Available treatments address the symptoms of CCD, not the underlying defect. Early diagnosis and aggressive salt replacement therapy result in normal growth and development, and generally good outcomes. Replacement of NaCl and KCl has been shown to be effective in children.

A potential treatment is butyrate.

In many cases of diarrhea, replacing lost fluid and salts is the only treatment needed. This is usually by mouth – oral rehydration therapy – or, in severe cases, intravenously. Diet restrictions such as the BRAT diet are no longer recommended. Research does not support the limiting of milk to children as doing so has no effect on duration of diarrhea. To the contrary, WHO recommends that children with diarrhea continue to eat as sufficient nutrients are usually still absorbed to support continued growth and weight gain, and that continuing to eat also speeds up recovery of normal intestinal functioning. CDC recommends that children and adults with cholera also continue to eat.

Medications such as loperamide (Imodium) and bismuth subsalicylate may be beneficial; however they may be contraindicated in certain situations.

Oral rehydration solution (ORS) (a slightly sweetened and salty water) can be used to prevent dehydration. Standard home solutions such as salted rice water, salted yogurt drinks, vegetable and chicken soups with salt can be given. Home solutions such as water in which cereal has been cooked, unsalted soup, green coconut water, weak tea (unsweetened), and unsweetened fresh fruit juices can have from half a teaspoon to full teaspoon of salt (from one-and-a-half to three grams) added per liter. Clean plain water can also be one of several fluids given. There are commercial solutions such as Pedialyte, and relief agencies such as UNICEF widely distribute packets of salts and sugar. A WHO publication for physicians recommends a homemade ORS consisting of one liter water with one teaspoon salt (3 grams) and two tablespoons sugar (18 grams) added (approximately the "taste of tears"). Rehydration Project recommends adding the same amount of sugar but only one-half a teaspoon of salt, stating that this more dilute approach is less risky with very little loss of effectiveness. Both agree that drinks with too much sugar or salt can make dehydration worse.

Appropriate amounts of supplemental zinc and potassium should be added if available. But the availability of these should not delay rehydration. As WHO points out, the most important thing is to begin preventing dehydration as early as possible. In another example of prompt ORS hopefully preventing dehydration, CDC recommends for the treatment of cholera continuing to give Oral Rehydration Solution during travel to medical treatment.

Vomiting often occurs during the first hour or two of treatment with ORS, especially if a child drinks the solution too quickly, but this seldom prevents successful rehydration since most of the fluid is still absorbed. WHO recommends that if a child vomits, to wait five or ten minutes and then start to give the solution again more slowly.

Drinks especially high in simple sugars, such as soft drinks and fruit juices, are not recommended in children under 5 years of age as they may "increase" dehydration. A too rich solution in the gut draws water from the rest of the body, just as if the person were to drink sea water. Plain water may be used if more specific and effective ORT preparations are unavailable or are not palatable. Additionally, a mix of both plain water and drinks perhaps too rich in sugar and salt can alternatively be given to the same person, with the goal of providing a medium amount of sodium overall. A nasogastric tube can be used in young children to administer fluids if warranted.

No specific treatment or cure exists. Affected children usually need total parenteral nutrition through a central venous catheter. Further worsening of liver damage should however be avoided if possible. Diarrhea will likely continue even though food stops passing through the gastrointestinal system. They can subsequently be managed with tube feeding, and some may be weaned from nutritional support during adolescence.

Treatment is directed largely towards management of underlying cause:

- Replacement of nutrients, electrolytes and fluid may be necessary. In severe deficiency, hospital admission may be required for nutritional support and detailed advice from dietitians. Use of enteral nutrition by naso-gastric or other feeding tubes may be able to provide sufficient nutritional supplementation. Tube placement may also be done by percutaneous endoscopic gastrostomy, or surgical jejunostomy. In patients whose intestinal absorptive surface is severely limited from disease or surgery, long term total parenteral nutrition may be needed.

- Pancreatic enzymes are supplemented orally in pancreatic insufficiency.

