A minority of patients can be treated medically with sodium restriction, diuretics to control ascites, anticoagulants such as heparin and warfarin, and general symptomatic management. The majority of patients require further intervention. Milder forms of Budd–Chiari may be treated with surgical shunts to divert blood flow around the obstruction or the liver itself. Shunts must be placed early after diagnosis for best results. The TIPS is similar to a surgical shunt: it accomplishes the same goal but has a lower procedure-related mortality—a factor that has led to a growth in its popularity. If all the hepatic veins are blocked, the portal vein can be approached via the intrahepatic part of inferior vena cava, a procedure called DIPS (direct intrahepatic portocaval shunt). Patients with stenosis or vena caval obstruction may benefit from angioplasty. Limited studies on thrombolysis with direct infusion of urokinase and tissue plasminogen activator into the obstructed vein have shown moderate success in treating Budd–Chiari syndrome; however, it is not routinely attempted.

Liver transplantation is an effective treatment for Budd–Chiari. It is generally reserved for patients with fulminant liver failure, failure of shunts or progression of cirrhosis that reduces the life expectancy to 1 year. Long-term survival after transplantation ranges from 69–87%. The most common complications of transplant include rejection, arterial or venous thromboses and bleeding due to anticoagulation. Up to 10% of patients may have a recurrence of Budd–Chiari syndrome after the transplant.

For patients who do not adequately respond to dietary fiber, osmotic laxatives such as polyethylene glycol, sorbitol, and lactulose can help avoid "cathartic colon" which has been associated with stimulant laxatives. Among the osmotic laxatives, doses of 17–26 g/d of polyethylene glycol have been well studied. Lubiprostone (Amitiza) is a gastrointestinal agent used for the treatment of idiopathic chronic constipation and constipation-predominant IBS. It is well tolerated in adults, including elderly patients. As of July 20, 2006, lubiprostone had not been studied in pediatric patients. Lubiprostone is a bicyclic fatty acid (prostaglandin E1 derivative) that acts by specifically activating ClC-2 chloride channels on the apical aspect of gastrointestinal epithelial cells, producing a chloride-rich fluid secretion. These secretions soften the stool, increase motility, and promote spontaneous bowel movements. Unlike many laxative products, lubiprostone does not show signs of tolerance, dependency, or altered serum electrolyte concentration.

Sedative drugs are often prescribed for vertigo and dizziness, but these usually treat the symptoms rather than the underlying cause. Lorazepam (Ativan) is often used and is a sedative which has no effect on the disease process, but rather helps patients cope with the sensation.

Anti-nauseants, like those prescribed for motion sickness, are also often prescribed but do not affect the prognosis of the disorder.

Specifically for Meniere's disease a medication called Serc (Beta-histine) is available. There is some evidence to support its effectiveness in reducing the frequency of attacks. Also Diuretics, like Diazide (HCTZ/triamterene), are effective in many patients. Finally, ototoxic medications delivered either systemically or through the eardrum can eliminate the vertigo associated with Meniere's in many cases, although there is about a 10% risk of further hearing loss when using ototoxic medications.

Treatment is specific for underlying disorder of balance disorder:

- anticholinergics

- antihistamines

- benzodiazepines

- calcium channel antagonists, specifically Verapamil and Nimodipine

- GABA modulators, specifically gabapentin and baclofen

- Neurotransmitter reuptake inhibitors such as SSRIs, SNRIs and Tricyclics

The use of antispasmodic drugs (e.g., anticholinergics such as hyoscyamine or dicyclomine) may help patients, especially those with cramps or diarrhea. A meta-analysis by the Cochrane Collaboration concludes if seven patients are treated with antispasmodics, one patient will benefit. Antispasmodics can be divided into two groups: neurotropics and musculotropics.

- Musculotropics, such as mebeverine, act directly at the smooth muscle of the gastrointestinal tract, relieving spasm without affecting normal gut motility. Since this action is not mediated by the autonomic nervous system, the usual anticholinergic side effects are absent. The antispasmodic otilonium may also be useful.

Dysequilibrium arising from bilateral loss of vestibular function – such as can occur from ototoxic drugs such as gentamicin – can also be treated with balance retraining exercises (vestibular rehabilitation) although the improvement is not likely to be full recovery.

