unk>  deficiency can manifest in a number of ways, including the following: * Prolonged neonatal jaundice, possibly leading to kernicterus (arguably the most serious complication of<unk>  deficiency) * Hemolytic crises in response to: * Illness (especially infections) * Certain drugs (see below) * Certain foods, most notably broad beans, from which the word favism derives * Certain chemicals * Diabetic ketoacidosis * Hemoglobinuria (red or brown urine) * Very severe crisis can cause acute kidney injury Favism is a hemolytic response to the consumption of fava beans, also known as broad beans. Though all individuals with favism show<unk>  deficiency, not all individuals with<unk>  deficiency show favism. The condition is known to be more prevalent in infants and children, and<unk>  genetic variant can influence chemical sensitivity. Other than this, the specifics of the chemical relationship between favism and<unk>  are not well understood.
Glucose-6-phosphate dehydrogenase deficiency
Pyruvate kinase deficiency
Ribose-5-phosphate isomerase deficiency
Hereditary spherocytosis
Glutaminase deficiency
Sickle cell disease
6-phosphogluconate dehydrogenase deficiency
Aldolase A deficiency