- Dietary modification is important in some conditions:

- Gluten-free diet in coeliac disease.

- Lactose avoidance in lactose intolerance.

- Antibiotic therapy to treat Small Bowel Bacterial overgrowth.

- Cholestyramine or other bile acid sequestrants will help reducing diarrhoea in bile acid malabsorption.

Common pharmacological treatments include:

- Mast cell stabilizers, including cromolyn sodium and natural stabilizers such as quercetin

- H1-antihistamines, such as cetirizine or ketotifen

- H2-antihistamines, such as ranitidine or famotidine

- Antileukotrienes, such as montelukast or zileuton as well as natural products (e.g., curcumin or St. John's wort extracts)

- Nonsteroidal anti-inflammatory drugs, including aspirin can be very helpful in reducing inflammation in some patients, while others can have dangerous reactions

Fillers, binders and dyes in many medications are often the culprit in causing reactions, not necessarily the active agent, so alternative formulations and compounding pharmacies should be considered.

Lifestyle changes may also be needed. Avoidance of triggers is important. It should be emphasized that MCAS patients can potentially react to any new exposure, including food, drink, medication, microbes and smoke via inhalation, ingestion or touch.

A low histamine diet and other elimination diets can be useful in identifying foods that trigger or worsen symptoms. Many MCAS patients already have high histamine levels, so ingesting foods with high histamine or histamine liberators can worsen many symptoms such as vasodilation that causes faintness and palpitations.

Bacterial overgrowth is usually treated with a course of antibiotics although whether antibiotics should be a first line treatment is a matter of debate. Some experts recommend probiotics as first line therapy with antibiotics being reserved as a second line treatment for more severe cases of SIBO. Prokinetic drugs are other options but research in humans is limited. A variety of antibiotics, including tetracycline, amoxicillin-clavulanate, fluoroquinolones, metronidazole, neomycin, cephalexin, trimethoprim-sulfamethoxazole, and nitazoxanide have been used; however, the best evidence is for the use of rifaximin.

A course of one week of antibiotics is usually sufficient to treat the condition. However, if the condition recurs, antibiotics can be given in a cyclical fashion in order to prevent tolerance. For example, antibiotics may be given for a week, followed by three weeks off antibiotics, followed by another week of treatment. Alternatively, the choice of antibiotic used can be cycled.

The condition that predisposed the patient to bacterial overgrowth should also be treated. For example, if the bacterial overgrowth is caused by chronic pancreatitis, the patient should be treated with coated pancreatic enzyme supplements.

Probiotics are bacterial preparations that alter the bacterial flora in the bowel to cause a beneficial effect. Animal research has demonstrated that probiotics have barrier enhancing, antibacterial, immune modulating and anti-inflammatory effects which may have a positive effect in the management of SIBO in humans. "Lactobacillus casei" has been found to be effective in improving breath hydrogen scores after 6 weeks of treatment presumably by suppressing levels of a small intestinal bacterial overgrowth of fermenting bacteria. The multi-strain preparation VSL#3 was found to be effective in suppressing SIBO. "Lactobacillus plantarum", "Lactobacillus acidophilus", and "Lactobacillus casei" have all demonstrated effectiveness in the treatment and management of SIBO. Conversely, "Lactobacillus fermentum" and "Saccharomyces boulardii" have been found to be ineffective. A combination of "Lactobacillus plantarum" and "Lactobacillus rhamnosus" has been found to be effective in suppressing bacterial overgrowth of abnormal gas producing organisms in the small intestine.

Probiotics are superior to antibiotics in the treatment of SIBO. A combination of probiotic strains has been found to produce better results than therapy with the antibiotic drug metronidazole and probiotics have been found to be effective in treating and preventing secondary lactase deficiency and small intestinal bacteria overgrowth in individuals suffering from post-infectious irritable bowel syndrome. Probiotics taken in uncomplicated cases of SIBO can usually result in the individual becoming symptom free. Probiotic therapy may need to be taken continuously to prevent the return of overgrowth of gas producing bacteria. A study by the probiotic yogurt producer Nestlé found that probiotic yogurt may also be effective in treating SIBO with evidence of reduced inflammation after 4 weeks of treatment.