Non-pharmacological treatments are effective in treating autoimmune disease and contribute to a sense of well-being. Women can:

- Eat healthy, well-balanced meals that includes fruits, vegetables, whole grains, fat-free or low-fat milk products, and lean sources of protein. A healthy diet limits saturated fat, trans fat, cholesterol, salt, and added sugars.

- Engage in regular physical activity without overdoing it. Consulting with a clinician about what types of physical activity is appropriate. A gradual and gentle exercise program often works well for people with long-lasting muscle and joint pain. Some types of yoga or tai chi may be helpful.

- Get enough rest. Rest allows body tissues and joints the time they need to repair. Sleeping is a great way to maintain health and helps both body and mind. Lack of sleep, stress levels and symptoms might get worsen. Immunity to other infections or diseases is reduced when sleep is not adequate. Rest cotributes to the ability to handle the stressors and problems. Many people need at least 7 to 9 hours of sleep each day to feel well-rested.

- Reduce stress. Stress and anxiety can trigger symptoms to flare up with some autoimmune diseases. Simplifying daily stressors will help contribute to a sense of well-being. Meditation, self-hypnosis, and guided imagery, may be effective in reducing stress, reducing pain, and the ability to deal with other aspects of living with the disease . Instructional materials can assist with learning these activities such as self-help books, audio sources, tapes, or with the help of an instructor. Joining a support group or talking with a counselor might also help manage stress and cope with the disease.

Several studies have attempted to predict the survival of patients with Budd–Chiari syndrome. In general, nearly 2/3 of patients with Budd–Chiari are alive at 10 years. Important negative prognostic indicators include ascites, encephalopathy, elevated Child-Pugh scores, elevated prothrombin time, and altered serum levels of various substances (sodium, creatinine, albumin, and bilirubin). Survival is also highly dependent on the underlying cause of the Budd–Chiari syndrome. For example, a patient with an underlying myeloproliferative disorder may progress to acute leukemia, independently of Budd–Chiari syndrome.

Gigantiform cementoma is a rare, autosomal dental tumor. It is benign, but without intervention it can result in severe disfigurement of the jaw. The cause of this tumor is currently unknown. This is an exceedingly rare tumor with only a handful of documented cases worldwide. The most famous case is of Novemthree Siahaan (who died on September 15, 2005), a young Indonesian boy from Batam Island who received medical care in Haulien, Taiwan through a Buddhist missionary from the Tzu Chi Foundation, which was documented on the Discovery Health Channel. Another famous case is a young Korean girl named Ayun Lee (August 26, 2003~) and her father Young-hak Lee whose case has shown that the tumor can be heritable. She is currently under treatment, which she may need to continue until her growth stops in her early 20s.

The term has been used in the past to describe florid cemento-osseous dysplasia, but it is now reserved for an autosomal dominant condition affecting the maxillae. It affects mostly Caucasian people under the age of 10. Treatment is difficult. Surgical removal of the affected bone is needed, and has to be followed by reconstruction.

Tolcapone inhibits the activity COMT, an enzyme which degrades dopamine. It has been used to complement levodopa; however, its usefulness is limited by possible complications such as liver damage. A similarly effective drug, entacapone, has not been shown to cause significant alterations of liver function. Licensed preparations of entacapone contain entacapone alone or in combination with carbidopa and levodopa.

Generally, acute myeloid leukemia is treated using chemotherapy consisting of an induction phase and consolidation phase (Dohner et al., 2009). Patients may also consider hematopoietic stem cell transplantation as a second mode of tackling the cancer. The most novel research is being done in tyrosine kinase inhibitors; however M2 acute myeloid leukemia treatment research involves molecules that inhibit the fusion oncoprotein AML1-ETO. Therefore, in terms of M2 subtype acute myeloid leukemia, the most prominent target is the abnormal AML1-ETO fusion protein. Similarly, chronic myeloid leukemia (CML) is comparable to acute myeloid leukemia M2 because it also forms a fusion oncoprotein – BCR-Abl. The developed tyrosine kinase inhibitor, imatinib mesylate, has had a tremendous effect on stopping cancer progression in the majority of chronic myeloid leukemia patients. BCR-Abl is constitutively active due chromosome translocation; therefore it over-phosphorylates the tyrosine kinase. Imatinib mesylate works to block BCR-Abl’s activity by blocking the active kinase domain (Fava et al., 2011).

