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Mast cell disease

Mast cell diseases comprise a heterogeneous spectrum of diseases involving the mast cells. The most common variants are:

  • Cutaneous mastocytoma
  • Urticaria pigmentosa
  • Telangiectasia macularis eruptiva perstans (TMEP)
  • Systemic mast cell disease
  • Mast cell leukemia
Mac Ardle disease
Macular degeneration
Mad cow disease
Maghazaji syndrome
Mal de debarquement
Malignant hyperthermia
Mallory-Weiss syndrome
Malouf syndrome
Marburg fever
Marfan syndrome
MASA syndrome
Mast cell disease
MAT deficiency
Maturity onset diabetes...
McArdle disease
McCune-Albright syndrome
Mediterranean fever
Megaloblastic anemia
Meleda Disease
Meniere's disease
Mental retardation
Mercury (element)
Metabolic acidosis
Metabolic disorder
Methylmalonic acidemia
Microscopic polyangiitis
Microtia, meatal atresia...
Miller-Dieker syndrome
Mitochondrial Diseases
Mitral valve prolapse
Mobius syndrome
MODY syndrome
Moebius syndrome
Molluscum contagiosum
MOMO syndrome
Mondini Dysplasia
Mondor's disease
Monoclonal gammopathy of...
Morquio syndrome
Motor neuron disease
Moyamoya disease
MPO deficiency
Mullerian agenesis
Multiple chemical...
Multiple endocrine...
Multiple hereditary...
Multiple myeloma
Multiple organ failure
Multiple sclerosis
Multiple system atrophy
Muscular dystrophy
Myalgic encephalomyelitis
Myasthenia gravis
Mycosis fungoides
Myelodysplastic syndromes
Myeloperoxidase deficiency
Myoadenylate deaminase...
Myositis ossificans


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The Role of the Brain and Mast Cells in MCS
From Townsend Letter for Doctors and Patients, 1/1/01 by Gunnar Heuser

Multiple Chemical Sensitivity (MCS) was first described in the 1980s, yet it has remained controversial. The resistance to the concept of MCS has come from scientists who pointed out the lack of solid scientific diagnostic tests. It has also come from the industry which has trouble accepting the proposition that their products make a great number of people sick.

My personal experience (I have evaluated several thousands of chemically injured patients) has convinced me that MCS is based on a physiological and not on a psychological mechanism. This is why I have been interested in finding objective evidence for MCS. In this paper I will present a mast cell hypothesis, a limbic system hypothesis, and an office approach to objective testing for MCS.

Mast Cell Disorder and MCS

Patients with mastocytosis can be exquisitely sensitive to even small amounts of chemicals. When mast cells discharge histamines and other compounds, patients often develop flushing and a metallic taste in their mouth.

A few years ago I decided to test some of my patients for mast cell disease. Some of these patients with MCS actually turned out to have mastocytosis. Other patients were found to have a mast cell disorder.

All diagnoses were made on the basis of skin biopsies done in an area which on inspection and palpation, showed no evidence of abnormality. It was also made on the basis of an elevated tryptase (an enzyme produced by mast cells) level. If mast cells were present in excess and/or if tryptase levels were elevated we would make a diagnosis of mast cell disease or disorder, if the clinical picture was also consistent with that diagnosis. In a few patients we also used a bone marrow biopsy to assist in the diagnosis.

Mastocytosis is considered to be a very rare disease. Yet, I have accumulated more then 20 patients with that diagnosis in a matter of two to three years.

At this time our testing is done on a random basis. We are now developing a protocol by which we will introduce a challenge (e.g. perfume, nail polish, chemicals found in a carpet store, etc.) and then test at a time when the patient is symptomatic from that challenge.

We also hope to work with the Mastocytosis Society [1] in further developing diagnostic approaches to the overlapping syndromes of mastocytosis and MCS.

At this time the diagnosis of MCS is considered justified only in the absence of diseases such as mastocytosis and porphyria. [2] This exclusion will require that all patients with MCS be tested for mast cell disorder and porphyrinopathy. I believe that this indeed should be done.

In summary I postulate that chemical injury can trigger a mast cell disorder which in turn can cause MCS. This concept was recently published. [3]

Limbic Hypermetabolism and MCS

Patients with MCS often show emotional instability during their reactions to small amounts of chemicals. This has been likened to the epileptogenic effects of kindling which is particularly effective in the limbic system of the brain. Yet no proof of this concept has come forward to date.

We started doing PET brain scans on some of our patients with MCS and found that the limbic, hypothalamic and brain stem areas are hypermetabolic (in terms of their radioactive glucose uptakes) and therefore hyperactive (almost as seen during focal seizure activity).

