Nonbacterial thrombotic endocarditis (NBTE) is a form of endocarditis in which small sterile vegetations are deposited on the valve leaflets. Formerly known as marantic endocarditis, which comes from the Greek marantikos, meaning "wasting away". The term "marantic endocarditis" is still sometimes used to emphasize the association with a wasting state such as cancer. Risk factors
Marantic vegetations are often associated with previous rheumatic fever. Other risk factors include:
hypercoagulable states
malignant cancers, especially mucin-producing adenocarcinomas (most commonly associated with pancreatic adenocarcinomas)
systemic lupus erythematosus: Referred to as Libman-Sacks endocarditis
trauma (e.g., catheters)

Valve predilection
The disease affects the valves with following predilection: mitral valve > aortic valve > tricuspid valve > pulmonary valve

Histopathology
Grossly, vegetations form along lines of valve closure and are generally symmetric with a smooth or verrucoid (warty) texture. Histologically, lesions are composed of fibrin (eosinophilic) and platelets but, unlike bacterial etiologies, contain little evidence of PMNs, microorganisms or inflammation. Diagnosis
Due to the non-invasive nature of NBTE, clinical examination may or may not reveal a new murmur. An embolic stroke may be the first feature to suggest diagnosis of NBTE. An echocardiograph may be used to further assess for valvular lesions. References


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Lysinuric protein intolerance (LPI) is an autosomal recessive metabolic disorder affecting amino acid transport. About 140 patients have been reported, almost half of them of Finnish origin. Individuals from Japan, Italy, Morocco and North Africa have also been reported plus one in Bixby, Oklahoma. Signs and symptoms
Infants with LPI are usually symptom-free when breastfed because of the low protein concentration in human milk, but develop vomiting and diarrhea after weaning. The patients show failure to thrive, poor appetite, growth retardation, enlarged liver and spleen, prominent osteoporosis and osteopenia, delayed bone age and spontaneous protein aversion. Forced feeding of protein may lead to convulsions and coma. Mental development is normal if prolonged episode of hyperammonemia can be avoided. Some patients develop severe pulmonary and kidney complications. High levels of plasma glutamine and glycine are observed. Causes
It has been associated with SLC7A7. Mechanism
In LPI, urinary excretion of cationic amino acids (ornithine, arginine and lysine) is increased and these amino acids are poorly absorbed from the intestine. Therefore, their plasma concentrations are low and their body pools become depleted. Deficiency of arginine and ornithine restricts the function of the urea cycle and leads to hyperammonemia after protein-rich meals. Deficiency of lysine may play a major role in the skeletal and immunological abnormalities observed in LPI patients.