Immunosuppressive therapies, encompassing corticosteroids, azathioprine, methotrexate and more recently, rituximab, are the mainstay of therapy. Other treatments include PE, IVIG, and thymectomy. Patients reportedly exhibited a heterogenous response to immunomodulation.

Antiepileptics can be used for symptomatic relief of peripheral nerve hyperexcitability. Indeed, some patients have exhibited a spontaneous remission of symptoms.

Prognosis is poor, however, current analysis suggests that those associated with thymoma, benign or malignant, show a less favorable prognosis (CASPR2 Ab positive).

Prevention focuses on improving sanitation of water and food sources.

Treatment focuses on addressing the central components of intestinal inflammation, bacterial overgrowth and nutritional supplementation.

There are multiple large-field, multi-country research initiatives focusing on strategies to prevent and treat EE.

- The MAL-ED project

- The Alive and Thrive nutrition project

- The Sanitation, Hygiene and Infant Nutrition Efficacy (SHINE) Trial (ClinicalTrials.gov identifier: NCT01824940)

- The WASH Benefits Study

In January 2001, researchers at Fordham University and Massachusetts General Hospital simultaneously reported finding the genetic mutation that causes FD, a discovery that opens the door to many diagnostic and treatment possibilities.

Despite that it probably would not happen in the near future, some expect that stem-cell therapy will result. Eventually, treatment could be given in utero.

While that may be years ahead, genetic screening became available around April 2001, enabling Ashkenazi Jews to find out if they are carriers. Screening organization Dor Yeshorim offers to test as part of its panel, which also includes Tay-Sachs disease and cystic fibrosis.

In the meantime, more research into treatments is being funded by the foundations that exist. These foundations are organized and run by parents of those with FD. There is no governmental support beyond recognizing those diagnosed with FD as eligible for certain programs.

Prenatal stress (or prenatal maternal stress) is exposure of an expectant mother to stress, which can be caused by stressful life events or by environmental hardships. The resulting changes to the mother's hormonal and immune system may harm the fetus's (and after birth, the infant's) immune function and brain development.

Prenatal stress is shown to have several affects in fetal brain development. In the hippocampus of adult male rats, prenatal stress has shown to decrease the rate of proliferation and cell death in the hypothalamus-pituitary axis. Prenatal stressed animals have prolonged corticosterone response. Removing the adrenal glands of the mother eliminates the effect of the pup's corticosterone response. Supplementing the adrenalectamized mother with corticosterone, rescued the hypothalamic-pituitary-axis response to maternal stress for prenatally stressed offspring. Prenatal stress caused high glucocorticoids, which in turn affects the hypothalamic-pituitary-axis negative feedback.

A study by García-Cáceres et al. showed that prenatal stress decreases cell turnover and proliferation in the hypothalamus of adult rats, which reduces structural plasticity and reduces the response to stress in adulthood. This study also showed that when prenatally stressed rats were stressed in adulthood the females showed an increase in corticotropin-releasing hormone suggesting it to be an up-regulation in the hypothalamic-pituitary adrenal axis. Males showed no elevation of corticosterone levels. Increase in adrenocorticotropic hormone with no effect of adult stress and a decrease in the corticotropin-releasing hormone mRNA in the hypothalamus showed a down-regulation. The author concludes that this makes prenatally stressed females less reactive to later life stressors than males.

Patient advocacy groups have been helping to determine research priorities.

Atypical hemolytic uremic syndrome (aHUS) has also been referred to as diarrhea-negative hemolytic-uremic syndrome (D HUS).

Currently, there is no cure for Devic's disease, but symptoms can be treated. Some patients recover, but many are left with impairment of vision and limbs, which can be severe.

Attacks are treated with short courses of high dosage intravenous corticosteroids such as methylprednisolone IV.

Plasmapheresis can be an effective treatment when attacks progress or do not respond to corticosteroid treatment. Clinical trials for these treatments contain very small numbers, and most are uncontrolled, though some report high success percentage.

Treatment in DOCK8 deficiency focuses on preventing and treating infections. Broad-spectrum antibiotics are a common mode of treatment when infection is present, though some infections (like lung abscesses) require surgical treatment. Pneumatocele may be treated with surgery, but the benefit is unclear.

Surgical treatment is also recommended for skin abscesses, along with topical and systemic antibiotics and antifungals.

Long-term treatment with systemic antibiotics, including trimethoprim/sulfamethoxazole, penicillins, and cephalosporins, is effective in preventing skin and lung infections. Other treatments used in DOCK8 deficiency include sodium cromoglycate, which improves white blood cell function, and isotretinoin, which improves skin condition.