Since the limbic system contributes emotional reactions and interpretations to sensory input, and since patients with amygdaloid (the amygdala is part of the limbic system) seizures can develop panic and related attacks during an amygdaloid seizure, our data appear to explain the emotional instability during a reaction to chemicals.

The previously mentioned structures also serve memory and cognitive as well as neuroendocrine and autonomic nervous system functions, all of which can be deranged in a patient with MCS.

In summary, I have shown that patients with MCS can develop hyperactivity in deep structures of the brain and that this may explain their emotional instability which therefore develops on a physiological rather than psychological basis.

It should be mentioned at this time that patients who are impaired and/or disabled from chemical injury and resultant MCS often become depressed. This depression would obviously be a natural reaction to their impairment and/or disability and therefore be a secondary depression.

Our findings were first published in 1999 [4] and will soon be published [5] in proceedings of a meeting on Chemical Intolerance. In this volume, kindling and related mechanisms are also discussed.

Challenge Testing in the Medical Office

A few years ago, at a meeting on MCS, testing of patients in an environmental chamber was suggested as the most scientific approach to proving MCS. This suggestion proved impractical which is why so few publications exist which provide a protocol for testing a patient for MCS.

In my office we have developed a protocol by which a patient first undergoes baseline testing of pulmonary and immune functions as well as 24-hour urine collection for porphyrin fractions. Then the patient voluntarily inhales (via mouth and nose) nail polish, perfume, or exposes himself/herself to a chemical environment. Once symptomatic from that exposure, the patient undergoes follow-up testing of the same parameters and of course, undergoes a follow-up physical examination with special attention to neurological abnormalities and/or changes on auscultation of the lungs.

Ideally, the patient brings a nonsensitive person (age and sex matched) who undergoes the same testing. Patient and volunteer (control) are carefully observed by my office staff who make detailed notes.

Table 1 shows comparison of some immune parameters with regard to the above-mentioned tests. So far, we have found that MCS patients indeed respond more to chemical exposure than their controls. This is also true of pulmonary function which is more impaired when the patient becomes symptomatic after exposure to a small amount of chemicals (see table 2).

We addressed elevation of TA1 (CD3+CD26+) cells in an earlier publication. [6] Our data on T3+ (CD3) cells are unpublished. These cells can, in my opinion, be used as indicators of reactions to chemicals although they do not seem to contribute to any symptomatology.

We are in the process of adding additional measurements (e.g. cerebral blood flow, tryptase blood levels, and others) to our protocol. Naturally, we do challenge testing only when the patient needs to prove MCS to Social Security, insurance carriers (long-term disability) and the courts. We are slowly accumulating data for future publication in a peer-reviewed journal.

If other interested physicians were to use our approach, data would quickly accumulate and hopefully become statistically significant much sooner than using an environmental chamber approach in an academic setting.

In summary, I have shown approaches to MCS which in my opinion are promising and will help to further define the mechanisms underlying the development of MCS.


Gunnar Heuser, MD, PhD, FACP, FACFE, BCFE

NeuroMed and NeuroTox Associates

A Medical Group

28240 W. Agoura Rd., Suite 203

Agoura Hills, California 91301 USA


Fax 818-865-8814


(1.) The Mastocytosis Society, Inc. 2010 North Grand Avenue, Connersville, IN 47331.

(2.) Bartha L, et al, Multiple chemical sensitivity: A 1999 consensus. Arch Environ Hlth 1999;54:147-149.

(3.) Heuser G, Letter to the editor regarding Mast coil disorder to be ruled out in MCS. Arch Environ Hlth 2000; 55:284-285.

(4.) Heuser G, Wu JC, Subcortical hypermetabolism and cortical hypometabolism after neurotoxic exposure. Human PET studies. 7th International symposium on neurobehavioral methods and effects in occupational and environmental health. Stockholm, Sweden June 20-23, 1999.

(5.) Heuser G, Wu JC, Deep subcortical (incl. limbic) hypermetabolism in patients with chemical intolerance. Human PET studies. Annals of the NY Academy of Sciences. 2001(in press).

(6.) Heuser G, Wojdani A, Heuser S, Diagnostic markers of multiple chemical sensitivity. In: Multiple Chemical Sensitivities, Addendum to Biologic Markers in Immunotoxicology. Notional Academy Press, Washington, D.C. 1992; 117-138.

shows changes from baseline in two chemically sensitive patients exposed to perfume. Note lesser or no change in age and sex matched control when counting TA1 and T3 + cells four and twenty hours after exposure.

COPYRIGHT 2001 The Townsend Letter Group
COPYRIGHT 2001 Gale Group

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