Skip to content

treatment

Gastroparesis: Diabetes and gastroparesis (Part 3)

Diabetes is one of the most common causes of gastroparesis. 40% of patients with long term diabetes mellitus type I and 20% with diabetes mellitus type II have delayed gastric emptying.   In 1995, 21% patient of gastroparesis patients had DM; in 2004, 26.7%.

Diabetes patients are more likely to have nausea and vomiting as the cardinal GP symptoms, rather than epigastric pain seen more frequently in idiopathic GP.  `Diabetic GP is known to cause more severe gastric retention than idiopathic GP.

Diabetic patients with gastroparesis are at risk for developing difficulty in managing sugar levels.  Poor control of blood sugar can contribute to delayed gastric emptying.  Hyperglycemia is associated with decreased movement of the stomach, an effect more pronounced above 250 mg/dL.  Additionally, some medications used for diabetes, like exenatide for type II diabetes, can delay gastric emptying.  Persistent hyperglycemia is often cited as contributing to vagus nerve damage, which can also result in GP.

In one series, 58% of DM patients had increased tone in the pyloric sphincter, through which food passes from the stomach into the small intestine.  Pyloric tone is often elevated in GP patients.  Botox injections into the pyloric sphincter has been associated with increased gastric emptying and relief of symptoms in diabetic GP patients.

Gastric electric stimulation is more likely to be successful in diabetic patients versus those whose GP is not associated with diabetes, showing 50% reduction in symptoms over those with idiopathic GP.  Patients also experience better glycemic control when GP is more controlled, as reflected by reduction in hemoglobin A1C.

Gastroparesis in diabetes patients is well studied.  Curiously, improving glycemic control is not associated with symptom improvement (or change at all) in patients with type II diabetes.  In type I diabetics, symptom change has only correlated well with depression.

References:

Sarosiek, Irene, et al. Surgical approaches to treatment of gastroparesis: Gastric electrical stimulation, pyloroplasty, total gastrectomy and enteral feeding tubes.  Gastroenterol Clin N Am 44 (2015) 151-167.

Pasricha, Pankaj Jay, Parkman, Henry P. Gastroparesis: Definitions and Diagnosis. Gastroenterol Clin N Am 44 (2015) 1-7.

Parkman, H. P. Idiopathic Gastroparesis. Gastroenterol Clin N Am 44 (2015) 59-68.

Nguyen, Linda Anh, Snape Jr., William J. Clinical presentation and pathophysiology of gastroparesis.  Gastroenterol Clin N Am 44 (2015) 21-30.

Bharucha, Adil E. Epidemiology and natural history of gastroparesis. Gastroenterol Clin N Am 44 (2015) 9-19.

Camilleri, Michael, et al. Clinical guideline: Management of gastroparesis. Am J Gastroenterol 2013; 108: 18-37.

Gastroparesis: Treatment (part 2)

Initial management of gastroparesis often focuses on treating dehydration and electrolyte and nutritional deficits.  One study found that 64% of gastroparesis patients were not consuming enough daily calories to support the needs of their bodies, which can worsen symptoms.  Vitamins A, B6, C, and K, as well as iron, potassium and zinc are frequently deficient in this population.  Small meals low in fat and fiber are recommended for gastroparesis patients.  Liquids or blended solids often empty normally from the stomach.

For cases in which oral diet is unable to provide sufficient calories and nutrition, placement of a feeding tube may be necessary.  Jejunal feeding tubes are often used successfully.  Prior to surgical placement of a feeding tube, a nasojejunal tube should be used successfully.  PEG-J or Jet-PEG tubes allow venting of gastric secretions to reduce vomiting and nausea while providing a feeding route.

TPN (total parental nutrition) is given intravenously, but carries risks, including central line infections.  For patients in whom oral feeding is not feasible, a feeding tube is often considered the safer option.

