There is no permanent cure for this syndrome, although patients can be treated according to their specific symptoms. The prognosis for those with Cockayne syndrome is poor, as death typically occurs by the age of 12. Treatment usually involves physical therapy and minor surgeries to the affected organs, like cataract removal. Also wearing high-factor sunscreen and protective clothing is recommended as patients with Cockayne syndrome are very sensitive to UV radiation. Optimal nutrition can also help. Genetic counseling for the parents is recommended, as the disorder has a 25% chance of being passed to any future children, and prenatal testing is also a possibility. Another important aspect is prevention of recurrence of CS in other sibling. Identification of gene defects involved makes it possible to offer genetic counseling and antenatal

diagnostic testing to the parents who already have one affected child.

The opioid antagonist naloxone allowed a woman with congenital insensitivity to pain to experience it for the first time. Similar effects were observed in Na1.7 null mice treated with naloxone. As such, opioid antagonists like naloxone and naltrexone may be effective in treating the condition.

CIPA sufferers have to live an extremely cautious life, incorporating numerous controls as part of their daily routine. Every morning it will be necessary to check for bruises, scratches or other injuries that might have taken place during sleeping hours, as it is very common for CIPA patients to injure themselves unknowingly. Temperature measuring must be done constantly, as well as urination control, by setting alarms or other reminders.

If any kind of accident has been suffered, regardless of its type and severity, CIPA patients must go through a thorough check for compromising injuries.

At young ages, permanent surveillance is vital. A lack of awareness of the extreme dangers this condition represents condemns the infant to a complete lack of tools against risk situations.

There are several other procedures a CIPA patient has to undergo in order to live a safe life. Those mentioned above were extracted from a “Doctor House” episode (Insensitive).

Treatments for CCCA remain investigational. Altering hair care practices has not been proven to assist in hair rejuvenation. High-dose topical steroids, antibiotics, immunomodulators such as tacrolimus (Protopic) and pimecrolimus (Elidel), and anti-androgen/5alpha Reductase inhibitors have been used with unknown efficacy.

SJS constitutes a dermatological emergency. Patients with documented "Mycoplasma" infections can be treated with oral macrolide or oral doxycycline.

Initially, treatment is similar to that for patients with thermal burns, and continued care can only be supportive (e.g. intravenous fluids and nasogastric or parenteral feeding) and symptomatic (e.g., analgesic mouth rinse for mouth ulcer). Dermatologists and surgeons tend to disagree about whether the skin should be debrided.

Beyond this kind of supportive care, no treatment for SJS is accepted. Treatment with corticosteroids is controversial. Early retrospective studies suggested corticosteroids increased hospital stays and complication rates. No randomized trials of corticosteroids were conducted for SJS, and it can be managed successfully without them.

Other agents have been used, including cyclophosphamide and cyclosporin, but none has exhibited much therapeutic success. Intravenous immunoglobulin treatment has shown some promise in reducing the length of the reaction and improving symptoms. Other common supportive measures include the use of topical pain anesthetics and antiseptics, maintaining a warm environment, and intravenous analgesics.

An ophthalmologist should be consulted immediately, as SJS frequently causes the formation of scar tissue inside the eyelids, leading to corneal vascularization, impaired vision, and a host of other ocular problems. Those with chronic ocular surface disease caused by SJS may find some improvement with PROSE treatment (prosthetic replacement of the ocular surface ecosystem treatment).

Surgery remains the front-line therapy for HNPCC. There is an ongoing controversy over the benefit of 5-fluorouracil-based adjuvant therapies for HNPCC-related colorectal tumours, particularly those in stages I and II.

There is no cure for IBS but in the future gene therapy may offer a cure.

Treatments for IBS generally attempt to improve the appearance of the skin and the comfort of the sufferer. This is done by exfoliating and increasing the moisture of the skin. Common treatments include:

- Emollients: moisturisers, petroleum jelly or other emolients are used, often several times a day, to increase the moisture of the skin.

- Baths: long baths (possibly including salt) several times a week are used to soften the skin and allow exfoliation.

- Exfoliating creams: creams containing keratolytics such as urea, salicylic acid and lactic acid may be useful.

- Antiseptic washes: antiseptics may be used to kill bacteria in the skin and prevent odour.

- Retenoids: very severe cases may use oral retinoids to control symptoms but these have many serious side effects including, in the case of IBS, increased blistering.

The most common problem with syndactyly correction is creeping of the skin towards the fingertip over time. This is likely due to tension at the site of the repair between the digits. Additional surgery may be required to correct this. One critique of using skin grafts is that the grafts darken in the years after surgery and become more noticeable. Also, if the skin grafts are harvested from the groin area, the skin may grow hair. Finally, the fingers may deviate after surgery. This is most commonly seen in complex syndactyly (when there has been a bony joining of the fingers).

