Exposure to Toxins and Multiple Chemical Sensitivity
Kyle Brauer Boone in Neuropsychological Evaluation of Somatoform and Other Functional Somatic Conditions, 2017
Immunologic deficits are one of the earliest and most popular explanations for MCS. Exposure to an allergen is known to cause immunochemical changes such that further exposure to the allergen creates a markedly greater response from the organism even at the same or lesser level of exposure (Turner-Warwick, 1977). This hypersensitive response can lead to inflammation and tissue damage that often presents as classic serum sickness with fever, urticaria, fatigue and malaise, arthritis, and sometimes renal failure. These types of immune complexes have been associated with autoimmune diseases and a host of other clinical conditions (Cochran, 1988). The suggested process with chemical exposure starts with the chemical causing tissue irritation, which then leads to inflammation and recruitment of macrophages to the area. These carry antigens to the lymphocyte to create an immune response to the antigen. This can be measured by laboratory tests of immune function with consistent and reliable results in known medical diseases (Meggs, 1992). The problem with many MCS studies is that any results outside of accepted parameters are interpreted to be defects in the immune system or resulting from chemical overload without a replicable pattern for the purported disease.
Fibromyalgia Syndrome: Canadian Clinical Working Case Definition, Diagnostic and Treatment Protocols–A Consensus Document
I. Jon Russell in The Fibromyalgia Syndrome: A Clinical Case Definition for Practitioners, 2020
Mismanagement of sensory information: Research and clinical experience suggest there is a lower tolerance to noxious stimuli such as exposure to excessive noise, light, fast-paced and/or confusing environments. A significantly hypersensitive response to these auditory, visual and somatosensory stimuli may be a major factor in the production of some symptoms (249,250). Due to neurotransmitter/receptor dysfunctions, sensory information is not managed properly in the brain (251). Gating is the process whereby the prefrontal cortex [PFC] assigns relative importance to the sensory information it receives. Goldstein (251) has speculated that conditions like FMS and ME/CFS may suffer from the effects of abnormal gating due to dysregulation of the signal to noise ratio [for example-high relevance is given to insignificant distractions] resulting in patients being unable to exclude background noise. This dysregulation could be associated with overwhelming fatigue. A similar dysregulation also amplifies the sensory input of the olfactory system when previously tolerated foods, drugs and odors make one sick or give rise to panic attacks. This subset of FMS patients [about half] may also meet the criteria for multiple chemical sensitivity based on subjective questioning (252).
Radiobiology of Tumours
W. P. M. Mayles, A. E. Nahum, J.-C. Rosenwald in Handbook of Radiotherapy Physics, 2021
Fractional doses of the order of 0.2 Gy to 1.0 Gy correspond to the 10–50% isodoses in a treatment plan (for a 2 Gy per fraction prescription dose), and consequently, the presence of HRS in the cells in certain organs-at-risk could affect complication rates. In support of this suggestion, Simonsson et al. (2008) observed a hypersensitive response to low doses in epidermal skin 30 minutes following irradiation in prostate cancer patients. The field of predicting complication probability by analysing dose distributions and dose volume histograms in organs-at-risk (normal-tissue complication probability modelling – see Section 44.3) may therefore need to take account of HRS. For example, if a certain conformal or intensity-modulated technique reduces the volume of normal tissue irradiated at around 1 Gy per fraction but at the same time increases the normal-tissue volume irradiated at around 0.2 Gy per fraction, and if the cells involved exhibit HRS, then instead of this technique yielding a reduction in cell killing and consequently, in complication probability, it could conceivably result in an increased complication risk. Honoré (2002) has explored scenarios of this nature.