Metoclopramide, a dopamine D2 receptor antagonist, is approved for treatment of gastroparesis.  However, treatment beyond 12 weeks should be considered only if the improvement on this medication is significant enough to outweigh risks.  Metoclopramide can cause dystonia and tardive dyskinesia.  Benzodiazepines and antihistamines are sometimes used to treat these side effects.  Domperidone is also a dopamine D2 receptor antagonist, but has lower incidence of side effects.  It is not approved in the US, but can be obtained via special FDA approval for US patients.

Medications to increase gastric motor activity, like erythromycin, are often used in gastoparesis patients.  When taken orally, erythromycin often becomes less effective after several weeks of relief.  Proton pump inhibitors and H2 antihistamines may provide some relief as gastroparesis is often associated with and irritating to GERD.

Medications for management of nausea and vomiting are mainstays for many gastroparesis patients, with phenothiazines or antihistamines often used for this purpose.  5-HT3 receptor antagonists like ondansetron are also widely used.  The neurokinin receptor-1 antagonist aprepitant is sometimes used after failing other antiemetics.  Scopolamine patches and dronabinol are also options.  Tricyclic antidepressants can be used to manage nausea, vomiting and abdominal pain, with nortriptyline and desipramine often preferred over amitriptyline, which can cause delayed emptying.  Mirtazapine has been reported as successful in a case study.

Abdominal pain associated with gastroparesis can be difficult to manage because opiates can induce gastroparesis.  Gabapentin, tramadol, tapentadol, pregabalin and nortriptyline are non-opiate options for pain management.

For some patients, more invasive treatment is indicated.  Some patients with gastroparesis have increased tone in the pyloric canal, which can contribute to delayed gastric emptying.  Injection of botulinum toxin (Botox) into the pyloric sphincter is sometimes tried.  In double-blind studies, use of Botox increases gastric emptying but does not improve symptom profiles.

There are surgical options to manage gastroparesis, with varying results.  Gastric electrical stimulation is considered for patients with long term symptoms that have not improved despite treatment.  These devices are implanted and provide low grade electrical stimulation to the stomach and increase motility.  In diabetic gastoparesis patients, this method improved quality of life and decreased symptoms.  Patients who acquired gastroparesis following surgery, or whose gastroparesis is idiopathic, were less likely to improve using GES.  Pyloroplasty and gastrectomy (partial or complete) have been trialed in some patients, but there is not a clear trend in the data.

Acupuncture has been shown to benefit gastroparesis patients in a number of studies, including one blinded, randomized study. Symptom severity was improved in those receiving acupuncture and gastric emptying time was decreased.  Autogenic retraining using the program developed by NASA for space motion sickness has shown some benefit.  Autogenic retraining was found to be more successful in patients with intact autonomic function.

References:

Sarosiek, Irene, et al. Surgical approaches to treatment of gastroparesis: Gastric electrical stimulation, pyloroplasty, total gastrectomy and enteral feeding tubes.  Gastroenterol Clin N Am 44 (2015) 151-167.

Pasricha, Pankaj Jay, Parkman, Henry P. Gastroparesis: Definitions and Diagnosis. Gastroenterol Clin N Am 44 (2015) 1-7.

Parkman, H. P. Idiopathic Gastroparesis. Gastroenterol Clin N Am 44 (2015) 59-68.

Nguyen, Linda Anh, Snape Jr., William J. Clinical presentation and pathophysiology of gastroparesis.  Gastroenterol Clin N Am 44 (2015) 21-30.

Bharucha, Adil E. Epidemiology and natural history of gastroparesis. Gastroenterol Clin N Am 44 (2015) 9-19.

Camilleri, Michael, et al. Clinical guideline: Management of gastroparesis. Am J Gastroenterol 2013; 108: 18-37.