An elemental diet taken for two weeks is an alternative to antibiotics for eliminating SIBO. An elemental diet works via providing nutrition for the individual while depriving the bacteria of a food source. Additional treatment options include the use of prokinetic drugs such as 5-HT4 receptor agonists or motilin agonists to extend the SIBO free period after treatment with an elemental diet or antibiotics. A diet void of certain foods that feed the bacteria can help alleviate the symptoms. For example, if the symptoms are caused by bacterial overgrowth feeding on indigestible carbohydrate rich foods, following a FODMAP restriction diet may help.

WAD is typically self-limited, generally resolving without specific treatment. Oral rehydration therapy with rehydration salts is often beneficial to replace lost fluids and electrolytes. Clear, disinfected water or other liquids are routinely recommended.

Hikers who develop three or more loose stools in a 24-hour period – especially if associated with nausea, vomiting, abdominal cramps, fever, or blood in stools – should be treated by a doctor and may benefit from antibiotics, usually given for 3–5 days. Alternatively, a single dose azithromycin or levofloxacin may be prescribed. If diarrhea persists despite therapy, travelers should be evaluated and treated for possible parasitic infection.

"Cryptosporidium" can be quite dangerous to patients with compromised immune systems. Alinia (nitazoxanide) is approved by the FDA for treatment of "Cryptosporidium".

There is no cure for MCAS. For most, symptoms wax and wane, but many can experience a general worsening trend over time. Lifespan for those with MCAS appears to be normal, but quality of life can range from mild discomfort to severely impaired. Some patients are impaired enough to be disabled and unable to work.

It is nearly always fatal unless, like short bowel syndrome patients, treated with parenteral nutrition or an intestinal transplant. The patient is often classified as being in "intestinal failure" and treated with the cohort of patients known as "short bowel syndrome" patients.

Bile acid sequestrants are the main agents used to treat bile acid malabsorption. Cholestyramine and colestipol, both in powder form, have been used for many years. Unfortunately many patients find them difficult to tolerate; although the diarrhea may improve, other symptoms such as pain and bloating may worsen. Colesevelam is a tablet and some patients tolerate this more easily. A proof of concept study of the farnesoid X receptor agonist obeticholic acid has shown clinical and biochemical benefit.

As of March 15, 2016, Novartis Pharmaceuticals is conducting a phase II clinical study involving a farnesoid X receptor agonist named LJN452.

Dysentery is initially managed by maintaining fluid intake using oral rehydration therapy. If this treatment cannot be adequately maintained due to vomiting or the profuseness of diarrhea, hospital admission may be required for intravenous fluid replacement. Ideally, no antimicrobial therapy should be administered until microbiological microscopy and culture studies have established the specific infection involved. When laboratory services are not available, it may be necessary to administer a combination of drugs, including an amoebicidal drug to kill the parasite and an antibiotic to treat any associated bacterial infection.

Anyone with bloody diarrhea needs immediate medical help. Treatment often starts with an oral rehydrating solution—water mixed with salt and carbohydrates—to prevent dehydration. (Emergency relief services often distribute inexpensive packets of sugars and mineral salts that can be mixed with clean water and used to restore lifesaving fluids in dehydrated children gravely ill from dysentery.)

If "Shigella" is suspected and it is not too severe, the doctor may recommend letting it run its course—usually less than a week. The patient will be advised to replace fluids lost through diarrhea. If the infection is severe, the doctor may prescribe antibiotics, such as ciprofloxacin or TMP-SMX (Bactrim). Unfortunately, many strains of "Shigella" are becoming resistant to common antibiotics, and effective medications are often in short supply in developing countries. If necessary, a doctor may have to reserve antibiotics for those at highest risk for death, including young children, people over 50, and anyone suffering from dehydration or malnutrition.