Because the circumference of the conjoined fingers is smaller than the circumference of the two separated fingers, there is not enough skin to cover both digits once they are separated at the time of surgery. Therefore, the surgeon must bring new skin into the area at the time of surgery. This is most commonly done with a skin graft (from groin or anterior elbow). Skin can also be used from the back of the hand by mobilizing it (called a "graftless" syndactyly correction), which requires planning over a period of months prior to surgery.

Advantages of patient-controlled analgesia include self-delivery of pain medication, faster alleviation of pain because the patient can address pain with medication, and dosage monitoring by medical staff (dosage can be increased or decreased depending on need). With a PCA the patient spends less time in pain and as a corollary to this, patients tend to use less medication than in cases in which medication is given according to a set schedule or on a timer.

Disadvantages include the possibility that a patient will use the pain medication nonmedically, self-administering the pain medication to get high. If a PCA device is not programmed properly for the patient this can result in an under-dose or overdose in a medicine. The system may also be inappropriate for certain individuals, for example patients with learning difficulties or confusion. Also, patients with poor manual dexterity may be unable to press the buttons as would those who are critically ill. PCA may not be appropriate for younger patients.

Cockayne syndrome (CS), also called Neill-Dingwall syndrome, is a rare and fatal autosomal recessive neurodegenerative disorder characterized by growth failure, impaired development of the nervous system, abnormal sensitivity to sunlight (photosensitivity), eye disorders and premature aging. Failure to thrive and neurological disorders are criteria for diagnosis, while photosensitivity, hearing loss, eye abnormalities, and cavities are other very common features. Problems with any or all of the internal organs are possible. It is associated with a group of disorders called leukodystrophies, which are conditions characterized by degradation of neurological white matter. The underlying disorder is a defect in a DNA repair mechanism. Unlike other defects of DNA repair, patients with CS are not predisposed to cancer or infection. Cockayne syndrome is a rare but destructive disease usually resulting in death within the first or second decade of life. The mutation of specific genes in Cockayne syndrome is known, but the widespread effects and its relationship with DNA repair is yet to be well understood.

It is named after English physician Edward Alfred Cockayne (1880–1956) who first described it in 1936 and re-described in 1946. Neill-Dingwall syndrome was named after Mary M. Dingwall and Catherine A. Neill. These women described the case of two brothers with Cockayne syndrome and asserted it was the same disease described by Cockayne. In their article the women contributed to the symptoms of the disease through their discovery of calcifications in the brain. They also compared Cockayne syndrome to what is now known as Hutchinson–Gilford progeria syndrome (HGPS), then called progeria, due to the advanced aging that characterizes both disorders.

Hospitalization and IV hydration should be the first step in any patient suspected of having myoglobinuria or rhabdomyolysis. The goal is to induce a brisk diuresis to prevent myoglobin precipitation and deposition, which can cause acute kidney injury. Mannitol can be added to assist with diuresis. Adding sodium bicarbonate to the IV fluids will cause alkalinzation of the urine, believed to reduce the breakdown of myoglobin into its nephrotoxic metabolites, thus preventing renal damage. Often, IV normal saline is all that is needed to induce diuresis and alkalinize the urine.

The primary treatment of TEN is discontinuation of the causative factor(s), usually an offending drug, early referral and management in burn units or intensive care units, supportive management, and nutritional support.

Current literature does not convincingly support use of any adjuvant systemic therapy. Initial interest in Intravenous immunoglobulin (IVIG) came from research showing that IVIG could inhibit Fas-FasL mediated keratinocyte apoptosis in vitro. Unfortunately, research studies reveal conflicting support for use of IVIG in treatment of TEN. Ability to draw more generalized conclusions from research to date has been limited by lack of controlled trials, and inconsistency in study design in terms of disease severity, IVIG dose, and timing of IVIG administration.

Larger, high quality trials are needed to assess the actual benefit of IVIG in TEN.

Numerous other adjuvant therapies have been tried in TEN including, corticosteroids, cyclosporin, cyclophosphamide, plasmapheresis, pentoxifylline, N-acetylcysteine, ulinastatin, infliximab, and Granulocyte colony-stimulating factors (if TEN associated-leukopenia exists). There is mixed evidence for use of corticosteriods and scant evidence for the other therapies.

90 percent of babies born SGA catch up in growth by the age of 2. However, all SGA babies should be watched for signs of Failure-to-Thrive (FTT), hypoglycemia and other conditions common to SGA babies (see below). Hypoglycemia is common in asymmetrical SGA babies because their larger brains burn calories at a faster rate than their usually limited fat stores hold. Hypoglycemia is treated by frequent feedings and/or additions of cornstarch-based products (such as Duocal powder) to the feedings.