Mast cell disease fact sheet

Mast Cell Disease

  • Mast cell disease includes all forms of disease in which your body makes too many mast cells or those mast cells do not function correctly.
  • Mast cell disease is rare, affecting less than 200,000 people in the US.
  • 90% of mast cell disease only affects the skin (edited to add: based upon estimates of mastocytosis population – counts of MCAS/MCAD not yet available).
  • The remaining 10% is systemic disease.
  • Multiple people in a family sometimes have mast cell disease, but the heritable gene has not been identified.
  • Cutaneous and systemic mastocytosis, mast cell sarcoma and mast cell leukemia are proliferative, meaning your body makes too many mast cells.
  • Mast cell activation syndrome/mast cell activation disorder are not proliferative, meaning there is a normal amount of mast cells behaving badly.
  • Monoclonal mast cell activation syndrome is borderline for proliferation, meaning the body is thinking about making too many mast cells or is just starting to.
  • The biggest risk for most mast cell patients is anaphylaxis, a severe, life-threatening allergic reaction that can be triggered by many things.
  • There is no cure for mast cell disease, but children sometimes grow out of it for unknown reasons.

Types of mast cell disease

  • Cutaneous mastocytosis (CM) is too many mast cells in the skin.
    • This causes rashes (sometimes permanent), hiving and blistering.
    • Urticaria pigmentosa (UP), telangiectasia macularis eruptive perstans (TMEP) and diffuse cutaneous mastocytosis (DCM) are the types of cutaneous mastocytosis. (Edited to include DCM.)
    • It is diagnosed by skin biopsy.
    • You can also have mast cell symptoms that aren’t related to the skin, like nausea, vomiting, weakness, headache, palpitations, etc.
    • Solitary mastocytoma is a benign mast cell tumor usually found on the skin, but sometimes elsewhere. It is sometimes included in the cutaneous mastocytosis category.
    • Children sometimes outgrow cutaneous mastocytosis.
    • When adults develop cutaneous mastocytosis, they usually also have systemic mastocytosis.
  • Systemic mastocytosis is too many mast cells in an organ that is not the skin.
    • The bone marrow is usually where too many mast cells are found, but it is sometimes found in other organs.
    • You can have systemic mastocytosis with or without cutaneous mastocytosis.
    • It is diagnosed by biopsy of an organ other than skin. Other testing like scans and organ tests may be necessary.
    • Indolent systemic mastocytosis (ISM) is stable with no organ damage. Life span is normal.
    • Smoldering systemic mastocytosis (SSM) is progressing towards a more damaging form with some signs that organ damage is beginning. Life span may be shortened if progression is not controlled.
    • Aggressive systemic mastocytosis (ASM) is a dangerous form with organ damage that requires chemotherapy to control. Life span is shorter.
    • Mast cell leukemia (MCL) is a malignant form with organ damage that requires chemotherapy. Life span is significantly reduced.
    • Mast cell sarcoma(MCS) is a malignant form with organ damage that requires chemotherapy. Life span is significantly reduced.
  • Mast cell activation syndrome (MCAS)/ Mast cell activation disorder (MCAD) is when a normal amount of mast cells behave badly. (Edited to change mast cell activation disease to mast cell activation disorder.)
    • It is clinically similar to indolent systemic mastocytosis. Life span is normal.
    • Biopsies are negative.
  • Monoclonal mast cell activation syndrome (MMAS) is when a person meets some of the criteria for systemic mastocytosis but not all. It indicates the mast cells are starting to think about abnormal proliferation.
    • It is clinically similar to indolent systemic mastocytosis. Life span is normal.
    • Biopsies are positive for one or two minor criteria for systemic mastocytosis.

Symptoms

  • Anaphylaxis
  • Skin
    • Flushing is one of the hallmark signs of mast cell disease
    • Other skin symptoms include rashes, hives, itching, angioedema, dermatographism
  • Gastrointestinal
    • Abdominal pain, diarrhea, constipation, swelling of GI tract, difficulty swallowing
  • Neurologic
    • Headache, migraine, feeling faint, numbness, pins and needles, tremors, tics, neuropathy
  • Psychiatric
    • Depression, anxiety, memory difficulties, insomnia, sleep disorders*
  • Cardiovascular
    • Weakness, dizziness, high or low blood pressure, slow or rapid heartbeat, abnormal heart rhythm, chest pain, palpitations

*Edited to add: Psychiatric symptoms are organic symptoms of mast cell disease, rather than reactive conditions from chronic illness.