Mitral valve prolapse
Published in Expert Review of Cardiovascular Therapy, 2019
Aeshah Althunayyan, Steffen E Petersen, Guy Lloyd, Sanjeev Bhattacharyya
The mechanism for symptoms is not fully understood although may be related to autonomic nervous system dysfunction [29–31]. Boudoulas et al. demonstrated increased adrenergic tone in symptomatic patients with MVP [29]. Symptomatic MVP patients had a hypersensitive response to adrenergic stimulation which reproduced symptoms in the majority of patients [30]. This response may be related to polymorphisms of β1 adrenergic receptors [31]. Bashore et al. demonstrated patients with symptomatic MVP and no significant regurgitation had reduced exercise tolerance compared to normal subjects. Furthermore, during upright exercise, there is a lack of increment in left ventricular end-diastolic volume suggesting impaired cardiac filling during upright exercise. This may be explained by reduced venous return and an inappropriate response of the venous capacitance system [32].
Nonlinearities in the cellular response to ionizing radiation and the role of p53 therein
Published in International Journal of Radiation Biology, 2021
David Murray, Razmik Mirzayans
It has long been anticipated that DNA repair processes should become saturated after high/supra-lethal doses of IR (e.g. Wheeler and Nelson 1987). However, a major challenge to the linearity of the DDR even at low doses was presented by the discovery of the low dose hyper-radiosensitivity-increased radioresistance (HRS-IRR) phenomenon in which many cell lines were found to exhibit clonogenic survival curves with an initial hypersensitive response (typically up to ∼25 cGy), followed by a region (typically at ∼50 cGy) in which the cells displayed increasing radioresistance (reviewed in Marples and Collis 2008). Such behavior was presumed to reflect a failure of cells to trigger some critical cytoprotective aspect(s) of the DDR network after doses below ∼50 cGy. An impaired rejoining of DSBs in the HRS region has been reported in some but not all human cell lines (reviewed in Murray and Weinfeld 2010), so this does not seem to represent a general mechanism. Activation of an ATM-dependent early-G2 cell-cycle checkpoint was also seen to have a threshold dose of ∼30 cGy in cell types that exhibit HRS but not in those that lack the HRS phenotype (Krueger et al. 2007; Marples and Collis 2008).
Ophthalmic and Neuro-ophthalmic Manifestations of Coronavirus Disease 2019 (COVID-19)
Published in Ocular Immunology and Inflammation, 2020
Amparo Ortiz-Seller, Lucía Martínez Costa, Antonio Hernández-Pons, Elia Valls Pascual, Alicia Solves Alemany, Mara Albert-Fort
Her best corrected visual acuity (BCVA) was 20/25 in both eyes. Slit-lamp examination revealed poorly reacting pupils. Pupillary dilation was more pronounced in bright illumination, with light-near dissociation. Abnormal pupillary response was not present in previous examinations. Topical dilute 0.1% pilocarpine was instilled into both eyes and hypersensitive response was demonstrated by constriction of both pupils (Figure 1). This finding suggested bilateral Adie tonic pupil. Moreover, funduscopic examination showed multiple bilateral white-yellowish placoid lesions located at the posterior pole and the mid-peripheral retina (Figure 2a-b). Ultra-wide-field (UWF) fundus autofluorescence revealed weak hyperautofluorescence of lesions (Figure 2c-d), whereas UWF fluorescein angiography (FA) displayed right patchy areas of choroidal hypofluorescence in the early phase with late hyperfluorescence (Figure 2e-h). Optical coherence tomography angiography (OCT-A) demonstrated bilateral areas of nonperfusion at the level of the choriocapillaris (Figure 3a-b). Spectral domain OCT showed inner retinal thinning temporal to the fovea in both eyes, and focal disruptions of the outer retinal layers (Figure 3c-d). The diagnosis of inflammatory chorioretinal disease and Adie’s syndrome possibly associated with COVID-19 was established.
Related Knowledge Centers
- Animal
- Innate Immune System
- Phytophthora Infestans
- Virus
- Infection
- Apoptosis
- Pathogen
- Systemic Acquired Resistance
- Species
- Nutrient