For the 10 percent of those that are SGA without catchup growth by the age of 2, an endocrinologist should be consulted. Some cases warrant growth hormone therapy (GHT).

There are some common conditions and disorders found in many that are SGA (and especially those that are SGA without catchup growth by age 2). They should be treated by the appropriate specialist:

- Gastroenterologist - for gastrointestinal issues such as: reflux (GERD) and/or delayed gastric emptying (DGE)

- Dietitian - to address caloric deficits. Dietitians are usually brought in for cases that include FTT. Also, according to the theory of thrifty phenotype, causes of growth restriction also trigger epigenetic responses in the fetus that are otherwise activated in times of chronic food shortage. If the offspring actually develops in an environment rich in food it may be more prone to metabolic disorders, such as obesity and type II diabetes.

- Speech Language Pathologist (SLP) or Occupational Therapist (OT) - for feeding issues. OTs may also treat sensory issues

- Behaviorist - for feeding issues, a behavioral approach may also be used, but usually for older children (over 2)

- Allergist - to diagnose or rule out food allergies (not necessarily more common in those SGA than the normal population)

- Ear, Nose and Throat doctor (ENT) - to diagnose enlarged adenoids or tonsils (not necessarily more common in those SGA than the normal population)

For IUGR (during pregnancy), possible treatments include the early induction of labor, though this is only done if the condition has been diagnosed and seen as a risk to the health of the fetus.

Treatment is typically achieved via diet and exercise, although metformin may be used to reduce insulin levels in some patients (typically where obesity is present). A referral to a dietician is beneficial. Another method used to lower excessively high insulin levels is cinnamon as was demonstrated when supplemented in clinical human trials.

A low carbohydrate diet is particularly effective in reducing hyperinsulinism.

A healthy diet that is low in simple sugars and processed carbohydrates, and high in fiber, and vegetable protein is often recommended. This includes replacing white bread with whole-grain bread, reducing intake of foods composed primarily of starch such as potatoes, and increasing intake of legumes and green vegetables, particularly soy.

Regular monitoring of weight, blood sugar, and insulin are advised, as hyperinsulinemia may develop into diabetes mellitus type 2.

It has been shown in many studies that physical exercise improves insulin sensitivity. The mechanism of exercise on improving insulin sensitivity is not well understood however it is thought that exercise causes the glucose receptor GLUT4 to translocate to the membrane. As more GLUT4 receptors are present on the membrane more glucose is taken up into cells decreasing blood glucose levels which then causes decreased insulin secretion and some alleviation of hyperinsulinemia. Another proposed mechanism of improved insulin sensitivity by exercise is through AMPK activity. The beneficial effect of exercise on hyperinsulinemia was shown in a study by Solomon et al. (2009), where they found that improving fitness through exercise significantly decreases blood insulin concentrations.

Marfanoid–progeroid–lipodystrophy syndrome (MPL), also known as Marfan lipodystrophy syndrome (MFLS) or progeroid fibrillinopathy, is an extremely rare medical condition which manifests as a variety of symptoms including those usually associated with Marfan syndrome, an appearance resembling that seen in neonatal progeroid syndrome (NPS; also known as Wiedemann–Rautenstrauch syndrome), and severe partial lipodystrophy. It is a genetic condition that is caused by mutations in the "FBN1" gene, which encodes profibrillin, and affects the cleavage products of profibrillin, fibrillin-1, a fibrous structural protein, and asprosin, a glucogenic protein hormone. As of 2016, fewer than 10 cases of the condition have been reported. Lizzie Velasquez and Abby Solomon have become known publicly through the media for having the condition.

In addition to severe lipodystrophy (loss of adipose tissue), individuals with MPL show a concomitant marked loss of lean tissue mass, which also contributes to their "skinny" appearance. Based on visual inspection, it was originally thought that the lipodystrophy associated with MPL was generalized. However, it appears in fact to be partial, being confined to the face, distal extremities, and the and lateral regions of the buttocks. Normal amounts of subcutaneous fat are found in the torso over the chest and abdomen. As such, the breasts are normal in females with MPL.

Individuals with MPL have an appearance of being prematurely aged, but this is not due to actual early aging and is instead due to their paucity of subcutaneous fat. As such, MPL is not truly a form of progeria.

In 2016, it was discovered that the partial lipodystrophy associated with MPL is caused by loss of the C-terminal domain cleavage product of profibrillin and novel glucogenic protein hormone, which has been named asprosin. Due to asprosin deficiency, individuals with MPL eat less, and do not gain weight or develop symptoms of diabetes like insulin resistance. MPL patients burn less energy than normal individuals, but also consume less, and their net energy balance is moderately reduced. In contrast to MPL patients, whose asprosin is undetectable in the blood, individuals with obesity and diabetes have elevated levels of asprosin. As such, "FBN1" has been nicknamed the "thin gene", and drug development for targeted inhibition of asprosin signaling is considered to be an "unusually promising" potential therapeutic route in the treatment of obesity and diabetes.