This list is not exhaustive.

Triggers

  • Many things can cause mast cell reactions or anaphylaxis in mast cell patients.
  • Allergy testing (skin prick or blood testing) is inaccurate in mast cell patients as these tests assess IgE allergies and mast cell patients often have non-IgE reactions.
  • Triggers can change over time and can include:
    • Heat, cold, or rapid change in temperature
    • Friction, especially on the skin
    • Sunlight
    • Illness, such as viral or bacterial infection
    • Exercise
    • Many foods, especially high histamine foods
    • Many preservatives and dyes
    • Many medications
    • Scents and fragrances
    • Physical stress, such as surgery
    • Emotional or psychological stress

Diagnosis: Blood and Urine Testing

  • Blood test: Serum tryptase
    • This tests for the total amount of mast cells in the body, the “mast cell burden”
    • Should be tested during a non-reactive period for baseline and during a reaction
    • Time sensitive: should be tested 1-4 hours after start of reaction
    • Normal range for adults is under 11 ng/ml. (Edited to remove out of place words “is abnormal” at the end of this statement)
    • 2 ng/ml + 20% increased from baseline is indicative of mast cell activation
    • Baseline over 20 ng/ml is a minor criteria for diagnosis systemic mastocytosis
  • 24 hour urine tests:
    • N-methylhistamine
      • Breakdown product of histamine
      • Released by mast cells when reacting
      • Very temperature sensitive
      • Sample must be refrigerated and transported on ice (unless preservative is provided)
      • Measured as a ratio of another molecule, creatinine
      • Normal range for adults is 30-200 mcg/g creatinine
      • One study found that if level was 300 mcg/g creatinine, a bone marrow biopsy was likely to be positive for systemic mastocytosis
    • D2 prostaglandin and 9a,11b-F2 prostaglandin
      • Released by mast cells when reacting
      • Very temperature sensitive
      • Sample must be refrigerated and transported on ice (unless preservative is provided)
      • Normal range for both is under 1000 ng
      • 9a,11b-F2 prostaglandin is a breakdown product of D2 prostaglandin
      • 9a,11b-F2 prostaglandin is the marker for which MCAS/MCAD patients are most often positive
      • If taking aspirin or NSAIDs, these may be discontinued five days before the test or as directed by your physician
      • Other tests sometimes done in blood include heparin, histamine, prostaglandin D2 and chromogranin A.
      • Serum tryptase and 24 hour urine n-methylhistamine, D2 prostaglandin and 9a,11b-F2 prostaglandin are the tests considered to be most reliable indicators of mast cell disease.

Diagnosis: Biopsies

  • Bone marrow biopsy
    • Obtained by bone marrow biopsy and aspiration procedure
    • Stained with Giemsa and tryptase stains
    • Tested with antibodies for CD117, CD2, CD25 and CD34
    • Looking for clusters of mast cells in groups of 15 or more
    • Looking for mast cells that are shaped abnormally, like spindles
    • DNA from the biopsy should be tested for the CKIT D816V mutation, a marker for systemic mastocytosis
  • Skin biopsy
    • Obtained by punch biopsy
    • Stained with Giemsa and tryptase stains
    • Tested with antibodies for CD117, CD2, CD25 and CD34
    • Looking for clusters of mast cells in groups of 15 or more
    • Looking for mast cells that are shaped abnormally, like spindles
    • DNA from the biopsy should be tested for the CKIT D816V mutation, a marker for systemic mastocytosis
  • GI biopsies
    • Obtained by scoping procedures
    • Stained with Giemsa and tryptase stains
    • Tested with antibodies for CD117, CD2, CD25 and CD34
    • Looking for clusters of mast cells in groups of 15 or more
    • Looking for mast cells that are shaped abnormally, like spindles
    • DNA from the biopsy should be tested for the CKIT D816V mutation, a marker for systemic mastocytosis (less likely to be positive than bone marrow biopsies)
    • Mast cells should be counted in five high powered (60X or 100X) fields and the count then averaged
    • Some researchers consider an average of more than 20 mast cells in a high powered field to be high, but this is not agreed upon
    • Some researchers consider an average of more than 20 mast cells in a high powered field to be diagnostic for mastocytic enterocolitis

