In more extreme cases, known as a kinked flatfoot, the entire inner edge of the footprint may actually bulge outward, where in a normal to high arch this part of the sole of the foot does not make contact with the ground at all. On plain radiography, flat feet can be diagnosed and graded by several measures, the most important in adults being the talonavicular coverage angle, the calcaneal pitch, and the talar-1st metatarsal angle (Mearys angle). The talonavicular coverage angle is abnormally laterally rotated in flat feet. It is normally up to 7 degrees laterally rotated, so a greater rotation indicates flat feet. Radiographies generally need to be taken on weightbearing feet in order to detect misalignment. Treatment
Most flexible flat feet are asymptomatic, and do not cause pain. In these cases, there is usually no cause for concern. Flat feet were formerly a physical-health reason for service-rejection in many militaries. However, three military studies on asymptomatic adults (see section below), suggest that persons with asymptomatic flat feet are at least as tolerant of foot stress as the population with various grades of arch. In a study performed to analyze the activation of the tibialis posterior muscle in adults with pes planus, it was noted that the tendon of this muscle may be dysfunctional and lead to disabling weightbearing symptoms associated with acquired flat foot deformity. The results of the study indicated that while barefoot, subjects activated additional lower-leg muscles to complete an exercise that resisted foot adduction.
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.