Because of spam, I personally moderate all comments left on my blog. However, because of health issues, I will not be able to do so in the future.

If you have a personal question about LI or any related topic you can send me an email at I will try to respond.

Otherwise, this blog is now a legacy site, meaning that I am not updating it any longer. The basic information about LI is still sound. However, product information and weblinks may be out of date.

In addition, my old website, Planet Lactose, has been taken down because of the age of the information. Unfortunately, that means links to the site on this blog will no longer work.

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Saturday, March 04, 2006

The Different Types of Dairy Allergy

Allergy. Hypersensitivity. Which one affects you or your family? How do you distinguish between them?

I took a stab at answering this in a simple way on my web site with Lactose Intolerance versus Milk Allergy.

I know that some of you want a deeper insight on the way the body works. Fortunately, a recent dissertation has addressed this question in depth.

Effects of Cow’s Milk and its Processing on Gastrointestinal
Symptoms and Delayed-Type Immune Responses,by Laura Paajanen.

The dissertation is a huge (83-page) .pdf file, so those with slow connections should be warned that it might be a long download.

The background information on allergies and intolerances is more important for readers than the study itself, so that should cut down on a lot of reading.

One part that I particularly want to highlight is the section on types of allergies. There are four major types, although just two are ones you normally have to worry about, true allergies and hypersensitivities. Paajanen writes:

Allergic reactions are traditionally classified under four types of hypersensitivity reaction which may lead to tissue damage, as described by Coombs and Gell (see Britton 2002, Hay & Westwood 2002, Male 2002, Platts-Mills 2002). It is not clear whether all four types of reaction are involved in the pathogenesis of food allergy, either in the gut itself or in remote organs. More than one mechanism may be involved in any allergic reaction, but the most plausible mechanisms are IgE-mediated reactions (Type I), and the non-IgE-mediated activation of T lymphocytes (Type IV): allergies may be exclusively IgE-mediated, partially IgEmediated or exclusively cell-mediated (Sampson 2001).

Type I, immediate anaphylactic hypersensitivity is characterised by the production of IgE antibodies against foreign proteins (Platts-Mills 2002). IgE antibodies bind to high-affinity Fc_RI receptors on mast cells and basophils. When an allergen binds between two IgE antibodies, it induces degranulation of a mast cell/basophil, which leads to the rapid release of histamine and the more gradual release of other mediators such as leukotrienes and cytokines. The combined effect of these agents is to constrict smooth muscle, dilate capillaries and induce cell infiltration. This mechanism underlies the common problem of atopic allergy….

Type IV, delayed cell-mediated hypersensitivity reactions take more than 12 hours to develop (Britton 2002). T cells identify antigens, and the antigen-sensitised T cells produce cytokines and other soluble factors which mediate the hypersensitivity reaction, or else they develop cytotoxicity. Th cell-activated macrophages destroy intracellular bacteria by releasing inflammatory mediators. Activated cytotoxic T cells and natural killer cells destroy virus-infected cells and transformed human cells, i.e. cancer cells and tissue transplants. Tissue damage occurs as a result of persistent antigenic stimulation, either because of continuing infection or because of autoimmunisation. Type IV hypersensitivity has been classified under three varieties: contact hypersensitivity and tuberculin-type hypersensitivity, which both occur within 3 days of a challenge; and granulomatous hypersensitivity reactions, which develop over a period of 21-28 days and are clinically the most serious of the Type IV responses. More than one type of delayed hypersensitivity may follow a single antigenic challenge, and reactions may overlap.

One other section is also a must read.

3.1 Different types of cow’s milk allergy
CMA before school age

CMA is usually the first major food allergy, since cow’s milk rpoteins are the first source of foreign antigens massively ingested in infancy. In several large clinical trials, the cumulative prevalence of allergy to cow’s milk has been approximately 2-3% during the first years of life in the general population (Jakobsson & Lindberg 1979, Hide & Guyer 1983, Bock 1987, Høst & Halken 1990, Schrander et al. 1993, Saarinen et al. 1999). In atopic infants, however, the prevalence is up to 50% (Sampson & McCaskill 1985, Isolauri & Turjanmaa 1996, Niggemann et al. 1999). CMA has been reported even in exclusively breast-fed infants (Høst et al. 1988, Isolauri et al. 1999, Järvinen et al. 1999, Österlund et al. 2004a). The majority of paediatric patients have symptoms from two or more organ systems: approximately 50-60% have cutaneous, 50-60% gastrointestinal and 20-30% respiratory symptoms (Høst 2002). In exclusively breast-fed infants with CMA, severe atopic eczema is a predominant symptom. In infants under the age of one year, CMA is reportedly IgE-mediated in 57-64% of the cases (Vanto et al. 1999, Saarinen & Savilahti 2000). The overall prognosis of CMA in infancy is good, with a remission rate of 85 or 90% by 3 years of age (Høst & Halken 1990, Høst 2002), non-IgE-mediated reactions being the quickest to recover (Vanto et
al. 2004)….