Treatment

  • H1 antihistamines
    • Second generation, longer acting, non-sedating for daily use
    • First generation, shorter acting, sedating, but more potent
    • Other medications with H1 antihistamine properties like tricyclic antidepressants
  • H2 antihistamines
  • Leukotriene inhibitors
  • Aspirin, if tolerated
  • Mast cell stabilizers
    • Cromolyn
    • Ketotifen
    • Quercetin
  • Epinephrine (should be on hand in case of anaphylaxis)
  • These are baseline medications for MCAS/MCAD, MMAS and ISM cell patients. If symptoms are uncontrolled, other medications may be used off label for mast cell disease.
  • Smouldering systemic mastocytosis patients may require chemotherapy.
  • Aggressive systemic mastocytosis, mast cell leukemia and mast cell sarcoma patients require chemotherapy.

Medications to Avoid

  • Medications that cause degranulation
    • Alcohol (ethanol, isopropanol)
    • Amphoteracin B
    • Atracurium
    • Benzocaine
    • Chloroprocaine
    • Colistin
    • Dextran
    • Dextromethorphan
    • Dipyridamole
    • Doxacurium
    • Iodine based radiographic dye
    • Ketorolac
    • Metocurine
    • Mivacurium
    • Polymyxin B
    • Procaine
    • Quinine
    • Succinylcholine
    • Tetracine
    • Tubocurarine
    • Vancomycin (especially when given intravenously)
    • In some patients, aspirin and NSAIDs (please ask if your doctor if these are appropriate for you)

 

  • Medications that interfere with the action of epinephrine
    • Alpha adrenergic blockers
      • Alfuzosin
      • Atipamezole
      • Carvedilol
      • Doxazosin
      • Idazoxan
      • Labetalol
      • Mirtazapine
      • Phenoxybenzamide
      • Phentolamine
      • Prazosin
      • Silodosin
      • Tamsulosin
      • Terazosin
      • Tolazoline
      • Trazodone
      • Yohimbine
    • Beta adrenergic blockers
      • Acebutolol
      • Atenolol
      • Betaxolol
      • Bisoprolol
      • Bucindolol
      • Butaxamine
      • Carteolol
      • Carvedilol
      • Celiprolol
      • Esmolol
      • Metoprolol
      • Nadolol
      • Nebivolol
      • Oxprenolol
      • Penbutolol
      • Pindolol
      • Propranolol
      • Sotalol
      • Timolol

Please note these lists are not exhaustive and you should check with your provider before starting a new medication. A pharmacist can review to determine if a medication causes mast cell degranulation or interferes with epinephrine. This list represents the medications for which I was able to find evidence of degranulation or a-/b-adrenergic activity.

Special Precautions

  • Mast cell patients require special precautions before major and minor procedures, including radiology procedures with and without contrast or dyes
  • They must premedicate using the following procedure:
    • Prednisone 50mg orally (20 mg for children under 12): 24 hours and 1-2 hours before procedure
    • Diphenhydramine 25-50 mg orally (12.5 mg for children under 12) OR hydroxyzine 25 mg orally, 1 hour before procedure
    • Ranitidiine 150 mg orally (20 mg for children under 12): 1 hour before procedure
    • Montelukast 10 mg orally (5 mg for children under 12): 1 hour before procedure
    • This protocol was developed for the Mastocytosis Society by Dr. Mariana Castells and the original can be found at www.tmsforacure.org/documents/ER_Protocol.pdf

Common coincident conditions

  • Ehlers Danlos Syndrome (EDS), especially hypermobility type (Type III)
  • Postural orthostatic tachycardia syndrome (POTS) or other types of dysautonomia
  • Mast cell disease, EDS and POTS are often found together
  • Autoimmune diseases
  • Myeloproliferative diseases, like essential thrombocythemia and polycythemia vera
  • Eosinophilic disorders

 

 

 

Chronic urticaria and angioedema: Part 5

Chronic urticaria has a very well described stepwise treatment standard, which I will describe briefly here. If resolution is not achieved with the method described in one step, the next step is executed.