Sometimes, Intravenous immunoglobulin is used as a treatment, but its benefits have not been proven. Levamisole is also ineffective. Mixed clinical outcomes have been found with interferon gamma and omalizumab. Though early research on hematopoietic stem cell transplantation was equivocal, later research has shown it to improve immune function. Two patients have been cured by bone marrow transplantation. Cyclosporine A is a current topic of research; preliminary results have shown it to be effective.

Children with DOCK8 deficiency do not tend to live long; sepsis is a common cause of death at a young age. CNS and vascular complications are other common causes of death.

The outlook for patients with FD depends on the particular diagnostic category. Patients with chronic, progressive, generalized dysautonomia in the setting of central nervous system degeneration have a generally poor long-term prognosis. Death can occur from pneumonia, acute respiratory failure, or sudden cardiopulmonary arrest in such patients.

Parents and patients should generally be educated regarding daily eye care and early warning signs of corneal problems as well as the use of punctal cautery. This education has resulted in decreased corneal scarring and need for more aggressive surgical measures such as tarsorrhaphy, conjunctival flaps, and corneal transplants.

Prenatal stress and negative mood during pregnancy has been shown to increase the risk for poor childbirth outcomes and postnatal maternal mood problems. Additionally, prenatal distress can interfere with the mother-infant attachment and child development outcomes. Despite the clear association between prenatal stress and child outcomes, frequently women do not receive screening, prevention, or treatment for mood or stress concerns.

Given the relationship between prenatal stress and child outcomes, it is essential to examine interventions that aim to reduce anxiety, depression, and stress during pregnancy. Mindfulness based stress reduction has been demonstrated to reduce anxiety and depression for people with stress-related and chronic medical conditions.

One pilot study shows promise for the potential of a mindfulness-based intervention to reduce negative affect and anxiety of women during pregnancy. Based out of the California Pacific Medical Center Research Institute, investigators Dr. Cassandra Vieten and Dr. John Astin conducted a wait-list control pilot study that tested a group-based mindfulness intervention. There were 31 women enrolled in the study: 13 women were assigned to the intervention and 18 women were assigned to the control group. Measures of anxiety, negative affect, positive affect, depression, mindfulness, perceived stress, and affect regulation were taken before intervention or control was assigned and after the intervention or control was completed. Measures were repeated at a follow-up visit 3 months after the intervention or control was completed. The investigators found a significant decrease in anxiety (p<.05) and negative affect (p <.04) in women who completed the mindfulness based intervention, but not a significant decrease in depression, positive affect, mindfulness, affect regulation, and perceived stress. These results suggest that mindfulness intervention during pregnancy reduce anxiety and negative affect of mothers. This study is a promising start to the potential impact that mindfulness based interventions could have on reducing prenatal stress, and thereby improving child outcomes.

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.

Due to the lack of knowledge around the underlying mechanism of MAP, an effective treatment method has not been developed. Treatment for this condition is symptomatic. However, several treatment methods have been tested and are still being developed as more information regarding the condition is found. Fibrinolytic and immunosuppresive therapeutic regimens were tested and found to be mostly unsuccessful as treatment methods.

After treating conditions comorbid with Degos disease, physicians have recently found improvement in symptoms with the use of eculizumab and treprostinil. Discovered by dermatopathologist, Cynthia Magro, response to eculizumab is often immediate and dramatic, but has been of limited duration and is expensive, needing to be infused every 14 days. Treprostinil use has been reported to result in clearing of gastrointestinal and central nervous system findings as well as clearing of cutaneous lesions, but reports are limited. Treprostinil may be more effective than other vasodilators because it may also increase the population of circulating endothelial cells, allowing angiogenesis.

An estimated 64 percent of patients with venous thromboembolism may have activated protein C resistance.

Due to the uncertainty about the pathogenesis of FM, current treatment approaches focus on management of symptoms to improve quality of life, using integrated pharmacological and non-pharmacological approaches. There is no single intervention shown to be effective for all patients and no gold treatment standard exists for FM. Multimodal/multidisciplinary therapy is recommended to target multiple underlying factors of FM. A meta-analysis of 1,119 subjects found "strong evidence that multicomponent treatment has beneficial short-term effects on key symptoms of FMS."

Activated protein C resistance (APCR) is a hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). This results in an increased risk of venous thrombosis, which can cause problems with circulation, such as pulmonary embolism.

The disorder can be acquired or inherited, the hereditary form having an autosomal dominant inheritance pattern.