Transcutaneous delivery systems, including iontophoretic systems, are available. These are popular for administration of opioids such as fentanyl, or local anesthetics such as lidocaine. Iontocaine is one example of such a system.

As the horn is composed of keratin, the same material found in fingernails, the horn can usually be removed with a sterile razor.However, the underlying condition will still need to be treated. Treatments vary, but they can include surgery, radiation therapy, and chemotherapy.

Congenital insensitivity to pain with anhidrosis may be misdiagnosed for leprosy, based on similar symptoms of severe injuries to the hands and feet.

SJS (with less than 10% of body surface area involved) has a mortality rate of around 5%. The mortality for toxic epidermal necrolysis (TEN) is 30–40%. The risk for death can be estimated using the SCORTEN scale, which takes a number of prognostic indicators into account. It is helpful to calculate a SCORTEN within the first 3 days of hospitalization. Other outcomes include organ damage/failure, cornea scratching, and blindness.. Restrictive lung disease may develop in patients with SJS and TEN after initial acute pulmonary involvement. Patients with SJS or TEN caused by a drug have a better prognosis the earlier the causative drug is withdrawn.

Corticosteroids and other immunosuppressive medications have historically been employed to reduce pemphigus symptoms, yet steroids are associated with serious and long-lasting side effects and their use should be limited as much as possible. Intravenous immunoglobulin, mycophenolate mofetil, methotrexate, azathioprine, and cyclophosphamide have also been used with varying degrees of success.

An established alternative to steroids are monoclonal antibodies such as rituximab, which are increasingly being used as first-line treatment. In numerous case series, many patients achieve remission after one cycle of rituximab. Treatment is more successful if initiated early on in the course of disease, perhaps even at diagnosis. Rituximab treatment combined with monthly IV immunoglobulin infusions has resulted in long-term remission with no recurrence of disease in 10 years after treatment was halted. This was a small trial study of 11 patients with 10 patients followed to completion.

The most common treatment is the acne medication isotretinoin. It may be combined with prednisone. Dapsone, which is normally used to treat leprosy, is a riskier medication but is sometimes prescribed in cases where the normal therapy is ineffectual. Antibiotics such as tetracycline or erythromycin may also be prescribed. An alternative option is to treat with carbon dioxide laser therapy, followed by topical tretinoin therapy.

Surgery may be necessary to remove large nodules. Alternatively, nodules can be injected with corticosteroids such as triamcinolone.

Because granuloma annulare is usually asymptomatic and self-limiting with a course of about 2 years, initial treatment is generally topical steroid creams, followed by oral steroids and finally intradermal injections at the site of each ring. Treatment success varies widely, with most patients finding only brief success with the above-mentioned treatments. New research out of India suggests that the combination of rifampin (600 mg), ofloxacin (400 mg), and minocycline hydrochloride (100 mg) once monthly, or ROM therapy, produces promising results. Most lesions of granuloma annulare disappear in pre-pubertal patients with no treatment within two years while older patients (50+) have rings for upwards of 20 years. The appearance of new rings years later is not uncommon.

CCCA tends to present itself in the 20s and progresses over 20–30 years. One should consider this diagnosis in African Americans with what appears to be a female-pattern hair loss.

Topical 5-fluorouracil (5-FU, Efudex, Carac) has been shown to be an effective therapy for diffuse, but minor actinic cheilitis. 5-fluorouracil works by blocking DNA synthesis. Cells that are rapidly growing need more DNA, so they accumulate more 5-fluorouracil, resulting in their death. Normal skin is much less affected. The treatment usually takes 2–4 weeks depending on the response. The typical response includes an inflammatory phase, followed by redness, burning, oozing, and finally erosion. Treatment is stopped when ulceration and crusting appear. There is minimal scarring. Complete clearance has been reported in about 50% of patients.

Imiquimod (Aldara) is an immune response modifier that has been studied for the treatment of actinic cheilitis. It promotes an immune response in the skin leading to apoptosis (death) of the tumor cells. It causes the epidermis to be invaded by macrophages, which leads to epidermal erosion. T-cells are also activated as a result of imiquimod treatment. Imiquimod appears to promote an “immune memory” that reduces the recurrence of lesions. There is minimal scarring. Complete clearance has been demonstrated in up to 45% of patients with actinic keratoses. However, the dose and duration of therapy, as well as the long-term efficacy, still need to be established in the treatment of actinic cheilitis.