  • A second generation H1 antihistamine like cetirizine is begun with standard daily dosing. Triggers should be avoided wherever possible.
  • Dosage of second generation H1 antihistamine is increased.
  • Another second generation H1 antihistamine is added to the regimen. (For example, cetirizine and fexofenadine taken together).
  • An H2 antihistamine is added. About 15% of histamine receptors in the skin are H2, so some patients see benefit from this.
  • A leukotriene receptor antagonist like montelukast is added.
  • A first generation H1 antihistamine like diphenhydramine is added at bedtime.
  • A strong antihistamine like hydroxyzine or doxepin is added and dosages increased accordingly.
  • If all else has failed, consider addition of medications like Xolair, cyclosporine, or other immunosuppressants.

Treatment of angioedema is dependent upon the cause of the angioedema (C1 esterase deficiency, ACE inhibitor, etc). However, it is generally agreed upon that upper airway swelling, even if mild, should be treated aggressively. Intramuscular epinephrine is indicated for this situation, with advisories in numerous papers to administer epinephrine as early as possible if airway swelling is present.

Reactions caused by IgE are the most likely to respond immediately to epinephrine. Hereditary and acquired angioedema are less likely to respond to epinephrine. If the patient is on beta blockers, glucagon is the drug of choice, as beta blockers interfere with action of epinephrine.

I am doing a detailed follow up post on treatment options for the various types of angioedema.

 

References:

Jonathan A. Bernstein, et al. The diagnosis and management of acute and chronic urticaria: 2014 update. J Allergy Clin Immunol Volume 133, Number 5.

Zuberbier T, Maurer M. Urticaria: current opinions about etiology, diagnosis and therapy. Acta Derm Venereol 2007;87:196-205.

Ferdman, Ronald M. Urticaria and angioedema. Clin Ped Emerg Med 2007; 8:72-80.

Initial diagnosis and treatment of mast cell activation disease: General notes for guidance

Mast cell disease is becoming more well known among both the public and medical providers, but there is still a lot of confusion regarding exactly what it is, how to diagnose and how to treat.

There are several tests that should be used when working up a patient for mast cell disease. Tryptase is the most well known of these tests, due to over 85% of patients with systemic mastocytosis (SM), a form of mast cell disease, having elevated tryptase. However, tryptase can be normal in mast cell patients, or may only be elevated during times of severe symptoms or anaphylaxis. While an elevated baseline tryptase can be used as confirmation for a mast cell disease (in the absence of frank hematologic disease), a normal tryptase test should not be used to discard the possibility of mast cell disease.

24-hour urine tests for mast cell mediators are most likely to capture evidence of mast cell activation when executed correctly. These tests measure n-methylhistamine, a metabolite of histamine, and prostaglandins D2 and F2a, which are all released by mast cells. Urine collected for this test should be kept refrigerated or on ice during collection and transport to the lab. I STRONGLY recommend communicating with the lab prior to beginning to this test to be sure that they understand the temperature requirements. The molecules being tested are not stable at room temperature and inappropriate storage can result in a negative test result in a positive patient. (For details on this topic and specific recommendations for testing, please refer to Afrin 2013).

Some providers also find utility in the measurement of other less specific mediators. Please refer to my previous post on this topic: https://www.mastattack.org/2014/10/mast-cell-mediators-recommended-testing-for-mcas-diagnosis/

Due to the well established time sensitive nature of these tests (Afrin 2013), a patient who presents a “mast cell clinical picture” and responds to typical mast cell medications may in fact have mast cell disease in the presence of negative tests.