Celastrol is a compound extracted from Tripterygium wilfordii that has anti-cancer properties. It was found to inhibit cell proliferation through the down regulation of AML1-ETO fusion oncoprotein. Celastrol inhibits the fusion oncoprotein by inducing mitochondrial instability and initiating caspase activity The decrease of AML1-ETO also results in lower levels of C-KIT kinases, Akt/PKB, STAT3, and Erk1/2 – all of which are involved in cell signaling and gene transcription (Yu et al., 2016).

Histone deacetylase inhibitors such as valproic acid (VPA), vorinostat, and all-trans retinoic acid (ATRA) are effective in targeting acute myeloid leukemia with the AML1-ETO fusion protein. The HDAC inhibitors are known to induce apoptosis through accumulation of DNA damage, inhibition of DNA repair, and activation of caspases. These inhibitors are extra sensitive to the fusion proteins. Vorinostat has been proven to cause a greater accumulation of DNA damage in fusion protein expressing cells and is directly correlated with the reduction of DNA repair enzymes (Garcia et al., 2008). Romidepsin, a drug in phase two clinical trials, has demonstrated higher efficacy in patients with AML1-ETO fusion protein leukemia (Odenike et al., 2008). Although many clinical evaluations have proven HDAC inhibitors have a promising effect on M2 subtype acute myeloid leukemia, it has not been approved as an official treatment.

In t(6;9) acute myeloid leukemia, FLT3-ITD and the DEK-NUP214 protein are potential targets for treatment. Sorafenib is a kinase inhibitor used as a treatment for kidney and liver cancer. The kinase inhibitor blocks serine-threonine kinase RAF-1 as well as FLT-ITD (Kindler, 2010). The drug has been proven to be effective in reducing FLT3-ITD overexpression (Metzelder et al., 2009). In patients with DEK-NUP214, it was found that the fusion oncoprotein caused an upregulation of mTORC1 (Sanden et al., 2013). Thus, a mTORC inhibitor could be a potential treatment.

Several dopamine agonists that bind to dopamine receptors in the brain have similar effects to levodopa. These were initially used as a complementary therapy to levodopa for individuals experiencing levodopa complications (on-off fluctuations and dyskinesias); they are now mainly used on their own as first therapy for the motor symptoms of PD with the aim of delaying the initiation of levodopa therapy and so delaying the onset of levodopa's complications. Dopamine agonists include bromocriptine, pergolide, pramipexole, ropinirole, piribedil, cabergoline, apomorphine and lisuride.

Though dopamine agonists are less effective than levodopa at controlling PD motor symptoms, they are usually effective enough to manage these symptoms in the first years of treatment. Dyskinesias due to dopamine agonists are rare in younger people who have PD but, along with other complications, become more common with older age at onset. Thus dopamine agonists are the preferred initial treatment for younger onset PD, and levodopa is preferred for older onset PD.

Dopamine agonists produce significant, although usually mild, side effects including drowsiness, hallucinations, insomnia, nausea, and constipation. Sometimes side effects appear even at a minimal clinically effective dose, leading the physician to search for a different drug. Agonists have been related to impulse control disorders (such as compulsive sexual activity, eating, gambling and shopping) even more strongly than levodopa. They tend to be more expensive than levodopa.

Apomorphine, a non-orally administered dopamine agonist, may be used to reduce off periods and dyskinesia in late PD. It is administered by intermittent injections or continuous subcutaneous infusions. Since secondary effects such as confusion and hallucinations are common, individuals receiving apomorphine treatment should be closely monitored. Two dopamine agonists that are administered through skin patches (lisuride and rotigotine) and are useful for people in the initial stages and possibly to control off states in those in the advanced state.

Although most autoimmune diseases cannot be cured, it is possible to manage the disease and participate in same activities that other women are able to do. Women with autoimmune diseases lead full, active lives. Seeing a specialist will assist in maintaining function and the maintenance of optimal health.

A 2007 review concluded that a period of nine months of growth hormone was required to reduce fibromyalgia symptoms and normalize IGF-1. A 2014 also found some evidence support its use. Sodium oxybate increases growth hormone production levels through increased slow-wave sleep patterns. However, this medication was not approved by the FDA for the indication for use in people with fibromyalgia due to the concern for abuse.

