Adverse reactions
Common side effects of primaquine administration include nausea, vomiting, and stomach cramps.In persons with cytochrome b5 reductase deficiency, primaquine causes methemoglobinemia, a condition in which the blood carries less oxygen that it does normally.Overdosing can reduce the number of function of various kinds of blood cells, including loss of red blood cells, methemoglobinemia, and loss of white blood cells.Persons with glucose-6-phosphate dehydrogenase deficiency (G6PD) may develop hemolytic anemia from primaquine. Pharmacology
Mechanism of action
Primaquine is lethal to P. vivax and P. ovale in the liver stage, and also to P. vivax in the blood stage through its ability to do oxidative damage to the cell. However, the exact mechanism of action is not fully understood. Liver hypnozoites aside, primaquine can possibly eliminate P. vivax merozoites in bone marrow as a result of accumulation there of hydrogen peroxide. Pharmacokinetics
Primaquine is well-absorbed in the gut and extensively distributed in the body without accumulating in red blood cells. Administration of primaquine with food or grapefruit juice increases its oral bioavailibity. In blood, about 20% of circulating primaquine is protein-bound, with preferential binding to the acute phase protein orosomucoid. With a half-life on the order of 6 hours, it is quickly metabolized by liver enzymes to carboxyprimaquine, which does not have anti-malarial activity. Renal excretion of the parent drug is less than 4%. Chemistry
Primaquine is an analog of pamaquine which was the first drug of the 8-aminoquinoline class; tafenoquine is another such drug.
The diffuse leprosy of Lucio and Latapí, also known as diffuse lepromatous leprosy or "pretty leprosy" is a clinical variety of lepromatous leprosy. It was first described by Lucio and Alvarado in 1852 and re-identified by Latapí in 1936. It is common in Mexico (23% of leprosy cases) and in Costa Rica and very rare in other countries. History
The spotted or lazarine leprosy was first described by Ladislao de la Pascua in 1844. Lucio and Alvarado published a description of the disease with the same names in 1852. Latapí re-described it in 1938 and reported it as spotted leprosy of Lucio in 1948. It was named the diffuse leprosy of Lucio and Latapí in 1963 by Frenken. The underlying pathology was explained by Chévez-Zamora as a diffuse generalised cutaneous infiltration. He named it pure and primitive diffuse lepromatosis, upon which necrotising lesions develop. He proposed the name Fenómeno de Lucio or erythema necrotisans for these lesions. Clinical features
This condition is characterized by:
a diffuse infiltration of all the skin which never transforms into nodule
a complete alopecia of eyebrows and eyelashes and body hair
an anhydrotic and dysesthesic zones of the skin
a peculiar type of lepra reaction named Lucios phenomenon or necrotic erythemaLucios phenomenon consists of well-shaped erythematous spots which later become necrotic with scabs, ulcerations and scars. These lesions are usually located on the lower extremities and may be extensive. They are frequently painful and rarely fatal. Pathology
The main pathological features of this disease are a vasculitis affecting all cutaneous vessels.