Its overall benefit has been described as "modest".Acamprosate may work better than naltrexone for eliminating alcohol abuse, while naltrexone may decrease the desire for alcohol to a greater extent.The Sinclair method is a method involving opiate antagonists such as naltrexone to treat alcoholism. The person takes the medication once, about an hour before consuming alcohol, to curb the urge to drink. The opioid antagonist is thought to block the positive reinforcement effects of alcohol and may assist the person to stop or reduce their drinking. Opioid use
Long-acting injectable naltrexone is an opioid receptor antagonist, blocking the effects of heroin and other opioids, and decreases heroin use compared to a placebo. Unlike methadone and buprenorphine, it is not a controlled medication. It may decrease cravings for opioids after a number of weeks, and decreases the risk of overdose, at least during the time period that naltrexone is still active, though concern about risk of overdose for those stopping treatment remains. It is given once per month and has better compliance and effect for opioid use than the oral formulation.A drawback of injectable naltrexone as compared to methadone and buprenorphine is the requirement for a period of opioid abstinence before starting the medication, as the injection can otherwise cause sudden and intense opioid withdrawal. This "hurdle" is responsible for worse patient uptake with long-acting injectable naltrexone as compared with buprenorphine.
Complement deficiency is an immunodeficiency of absent or suboptimal functioning of one of the complement system proteins. Because of redundancies in the immune system, many complement disorders are never diagnosed. Some studies estimate that less than 10% are identified. Hypocomplementemia may be used more generally to refer to decreased complement levels, while secondary complement disorder means decreased complement levels that are not directly due to a genetic cause but secondary to another medical condition. Signs and symptoms
The following symptoms (signs) are consistent with complement deficiency in general:

Complications
Vaccinations for encapsulated organisms (e.g., Neisseria meningitidis and Streptococcus pneumoniae)  is crucial for preventing infections in complement deficiencies. Among the possible complications are the following:

Deficiencies of the terminal complement components increases susceptibility to infections by Neisseria. Causes
The cause of complement deficiency is genetics (though cases of an acquired nature do exist post infection). The majority of complement deficiencies are inherited as autosomal recessive conditions, while properdin deficiency occurs through X-linked inheritance. MBL deficiency can be inherited by either manner. Inherited
Properdin deficiency is an X-linked disorder that also causes susceptibility to Neisseria infections. C1-inhibitor deficiency or hereditary angioedema will have low C4 with normal C1 levels. Acquired
Acquired hypocomplementemia may occur in the setting of bone infections (osteomyelitis), infection of the lining of the heart (endocarditis), and cryoglobulinemia. Systemic lupus erythematosus is associated with low C3 and C4. Membranoproliferative glomerulonephritis usually has low C3. Mechanism
The mechanism of complement deficiency consists of:

C2: In regard to C2 deficiency, about 5 different mutations in the C2 gene are responsible.