Patients with constitutional delay of puberty may be monitored by an endocrinologist, but definitive treatment may not be needed as there will eventually be progression to normal puberty. Secondary amenorrhea
Treatment for secondary amenorrhea varies greatly based on the root cause. Functional hypothalamic amenorrhoea is typically treated by weight gain through increased calorie intake and decreased expenditure. Multidisciplinary treatment with monitoring from a physician, dietitian, and mental health counselor is recommended, along with support from family, friends, and coaches. Although oral contraceptives can cause menses to return, oral contraceptives should not be the initial treatment as they can mask the underlying problem and allow other effects of the eating disorder, like osteoporosis, continue to develop.Patients with hyperprolactinemia are often treated with dopamine agonists to reduce the levels of prolactin and restore menstruation. Surgery and radiation may also be considered if dopamine agonists, such as cabergoline and bromocriptine are ineffective. Once prolactin levels are lowered, the resulting secondary amenorrhea is typically resolved. Similarly, treatment of thyroid abnormalities often resolves the associated amenorrhea. For example, administration of thyroxine in patients with low thyroid levels restored normal menstruation in a majority of patients.Although there is currently no definitive treatment for PCOS, various interventions are used to restore more frequent ovulation in patients. Weight loss and exercise have been associated with a return of ovulation in patients with PCOS due to normalization of androgen levels. Metformin has also been recently studied to regularize menstrual cycles in patients with PCOS.
This acts as an endotoxin and is responsible for septic shock and hemorrhage due to the destruction of red blood cells. Other virulence factors include a polysaccharide capsule which prevents host phagocytosis and aids in evasion of the host immune response. Adhesion is another key virulence strategy to successfully invade host cell. There are several known proteins that are involved in adhesion and invasion, or mediate interactions with specific host cell receptors. These include the Type IV pilin adhesin which mediates attachment of the bacterium to the epithelial cells of the nasopharynx, surface-exposed Opa and Opc proteins which mediate interactions with specific host cell receptors, and NadA which is involved in adhesion.Pathogenic meningococci that have invaded into the bloodstream must be able to survive in the new niche, this is facilitated by acquisition and utilisation of iron (FetA and Hmbr), resisting intracellular oxidative killing by producing catalase and superoxide dismutase and ability to avoid complement mediated killing (fHbp). Meningococci produce an IgA protease, an enzyme that cleaves IgA class antibodies and thus allows the bacteria to evade a subclass of the humoral immune system. A hypervirulent strain was discovered in China. Its impact is yet to be determined. Complement inhibition
Factor H binding protein (fHbp) that is exhibited in N. meningitidis and some commensal species is the main inhibitor of the alternative complement pathway. fHbp protects meningococci from complement-mediated death in human serum experiments, but has also been shown to protect meningococci from antimicrobial peptides in vitro.