No vaccine is available. There are several "Shigella" vaccine candidates in various stages of development that could reduce the incidence of dysentery in endemic countries, as well as in travelers suffering from traveler's diarrhea.

The risk of fecal-oral transmission of pathogens that cause diarrhea can be significantly reduced by good hygiene, including washing hands with soap and water after urination and defecation, and washing eating utensils with warm soapy water. Additionally a three-bowl system can be used for washing eating utensils.

Acrodermatitis enteropathica without treatment is fatal, and affected individuals may die within a few years. There is no cure for the condition. Treatment includes lifelong dietary zinc supplementation.

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.

Most asymptomatic individuals with Gitelman syndrome can be monitored without medical treatment. Potassium and magnesium supplementation to normalize low blood levels of potassium and magnesium is the mainstay of treatment. Large doses of potassium and magnesium are often necessary to adequately replace the electrolytes lost in the urine. Diarrhea is a common side effect of oral magnesium which can make oral replacement difficult but dividing the dose to 3-4 times a day is better tolerated. Severe deficits of potassium and magnesium require intravenous replacement. If low blood potassium levels are not sufficiently replaced with oral replacement, aldosterone antagonists (such as spironolactone or eplerenone) or epithelial sodium channel blockers such as amiloride can be used to decrease urinary wasting of potassium.

Concomitant pinworm infection should also be excluded, although the association has not been proven. Successful treatment of the infection with iodoquinol, doxycycline, metronidazole, paromomycin, and secnidazole has been reported. Resistance requires the use of combination therapy to eradicate the organism. All persons living in the same residence should be screened for "D. fragilis", as asymptomatic carriers may provide a source of repeated infection. Paromomycin is an effective prophylactic for travellers who will encounter poor sanitation and unsafe drinking water.

Medications may consist of stool softeners and laxatives in IBS-C and antidiarrheals (e.g., opiate, opioid, or opioid analogs such as loperamide, codeine, diphenoxylate) if diarrhea is predominant.

Drugs affecting serotonin (5-HT) in the intestines can help reduce symptoms. On the other hand, many IBS-D patients report that SSRI type medications exacerbate spasms and diarrhea. This is thought to be due to the large number of serotonin receptors in the gut. 5HT3 antagonists such as ondansetron are effective in postinfectious IBS and diarrhea-dominant IBS due to their blockade of serotonin on 5HT3 receptors in the gut; the reason for their benefit is believed to be that excessive serotonin in the gut is thought to play a role in the pathogenesis of some subtypes of IBS. Certain atypical antipsychotic medications, such as clozapine and olanzapine, may also provide relief due to serotonergic properties these agents possess, acting on the same receptors as other medications in this specific category. Benefits may include reduced diarrhea, reduced abdominal cramps, and improved general well-being. Any nausea present may also respond to 5HT3 antagonists owing to their antiemetic properties. Serotonin stimulates the gut motility and so agonists can help constipation-predominant irritable bowel, while antagonists can help diarrhea-predominant irritable bowel. Selective serotonin reuptake inhibitors, SSRIs, frequently prescribed for panic and/or anxiety disorder and depression, affect serotonin in the gut, as well as the brain. The bowels are highly dependent on serotonin for neural communication. "Selective serotonin reuptake inhibitor antidepressants seem to promote global well-being in some patients with irritable bowel syndrome and, possibly, some improvement in abdominal pain and bowel symptoms, but this effect appears to be independent of improved depression. Further research is required."

Mast cells and the compound that they secrete are central to the pathophysiology and implicated in the treatment of IBS; some of the secreted mast cell mediators (and associated receptors) which have been implicated in symptoms of IBS or specific subtypes include: histamine (HRH1, HRH2, HRH3), tryptase and chymase (PAR2), serotonin (5-HT3), PGD2 (DP1). Histamine also causes epithelial secretion of chloride ions and water (associated with secretory diarrhea) by signaling through a receptor or ligand-gated ion channel that has not been identified as of 2015. A 2015 review noted that both H1-antihistamines and mast cell stabilizers have shown efficacy in reducing pain associated with visceral hypersensitivity in IBS; other lower quality studies have also suggested the benefit of these agents for IBS. In a related review on idiopathic mast cell activation syndromes (including IBS), a combined treatment approach using antileukotrienes, H1/H2-antihistamines, and a mast cell stabilizer are suggested.

