Everything you need to know about cold-induced skin allergy.

Cold urticaria, often referred to as cold allergy, is a distinct form of urticaria triggered by cold exposure without any allergen being involved. Therefore, the term cold allergy, although frequently used, is actually incorrect. The areas most commonly affected are those most exposed, such as the hands and face. Clinically, this condition is classified among chronic inducible urticarias.

Cold urticaria can pose a medical challenge, as some atypical forms may progress to severe reactions such as cold-induced anaphylaxis.

Although advancements have been made in understanding and managing cold urticaria, many questions still remain. The average duration of the disease extends over several years, and its clinical presentation can vary, making personalized diagnosis and treatment sometimes complex.

The manifestations of cold urticaria occur rapidly following cold exposure, often within minutes.

They present as the appearance of red, swollen plaques, sometimes accompanied by edema, on directly exposed areas: hands in contact with a cold object, face, soles of the feet on a cold surface, or following ingestion of cold foods or beverages. These lesions are generally very pruritic and may be accompanied by burning or tingling sensations. They resolve spontaneously once exposure ceases, within minutes to a few hours.

In some individuals, cold urticaria may be accompanied by more generalized symptoms, reflecting a systemic reaction. Headaches, feelings of malaise, fever, and joint or abdominal pain may then develop. In more severe cases, respiratory distress, swelling of the lips or throat, or even an anaphylactic reaction can occur, particularly during significant exposures such as cold-water swimming. Although these scenarios are rare, they warrant special vigilance and immediate medical management.

Often mistaken for one another and both triggered by low temperatures, cold urticaria and eczema are nonetheless two distinct conditions.

In summary, cold urticaria is an acute, transient reaction directly triggered by cold, whereas eczema is a chronic condition whose symptoms can be exacerbated by winter conditions.

The precise causes of cold urticaria remain poorly understood.

However, several mechanisms are suspected. The main hypotheses include autoimmunity, autoallergy, and abnormalities in temperature detection by the skin. Exposure to cold could trigger the formation of new autoantigens, leading in sensitized individuals to an immunoglobulin E (IgE)-dependent mast cell activation, which results in the appearance of hives.

Some studies have demonstrated the presence of autoantibodies targeting IgE or mast cell receptors in certain patients, suggesting a possible role for type IIb autoimmunity. In some patients, circulating histamine-reactive factors may also contribute to cutaneous reactions independently of IgE. Furthermore, mast cells, which are immune cells, play a role in the onset of the allergic reaction. Their rapid degranulation following cold exposure triggers the release of histamine and other inflammatory mediators, such as prostaglandins and TNF-α.

In addition, cold-sensitive TRP-type ion channels (TRPM8 and TRPA1) appear to contribute to cutaneous cold detection and to the modulation of inflammatory responses. Other factors, such as the potential presence of cryoglobulins or abnormalities in the enzymatic regulation of mast cells, may play a secondary role in the disease’s pathophysiology.

Finally, there is a familial hereditary form of cold urticaria. In this case, it is a genetic condition with autosomal dominant inheritance that persists throughout a person’s life. This specific mode of inheritance means that the mutation is located on a non-sex chromosome and that a single copy of the gene must be affected for the condition to develop. This form of cold urticaria is extremely rare and may be linked to the gut microbiota.

Cold urticaria can suddenly occur in an otherwise healthy individual and then disappear without explanation a few years later. Young adults and women appear to be more frequently affected.

The diagnosis of cold urticaria is based primarily on the clinical history, which identifies a clear relationship between cold exposure and the rapid onset of urticarial plaques.

To confirm the diagnosis and assess its severity, cold provocation tests are generally performed in a medical setting. The simplest and most commonly used test is the ice cube test. It involves applying an ice cube, placed in a plastic bag or medical glove, to the inner forearm for about five minutes. After the ice cube is removed, the skin is examined approximately ten minutes later: the appearance of a localized urticarial wheal is considered a positive result. This test confirms cold sensitivity but does not precisely determine the temperature threshold that triggers the reaction.

For a more refined evaluation, particularly in atypical or severe forms, a standardized device such as the TempTest can be used. This device applies various controlled temperatures to the forearm skin, allowing precise determination of the minimum temperature capable of triggering an allergic reaction.

In certain cases, blood tests may also be prescribed. They do not directly establish a diagnosis of cold urticaria but can be useful for identifying associated causes or immunological abnormalities, particularly in secondary forms or in cases of unusual symptoms.

These tests must be strictly performed under medical supervision. It is strongly discouraged to attempt to replicate an ice cube test on your own, as unsupervised exposure to cold can trigger a significant, even systemic, reaction in some individuals.

The management of cold urticaria primarily relies on prevention and avoidance of the triggering factor, namely exposure to cold.

On a daily basis, this involves protective measures. For example, it is recommended to wear warm clothing in winter (gloves, scarf, hat), to avoid direct contact with cold objects, to be wary of iced beverages or foods, and to refrain from swimming in cold water (unheated pool, lake, sea).

From a medical perspective, treatment primarily relies on the administration of antihistamines orally, prescribed by the physician. These medications block the action of histamine, the key mediator of hives, and are generally effective at preventing the appearance of wheals or reducing their intensity. The dosage and duration of treatment with antihistamines are adjusted according to the severity and frequency of symptoms. In more severe cases, particularly when an episode of cold-induced anaphylaxis has already been observed, an epinephrine auto-injector can be prescribed as a preventive measure. It should be used immediately in the event of a severe systemic reaction.

In severe forms or those resistant to standard treatments, more targeted therapeutic options may be considered. A clinical study described the case of an adolescent with cold urticaria whose symptoms progressively worsened over two years despite treatment with H1-antihistamines and leukotriene antagonists. The reactions, initially cutaneous, became systemic during cold-water immersion, particularly in marine environments. The introduction of anti-IgE therapy resulted in complete resolution of clinical manifestations.

This marked improvement supports the hypothesis of a central role for IgE and its high-affinity receptor (FcεRI) in cold-induced mast cell activation. By reducing free IgE levels, this type of treatment could limit mast cell degranulation and the release of mediators responsible for cold urticaria symptoms. Although this finding is based on a single clinical case, it opens interesting perspectives for the management of severe forms of cold urticaria and highlights the need for further studies to confirm its efficacy and to define patient profiles most likely to benefit.

Finally, for certain individuals, a cold desensitization may be considered. It involves gradual, controlled, and localized exposure to cold, conducted exclusively in a specialized hospital setting. This approach requires close medical supervision.

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• BOYCE J. A. Successful treatment of cold-induced urticaria/anaphylaxis with anti-IgE. Food Allergy, Dermatologic Diseases, and Anaphylaxis (2006).

• MAURER M. & al. Cold urticaria – What we know and what we do not know. European Journal of Allergy and Clinical Immunology (2020).

• KRAUSE K. & al. Cold-induced urticarial autoinflammatory syndrome related to factor XII activation. Nature Communications (2020).

• MAURER M. & al. Risk factors for systemic reactions in typical cold urticaria: Results from the COLD-CE study. European Journal of Allergy and Clinical Immunology (2021).