CMA in school-aged children and adults

In most textbooks CMA is considered to be rare in adults. Only a restricted number of studies on the immunological mechanisms of adult CMA exist, supported by either double-blind, placebo controlled milk challenges or the open challenge procedure (Nørgaard & Bindslev-Jensen 1992, Nørgaard et al. 1995, Bengtsson et al. 1996b, Bengtsson et al. 1996a, Bengtsson et al. 1997, Werfel et al. 1997, Little et al. 1998, Ulanova et al. 2000, Lin et al. 2002, Magnusson et al. 2003). In recent years recovery from CMA has become a subject of controversy. Compared to the mainly IgE-mediated CMA of infants and small children, a new form of delayed-type gastrointestinal cow’s milk hypersensitivity, also known as cow’s milk sensitive enteropathy, has been described in school-aged children and adults, and it may be more common than previously thought (Bengtsson et al. 1996b, Bengtsson et al. 1996a, Bengtsson et al. 1997, Pelto et al. 1998, Pelto et al. 1999, Ulanova et al. 2000, Kokkonen et al. 2001a, Lin et al. 2002, Magnusson et al. 2003, Kokkonen et al. 2004). After childhood, reactions to milk are rarely IgE-mediated, and virtually only case reports of IgE-mediated CMA in adults exist. In one study, only 10% of the children with CMA in childhood had IgE-mediated reactions to milk protein at school age; however, half the children still reported gastrointestinal symptoms related to the ingestion of cow’s milk protein (Kokkonen et al. 2001a).

As for diagnosing allergies in infants and children:

In young infants, open controlled challenges have been shown to be reliable when performed under professional observation in a hospital (Høst & Halken 1990, Niggemann et al. 1994, Isolauri & Turjanmaa 1996). In children over 1-2 years of age and in adults, the double-blind placebo controlled food challenge is considered the gold standard for exclusion of psychological or causal reactions (Høst & Halken 1990, Niggemann et al. 1994), but is often too laborious in clinical work (Kaila et al. 2000). In patients with delayed reactions, a placebo-controlled food challenge would be the best method of diagnosis (Bindslev-Jensen et al. 2004), but this is often not practical in clinical work. In adults in particular it may be difficult to distinguish gastrointestinal allergies from other gastrointestinal symptoms such as those of lactose intolerance or irritable bowel syndrome.

In early infancy and especially in breast-fed infants who develop immediate reactions to cow’s milk, the presence of a specific elevation of IgE antibodies to cow’s milk or a skin prick test for cow’s milk may have diagnostic value. According to reports, the specificity of the skin prick test varies greatly, from 50 to 99%, and sensitivity, from 14 to 78%, when the cut-off size of the wheal diameter is set at 3 mm (Majamaa et al. 1999a, Vanto et al. 1999, Roehr et al. 2001, Saarinen et al. 2001, Strömberg 2002, Rancé 2004). In these particular studies, the atopy patch test was found to have better specificity (71 to 100%), especially in patients with skin symptoms, but its sensitivity for identifying all the disease cases was comparatively low (from 26 to 89%). When quantitatively assessed by the CAP System FEIA, cow’s milk specific IgE antibody titres of over 32 kU/l have been reported to predict IgE-mediated CMA with as high as 95% certainty in atopic patients (Sampson & Ho 1997). However, this finding was not supported by a recent study in which much higher cow’s milk-specific IgE titres (88.8 kU/l) were needed for predicting CMA with 90% probability, and the authors concluded that no meaningful predictive decision point could be calculated for predicting CMA (Celik-Bilgili et al. 2005). Skin tests are rarely useful in adults (Nørgaard & Bindslev-Jensen 1992). Increased IgA and IgG milk antibodies are not diagnostic, but merely a sign that milk has been ingested. Basophil histamine release is more frequently measured in other food allergies (Hansen et al. 2003, Østerballe et al. 2003) than in CMA (Prahl et al. 1988), and has not usually been found to be more predictive than skin prick testing or milk-specific IgE testing.

There's much more to read as well. It's a fine summary of the literature for anybody who wants more than the "allergy lite" you usually get online.

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