The muscle relaxants cyclobenzaprine, carisoprodol with acetaminophen and caffeine and tizanidine are sometimes used to treat fibromyalgia; however as of 2015 they are not approved for this use in the United States. The use of NSAIDs is not recommended as first line therapy.

Dopamine agonists (e.g. pramipexole and ropinirole) resulted in some improvement in a minority of people, but numerous side effects, including the onset of impulse control disorders like compulsive gambling and shopping, have led to concern about this approach.

There is some evidence that 5HT antagonists may be beneficial. Preliminary clinical data finds that low-dose naltrexone (LDN) may provide symptomatic improvement.

Very low quality evidence suggests quetiapine may be effective in fibromyalgia.

No high quality evidence exists that suggests synthetic cannabinoids help with fibromyalgia, and in general tolerability is poor.

The use of opioids is controversial. As of 2015, no opioid is approved for use in this condition by the FDA. The National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) in 2014 stated that there was a lack of evidence for opioids for most people. The Association of the Scientific Medical Societies in Germany in 2012 made no recommendation either for or against the use of weak opioids because of the limited amount of scientific research addressing their use in the treatment of FM. They strongly advise against using strong opioids. The Canadian Pain Society in 2012 said that opioids, starting with a weak opioid like tramadol, can be tried but only for people with moderate to severe pain that is not well-controlled by non-opioid painkillers. They discourage the use of strong opioids and only recommend using them while they continue to provide improved pain and functioning. Healthcare providers should monitor people on opioids for ongoing effectiveness, side effects and possible unwanted drug behaviors.

The European League Against Rheumatism in 2008 recommends tramadol and other weak opioids may be used for pain but not strong opioids. A 2015 review found fair evidence to support tramadol use if other medications do not work. Goldenberg "et al" suggest that tramadol works via its serotonin and norepinephrine reuptake inhibition, rather than via its action as a weak opioid receptor agonist. The combination of tramadol and paracetemol has demonstrated efficacy, safety and tolerability (for up to two years in the management of other pain conditions) without the development of tolerance. It is as effective as a combination of codeine (another mild opioid) and paracetamol but produces less sleepiness and constipation.

A large study of US people with fibromyalgia found that between 2005 and 2007 37.4% were prescribed short-acting opioids and 8.3% were prescribed long-acting opioids, with around 10% of those prescribed short-acting opioids using tramadol; and a 2011 Canadian study of 457 people with FM found 32% used opioids and two thirds of those used strong opioids.

Inhaled bronchodilators are the primary medications used, and result in a small overall benefit. The two major types are β agonists and anticholinergics; both exist in long-acting and short-acting forms. They reduce shortness of breath, wheeze, and exercise limitation, resulting in an improved quality of life. It is unclear if they change the progression of the underlying disease.

In those with mild disease, short-acting agents are recommended on an as needed basis. In those with more severe disease, long-acting agents are recommended. Long-acting agents partly work by improving hyperinflation. If long-acting bronchodilators are insufficient, then inhaled corticosteroids are typically added. With respect to long-acting agents, if tiotropium (a long-acting anticholinergic) or long-acting beta agonists (LABAs) are better is unclear, and trying each and continuing the one that worked best may be advisable. Both types of agent appear to reduce the risk of acute exacerbations by 15–25%. While both may be used at the same time, any benefit is of questionable significance.

Several short-acting β agonists are available, including salbutamol (albuterol) and terbutaline. They provide some relief of symptoms for four to six hours. Long-acting β agonists such as salmeterol, formoterol, and indacaterol are often used as maintenance therapy. Some feel the evidence of benefits is limited while others view the evidence of benefit as established. Long-term use appears safe in COPD with adverse effects include shakiness and heart palpitations. When used with inhaled steroids they increase the risk of pneumonia. While steroids and LABAs may work better together, it is unclear if this slight benefit outweighs the increased risks. Indacaterol requires an inhaled dose once a day, and is as effective as the other long-acting β agonist drugs that require twice-daily dosing for people with stable COPD.