Depending on the clinical picture, a provider may feel it necessary to order a bone marrow biopsy, skin biopsy or biopsy of another organ to determine if mast cell infiltrates are present. This is not always immediately done in the presence of positive tryptase, n-methylhistamine, D2 prostaglandin or F2a prostaglandin test and will not always affect treatment. It is common knowledge among mast cell fluent providers that a negative biopsy does not exclude mast cell disease, but it is instead used to rule in the presence of specific proliferative entities like systemic mastocytosis (Picard 2013, Molderings 2011). Furthermore, a single biopsy may fail to capture a positive specimen in a known-positive patient (Butterfield 2004).

For more specific details regarding differentiation among the diagnostic categories of mast cell disease, please refer to my previous post on this topic: https://www.mastattack.org/2014/07/diagnosis-of-mast-cell-diseases/

There are a number of well known, well tolerated medications that can be used to manage mast cell disease. First line medications include antihistamines, leukotriene inhibitors, and mast cell stabilizers (Cardet 2013, Picard 2013, Molderings 2011, Afrin 2013).

Histamine is released by activated mast cells in large quantities. Histamine acts on the body by interacting with four different types of receptors, called H1, H2, H3 and H4. Medications that block the H1 and H2 receptors are available in plentiful supply in many countries. Once diagnosed, mast cell patients generally begin daily treatment with both H1 and H2 antihistamines. Longer acting, non-sedating H1 blockers like cetirizine are typically used to provide a baseline H1 coverage. H2 coverage is achieved with medications like Zantac or Pepcid. Dosage can be increased as needed to provide effective symptom relief, and these medications are often taken in moderate to high doses by mast cell patients. It is not uncommon to take multiple drugs together to block one type of histamine receptor, but this should be managed by a provider.

Leukotrienes are also released by activated mast cells. Singulair is an example of a leukotriene inhibitor that is a common add-on for mast cell patients. This medication is not a replacement for antihistamines.

Mast cell stabilizers achieve effects by making mast cells less likely to release chemicals. Cromolyn is typically the first line mast cell stabilizer in the US. This medication can take several weeks to demonstrate its full effect, so patients and providers should be aware of this fact. Another mast cell stabilizer, ketotifen, is also available in the US through compounding pharmacies. Ketotifen is also an H1 antihistamine.

Medications should ideally be added one at a time to allow easy identification of a bad actor in the event of a med reaction. As a result, tweaking a patient’s medication regimen takes time and patience. If a patient reacts to a medication, care should be taken to determine if the medication is truly the issue or if it is an inactive ingredient in the preparation (lactose, etc).

Mast cell disease can result in a highly variable clinical picture and mast cell patients are often only diagnosed following years of investigation for other possible causes of their symptoms. For this reason, many mast cell patients have acquired a long list of diagnoses prior to a mast cell diagnosis. In some cases, these diagnoses may be accurate and co-existing. All existing prior diagnoses should be considered for their accuracy in light of a mast cell diagnosis.

Additionally, there are a number of conditions which are frequently comorbid with mast cell disease, including Ehlers Danlos syndrome, postural orthostatic tachycardia syndrome (POTS), a variety of autoimmune diseases and several digestive conditions.  Patients should be evaluated according to their clinical picture and laboratory findings.

 

References:

Afrin, Lawrence B. Presentation, Diagnosis and Management of Mast Cell Activation Syndrome. 2013. Mast Cells.

Juan-Carlos Cardet, Maria C. Castells, and Matthew J. Hamilton. Immunology and Clinical Manifestations of Non-Clonal Mast Cell Activation Syndrome. Curr Allergy Asthma Rep. Feb 2013; 13(1): 10–18.

Matthieu Picard, Pedro Giavina-Bianchi, Veronica Mezzano, Mariana Castells. Expanding Spectrum of Mast Cell Activation Disorders: Monoclonal and Idiopathic Mast Cell Activation Syndromes. Clinical Therapeutics, Volume 35, Issue 5, May 2013, Pages 548–562.

Gerhard J Molderings, Stefan Brettner, Jürgen Homann, Lawrence B Afrin. Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options. Journal of Hematology & Oncology 2011, 4:10.