In 1985 Edward Blau, a pediatrician in Marshfield, Wisconsin, reported a family that over four generations had granulomatous inflammation of the skin, eyes and joints. The condition was transmitted as an autosomal dominant trait. In the same year Jabs et al. reported a family that over two generations had granulomatous synovitis, uveitis and cranial neuropathies. The condition was transmitted in an autosomal dominant fashion. In 1981 Malleson et al. reported a family that had autosomal dominant synovitis, camptodactyly, and iridocyclitis. One member died of granulomatous arteritis of the heart and aorta. In 1982 Rotenstein reported a family with granulomatous arteritis, rash, iritis, and arthritis transmitted as an autosomal dominant trait over three generations. Then in 1990 Pastores et al. reported a kindred with a phenotype very similar to what Blau described and suggested that the condition be called Blau Syndrome (BS). They also pointed out the similarities in the families noted above to BS but also pointed out the significant differences in the phenotypes.

In 1996 Tromp et al. conducted a genome wide search using affected and non affected members of the original family. A marker D16S298gave a maximum LOD score of 3.75 and put the BS susceptibility locus within the 16p12-q21 interval. Hugot et al. found a susceptibility locus for Crohn disease a granulomatous inflammation of the bowel on chromosome 16 close to the locus for BS. Based on the above information Blau suggested in 1998 that the genetic defect in BS and Crohn Disease might be the same or similar.

Finally in 2001 Miceli-Richard et al. found the defect in BS to be in the nucleotide-binding domain of CARD15/NOD2. They commented in their article that mutations in CARD15 had also been found in Crohn's Disease. Confirmation of the defect in BS being in the CARD15 gene was made by Wang et al. in 2002 using the BS family and others. With that information the diagnosis of BS was not only determined by phenotype but now by genotype.

Early onset sarcoidosis is BS without a family history, BS has been diagnosed in patients who have not only the classic triad but granuloma in multiple organs. Treatment has included the usual anti inflammatory drugs such as adrenal glucocorticoids, anti-metabolites and also biological agents such as anti-TNF and infliximab all with varying degrees of success.

The elucidation that the gene defect in BS involves the CARD15/NOD2 gene has stimulated many investigators, to define how this gene operates as part of the innate immune system, that responds to bacterial polysaccharides, such as muramyl dipeptide, to induce signaling pathways that induce cytokine responses, and protect the organism. In BS the genetic defect seems to lead to over expression, and poor control of the inflammatory response leading to widespread granulomatous, inflammation and tissue damage This reference provides an excellent review of the clinical aspects of BS, and the presumed pathogenetic mechanisms brought about by the gene defect.

What stimulus activates the aberrant immune response, and what would then lead to the discovery of more precise therapy, and the relationship to the specific gene defect and phenotype, require further research.

- List of cutaneous conditions

The papules characteristic for this disease develop due to infractions, or blockages in small-medium arteries and veins. The underlying cause is unknown for this disease. Though not confirmed, some cases have shown signs of inheritance between first-degree relatives. It has been suggested that the disease has a familial inheritance pattern; it is thought to be an autosomal dominant disorder. In most cases of familial inheritance, the benign variant of the disease has been present.

Due to the lack of knowledge of the pathomechanism for this condition prevention strategies are not known. However, in order to prevent worsening of symptoms, consistent evaluations should be conducted by a physician.

One study looked at commercial buildings and their employees, comparing some environmental factors suspected of inducing SBS to a self-reported survey of the occupants, finding that the measured psycho-social circumstances appeared more influential than the tested environmental factors. The list of environmental factors in the study can be found here. Limitations of the study include that it only measured the indoor environment of commercial buildings, which have different building codes than residential buildings, and that the assessment of building environment was based on layman observation of a limited number of factors.

Research has shown that SBS shares several symptoms common in other conditions thought to be at least partially caused by psychosomatic tendencies. The umbrella term "autoimmune/inflammatory syndrome induced by adjuvants" has been suggested. Other members of the suggested group include Silicosis, Macrophagic myofascitis, The Gulf War syndrome, Post-vaccination phenomena.

Sick building syndrome can also occur due to factors of the home. Laminated flooring can cause more exposure to chemicals and more resulting SBS symptoms compared to stone, tile, and cement flooring. Recent redecorating and new furnishings within the last year were also found to be associated with increased symptoms, along with dampness and related factors, having pets, and the presence of cockroaches. The presence of mosquitoes was also a factor related to more symptoms, though it is unclear whether it was due to the presence of mosquitoes or the use of repellents.

Blau Syndrome is an autosomal dominant genetic inflammatory disorder which affects the skin, eyes, and joints. It is caused by a mutation in the NOD2 (CARD15) gene. Symptoms usually begin before the age of 4, and the disease manifests as early onset cutaneous sarcoidosis, granulomatous arthritis, and uveitis.

Morbidity and mortality range from both extremes as the significance correlate with the underlying systemic disease.