Two main anticholinergics are used in COPD, ipratropium and tiotropium. Ipratropium is a short-acting agent, while tiotropium is long-acting. Tiotropium is associated with a decrease in exacerbations and improved quality of life, and tiotropium provides those benefits better than ipratropium. It does not appear to affect mortality or the overall hospitalization rate. Anticholinergics can cause dry mouth and urinary tract symptoms. They are also associated with increased risk of heart disease and stroke. Aclidinium, another long acting agent, reduces hospitalizations associated with COPD and improves quality of life. Aclinidinium has been used as an alternative to tiotropium, but which drug is more effective is not known.

Corticosteroids are usually used in inhaled form, but may also be used as tablets to treat and prevent acute exacerbations. While inhaled corticosteroids (ICSs) have not shown benefit for people with mild COPD, they decrease acute exacerbations in those with either moderate or severe disease. By themselves, they have no effect on overall one-year mortality. Whether they affect the progression of the disease is unknown. When used in combination with a LABA, they may decrease mortality compared to either ICSs or LABA alone. Inhaled steroids are associated with increased rates of pneumonia. Long-term treatment with steroid tablets is associated with significant side effects.

Few medications are approved specifically for schizoaffective disorder. In general, medications are chosen to reduce symptoms of psychosis and mood disorder.

Antipsychotic medication is usually required both for acute treatment and the prevention of relapse. There is no single antipsychotic of choice in treating schizoaffective disorder, but atypical antipsychotics should be considered because they have mood-stabilizing activity. Paliperidone is an antipsychotic with FDA approval for the treatment of schizoaffective disorder. Antipsychotics should be used at the minimum dose necessary to control symptoms. Potential side effects include extrapyramidal symptoms, including tremor, muscle stiffness, and restlessness or akathisia. Atypical antipsychotics carry a risk of metabolic syndrome, including weight gain, increased blood sugar, and increased blood cholesterol, so regular monitoring of weight and bloodwork should be carried out. Some atypical antipsychotics, such as ziprasidone and aripiprazole, are associated with less risk than others, such as olanzapine. Medication choice is based on how effectively it reduces symptoms, how few side effects it causes, and cost.

In people with treatment-refractory psychosis, a clozapine trial should be considered. Clozapine is an atypical antipsychotic that is recognized as being particularly effective when other antipsychotic agents have failed. Clozapine should also be considered in people with chronic and persistent suicidal thinking and behaviour, as it has been shown to reduce the risk of suicide in patients with schizoaffective disorder and a history of suicidality. Between 0.5 and 2% of patients taking clozapine may develop a life-threatening complication called agranulocytosis, which is a significant drop in a type of white blood cell. Because of this risk, people taking clozapine must have regular monitoring of blood cell counts.

The management of the bipolar type of schizoaffective disorder is similar to the treatment of bipolar disorder, with the goal of preventing mood episodes and cycling. Lithium or anticonvulsant mood stabilizers such as valproic acid, carbamazepine, and lamotrigine are prescribed in combination with an antipsychotic.

For depression, if an antidepressant is prescribed, "extra attentiveness must be given" by the prescribing clinician due its risk for long-term mood cycle acceleration (that is, inducing more frequent episodes of depression per unit of time) and medication-induced psychosis or mania. For individuals who show emerging psychosis, mania, mixed episode symptoms, or mood cycle acceleration, switching to an antipsychotic plus lithium or lamotrigine is preferable to antidepressants.

For individuals who experience anxiety, anti-anxiety medications can be used, usually on a short-term basis. Benzodiazepines, including lorazepam, clonazepam and diazepam, are types of anti-anxiety medications. Care must be taken when prescribing benzodiazepines due to the risk of the patient developing tolerance and dependence.

The Boston brace is a plastic exterior that can be made with a small amount of lordosis to minimize stresses on discs that have experienced herniated discs.

In the case where Ehlers Danlos syndrome (EDS) is responsible, being properly fitted with a customized brace may be a solution to avoid strain and limit the frequency of instability.

Corticosteroid injections can be effective for temporary relief from symptoms while a person develops a long-term strategy that fits their lifestyle. This form of treatment is thought to reduce discomfort in those with CTS due to its ability to decrease median nerve swelling. The use of ultrasound while performing the injection is more expensive but leads to faster resolution of CTS symptoms. The injections are done under local anesthesia. This treatment is not appropriate for extended periods, however. In general, local steroid injections are only used until more definitive treatment options can be used. Corticosteroid injections do not appear to be very effective for slowing disease progression.

