All but amphilinids and gyrocotylids (which burrow through the gut or body wall to reach the coelom) are intestinal, though some life-cycle stages rest in muscle or other tissues. The definitive host is always a vertebrate but in nearly all cases, one or more intermediate hosts are involved in the lifecycle, typically arthropods or other vertebrates. Infections can be long-lasting; in humans, tapeworm infection may last as much as 30 years. No asexual phases occur in the lifecycle, as they do in other flatworms, but the lifecycle pattern has been a crucial criterion for assessing evolution among Platyhelminthes.Cestodes produce large numbers of eggs, but each one has a low probability of finding a host. To increase their chances, different species have adopted various strategies of egg release. In the Pseudophyllidea, many eggs are released in the brief period when their aquatic intermediate hosts are abundant (semelparity). In contrast, in the terrestrial Cyclophyllidea, proglottids are released steadily over a period of years, or as long as their host lives (iteroparity). Another strategy is to have very long-lived larvae; for example, in Echinococcus, the hydatid larvae can survive for ten years or more in humans and other vertebrate hosts, giving the tapeworm an exceptionally long time window in which to find another host.Many tapeworms have a two-phase lifecycle with two types of host. The adult Taenia saginata lives in the gut of a primate such as a human, its definitive host.
DXA may show abnormal bone mineral density which may correlate with disease severity, although bone mineral density in HPP patients may not be systemically reduced. Genetic analysis
All clinical sub-types of hypophosphatasia have been traced to genetic mutations in the gene encoding TNSALP, which is localized on chromosome 1p36.1-34 in humans (ALPL; OMIM#171760). Approximately 388 distinct mutations have been described in the TNSALP gene. "The Tissue Nonspecific Alkaline Phosphatase Gene Mutations Database". About 80% of the mutations are missense mutations. The number and diversity of mutations results in highly variable phenotypic expression, and there appears to be a correlation between genotype and phenotype in hypophosphatasia”. Mutation analysis is possible and available in 3 laboratories. Treatment
As of October 2015, asfotase alfa (Strensiq) has been approved by the FDA for the treatment of hypophosphatasia. Some evidence exists to support the use of teriparatide in adult-HPP.Current management consists of palliating symptoms, maintaining calcium balance and applying physical, occupational, dental and orthopedic interventions, as necessary. Hypercalcemia in infants may require restriction of dietary calcium or administration of calciuretics. This should be done carefully so as not to increase the skeletal demineralization that results from the disease itself. Vitamin D sterols and mineral supplements, traditionally used for rickets or osteomalacia, should not be used unless there is a deficiency, as blood levels of calcium ions (Ca2+), inorganic phosphate (Pi) and vitamin D metabolites usually are not reduced. Craniosynostosis, the premature closure of skull sutures, may cause intracranial hypertension and may require neurosurgical intervention to avoid brain damage in infants.