A different type of hypersensitivity reaction to molds results in a syndrome known as hypersensitivity pneumonitis. Repeated exposure to certain mold products triggers the cellular part of the immune system to attack the lungs. This is a much slower allergic reaction than the type caused by IgE.
A number of non-specific symptoms may occur in patients living or working in moisture-damaged buildings infested by hazardous microbiota. In the beginning, these symptoms are usually reversible, mild, and present as irritation of the mucosa and increased morbidity due to respiratory tract infections and asthma-like symptoms. Later, the disease may become chronic and the assessment of dampness and mold hypersensitivity syndrome (DMHS) may be warranted. DMHS presents with signs of irritation in the eyes, nose, and respiratory tract. Subsequently, the patient may experience recurrent sinusitis or bronchitis, and neurological manifestations such as headaches, nausea, and unexplained fatigue.
Some may develop rheumatic symptoms resembling fibromyalgia or neurological symptoms which may progress into pain and/or numbness in the legs and arms and the so-called “brain fog”. These patients have impaired cognition, inability to concentrate, and problems with both short- and long-term memories. Some patients develop new-onset asthma, or may present asthma-like conditions, such as dyspnea, burning sensation in the respiratory tract, and productive or nonproductive cough.
Carbamazepine is an aromatic antiepileptic drug that has been approved for treatment of epilepsy and trigeminal neuralgia. In approximately five to ten percent of patients, carbamazepine treatment is associated with carbamazepine-induced hypersensitivity reactions, which are generally cutaneous in nature. It is also rarely (0.01 to 0.1 percent of patients) associated with severe reactions, including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN).
The diagnosis of dampness and mold hypersensitivity syndrome (DMHS) is clinical and is based on the patient’s history and careful examination supplemented by risk assessment based on an HLA-DR test. A study has shown the following HLA gene combinations are implicated in mold hypersensitivity: HLA-DR7-DQ2-DR53; DR7-DQ3-DR53; DR13-DQ6-DR52; DR17-DQ2-DR52; and DR18-DQ4-DR52.
- Gray MR, Thrasher JD, Crago R, et al. Mixed mold mycotoxicosis: immunological changes in humans following exposure in water-damaged buildings. Arch Environ Health. 2003;58(7):410-20.
- Vlachopoulou E, Lahtela E, Wennerström A, et al. Evaluation of HLA-DRB1 imputation using a Finnish dataset. Tissue Antigens. 2014;83(5):350-5.
- Empting LD. Neurologic and neuropsychiatric syndrome features of mold and mycotoxin exposure. Toxicol Ind Health. 2009;25(9-10):577-81.
- Kilburn KH. Neurobehavioral and pulmonary impairment in 105 adults with indoor exposure to molds compared to 100 exposed to chemicals. Toxicol Ind Health. 2009;25(9-10):681-92.
- Knutsen AP, Vijay HM, Kumar V, et al. Mold-sensitivity in children with moderate-severe asthma is associated with HLA-DR and HLA-DQ. Allergy. 2010;65(11):1367-75.
There are no reviews yet.