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.

CFTR has been a drug target in efforts to find treatments for related conditions. Ivacaftor (trade name Kalydeco, developed as VX-770) is a drug approved by the FDA in 2012 for people with cystic fibrosis who have specific CFTR mutations Ivacaftor was developed by Vertex Pharmaceuticals in conjunction with the Cystic Fibrosis Foundation and is the first drug that treats the underlying cause rather than the symptoms of the disease. Called "the most important new drug of 2012", and "a wonder drug" it is one of the most expensive drugs, costing over US$300,000 per year, which has led to criticism of Vertex for the high cost.

Treatments are focused on the underlying cause of hyponatremia and include

- fluid restriction

- 0.9% saline and hypertonic saline intravenously

- 100 ml of 3% saline hourly

When EAH is treated early, complete recovery is expected.

In addition to the above treatments, athletes experiencing EAH encephalopathy may also receive high-flow oxygen and a rapid infusion of 100 ml of 3% NaCl to reduce brain edema.

Treatment remains largely supportive. The behavioral disturbances of MPS-III respond poorly to medication. If an early diagnosis is made, bone marrow replacement may be beneficial. Although the missing enzyme can be manufactured and given intravenously, it cannot penetrate the blood–brain barrier and therefore cannot treat the neurological manifestations of the disease.

Along with many other lysosomal storage diseases, MPS-III exists as a model of a monogenetic disease involving the central nervous system.

Several promising therapies are in development. Gene therapy in particular is under Phase I/II clinical trial in France since October 2011 under the leadership of Paris-based biotechnology company Lysogene. Other potential therapies include chemical modification of deficient enzymes to allow them to penetrate the blood–brain barrier, stabilisation of abnormal but active enzyme to prevent its degradation, and implantation of stem cells strongly expressing the missing enzyme. For any future treatment to be successful, it must be administered as early as possible. Currently MPS-III is mainly diagnosed clinically, by which stage it is probably too late for any treatment to be very effective. Neonatal screening programs would provide the earliest possible diagnosis.

The flavonoid genistein decreases the pathological accumulation of glycosaminoglycans in Sanfilippo syndrome. "In vitro", animal studies and clinical experiments suggest that the symptoms of the disease may be alleviated by an adequate dose of genistein. Despite its reported beneficial properties, genistein also has toxic side effects.

Several support and research groups have been established to speed the development of new treatments for Sanfilippo syndrome.

In terms of treatment of oculocerebrorenal syndrome for those individuals who are affected by this condition includes the following:

- Glaucoma control (via medication)

- Nasogastric tube feeding

- Physical therapy

- Clomipramine

- Potassium citrate

Carbamazepine is at least partly effective at reducing the number or severity of attacks in the majority of PEPD patients. High doses of this drug may be required, perhaps explaining the lack of effect in some individuals. While other anti-epileptic drugs, gabapentin and topiramate, have limited effect in some patients, they have not been shown to be generally effective. Opiate derived analgesics are also largely ineffective, with only sporadic cases of beneficial effect.

Treatment is directed towards (1) correcting hypotension, hypovolemia, electrolyte imbalances, and metabolic acidosis; (2) improving vascular integrity, and (3) providing an immediate source of glucocorticoids. Rapid correction of hypovolemia is the first priority.

Most patients show dramatic improvement within 24 to 48 hours of appropriate fluid and glucocorticoid therapy. Over the ensuing 2 to 4 days, a gradual transition from IV fluids to oral water and food is undertaken, and maintenance mineralocorticoid and glucocorticoid therapy is initiated. Failure to make this transition smoothly should raise suspicion of insufficient glucocorticoid supplementation, concurrent endocrinopathy (e.g. hypothyroidism), or cocurrent illness (especially renal damage).