Electroconvulsive therapy, or ECT, may be considered for patients with schizoaffective disorder experiencing severe depression or severe psychotic symptoms that have not responded to treatment with antipsychotics.

Generally accepted treatments include: physiotherapy, steroids either orally or injected locally, splinting, and surgical release of the transverse carpal ligament. Limited evidence suggests that gabapentin is no more effective than placebo for CTS treatment. There is insufficient evidence for therapeutic ultrasound, yoga, acupuncture, low level laser therapy, vitamin B6, and exercise. Change in activity may include avoiding activities that worsen symptoms.

The American Academy of Orthopedic Surgeons recommends proceeding conservatively with a course of nonsurgical therapies tried before release surgery is considered. A different treatment should be tried if the current treatment fails to resolve the symptoms within 2 to 7 weeks. Early surgery with carpal tunnel release is indicated where there is evidence of median nerve denervation or a person elects to proceed directly to surgical treatment. Recommendations may differ when carpal tunnel syndrome is found in association with the following conditions: diabetes mellitus, coexistent cervical radiculopathy, hypothyroidism, polyneuropathy, pregnancy, rheumatoid arthritis, and carpal tunnel syndrome in the workplace.

Since lumbar hyperlordosis is usually caused by habitual poor posture, rather than by an inherent physical defect like scoliosis or hyperkyphosis, it can be reversed. This can be accomplished by stretching the lower back, hip-flexors, hamstring muscles, and strengthening abdominal muscles.Dancers should ensure that they don't strain themselves during dance rehearsals and performances. To help with lifts, the concept of isometric contraction, during which the length of muscle remains the same during contraction, is important for stability and posture.

Lumbar hyperlordosis may be treated by strengthening the hip extensors on the back of the thighs, and by stretching the hip flexors on the front of the thighs.

Only the muscles on the front and on the back of the thighs can rotate the pelvis forward or backward while in a standing position because they can discharge the force on the ground through the legs and feet. Abdominal muscles and erector spinae can't discharge force on an anchor point while standing, unless one is holding his hands somewhere, hence their function will be to flex or extend the torso, not the hip.

Back hyper-extensions on a Roman chair or inflatable ball will strengthen all the posterior chain and will treat hyperlordosis. So too will stiff legged deadlifts and supine hip lifts and any other similar movement strengthening the posterior chain "without involving the hip flexors" in the front of the thighs. Abdominal exercises could be avoided altogether if they stimulate too much the psoas and the other hip flexors.

Controversy regarding the degree to which manipulative therapy can help a patient still exists. If therapeutic measures reduce symptoms, but not the measurable degree of lordotic curvature, this could be viewed as a successful outcome of treatment, though based solely on subjective data. The presence of measurable abnormality does not automatically equate with a level of reported symptoms.

A number of medications exist to treat incontinence including: fesoterodine, tolterodine and oxybutynin. While a number appear to have a small benefit, the risk of side effects are a concern. For every ten or so people treated only one will become able to control their urine and all medication are of similar benefit.

Medications are not recommended for those with stress incontinence and are only recommended in those who have urge incontinence who do not improve with bladder training.

In 1995, the Food and Drug Administration (FDA) approved the Varicella vaccine to prevent chickenpox. Its effect on postherpetic neuralgia is still unknown. The vaccine—made from a weakened form of the varicella-zoster virus—may keep chickenpox from occurring in nonimmune children and adults, or at least lessen the risk of the chickenpox virus lying dormant in the body and reactivating later as shingles. If shingles could be prevented, postherpetic neuralgia could be completely avoided.

In May 2006 the Advisory Committee on Immunization Practices approved a new vaccine by Merck (Zostavax) against shingles. This vaccine is a more potent version of the chickenpox vaccine, and evidence shows that it reduces the incidence of postherpetic neuralgia. The CDC recommends use of this vaccine in all persons over 60 years old.

Treatment options range from conservative treatment, behavior management, bladder retraining, pelvic floor therapy, collecting devices (for men), fixer-occluder devices for incontinence (in men), medications and surgery. The success of treatment depends on the correct diagnoses. Weight loss is recommended in those who are obese.