Materiały źródłowe

• #1 Cold urticaria – UpToDate

  https://www.uptodate.com/contents/cold-urticaria/print

  Cold urticaria is characterized by pruritic wheals (hives) and/or angioedema due to cutaneous mast cell degranulation and their release of proinflammatory mediators after cold exposure of the skin. […] The underlying pathophysiology of cold urticaria is largely unknown but is likely to involve immunoglobulin E (IgE) mediated mast cell activation in a subgroup of patients. Signs and symptoms result from degranulation of mast cells and the resulting release of histamine and other proinflammatory mediators. This results in pruritus, burning, and erythema from activation of cutaneous nerves and vasodilation of skin vessels with extravasation causing wheals and angioedema. Following a cold stimulation test (CST), cutaneous mast cells show signs of degranulation, and skin and serum levels of mast cell mediators are increased. […] On skin biopsy, cold urticaria lacks a late-phase cellular infiltrate, similar to most other forms of physical urticaria (except delayed pressure urticaria).

• #2 Cold urticaria – What we know and what we do not know – PubMed

  https://pubmed.ncbi.nlm.nih.gov/33249577/

  Cold urticaria (ColdU) is a common form of chronic inducible urticaria characterized by the development of wheals, angioedema or both in response to cold exposure. […] Today, its pathophysiology is thought to involve the cold-induced formation of autoallergens and IgE to these autoallergens, which provoke a release of proinflammatory mediators from skin mast cells. […] The classification of ColdU includes typical and atypical subtypes. […] The management of ColdU includes cold avoidance, the regular use of nonsedating antihistamines and the off-label use of omalizumab. […] However, many questions regarding ColdU remain unanswered.

• #3 What Is Acquired Cold Urticaria?

  https://www.icliniq.com/articles/allergies/acquired-cold-urticaria

  Acquired cold urticaria is a type I hypersensitivity reaction involving IgE antibodies (a protein released in response to allergy), mast cells (an immune cell), and inflammatory mediators release (essential components of allergic inflammation). […] Although several theories exist regarding the disease mechanism of acquired cold urticaria, none is proven. Various studies support the autoimmune theory. Weals (a raised red mark on the skin) and angioedema (tissue swelling) in acquired cold urticaria involve mast cell degranulation (which releases histamine, a chemical involved in allergic immune response and cytokines; immune mediators) with the generation of inflammatory mediators. […] These mediators induce vasodilatation (dilation of blood vessels), increased vessel permeability, and nerve endings stimulation. As a result, it leads to swelling, redness, and skin itching. The redness and itching can also be accompanied by fever, headache, tiredness, arthralgia (joint pain), and leukocytosis (increased circulating white blood cells). A weal is characterized by edema, mast cell degranulation, and an inflammatory infiltrate of cells (lymphocytes, monocytes, neutrophils, eosinophils, and basophils).

• #4 Cold urticaria – UpToDate

  https://www.uptodate.com/contents/cold-urticaria/print

  Cold urticaria is characterized by pruritic wheals (hives) and/or angioedema due to cutaneous mast cell degranulation and their release of proinflammatory mediators after cold exposure of the skin. […] The underlying pathophysiology of cold urticaria is largely unknown but is likely to involve immunoglobulin E (IgE) mediated mast cell activation in a subgroup of patients. Signs and symptoms result from degranulation of mast cells and the resulting release of histamine and other proinflammatory mediators. This results in pruritus, burning, and erythema from activation of cutaneous nerves and vasodilation of skin vessels with extravasation causing wheals and angioedema. Following a cold stimulation test (CST), cutaneous mast cells show signs of degranulation, and skin and serum levels of mast cell mediators are increased. […] On skin biopsy, cold urticaria lacks a late-phase cellular infiltrate, similar to most other forms of physical urticaria (except delayed pressure urticaria).

• #5 Urticaria: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/762917-overview

  Urticaria (hives) results from the release of histamine, bradykinin, leukotriene C4, prostaglandin D2, and other vasoactive substances from mast cells and basophils in the dermis. These substances cause extravasation of fluid into the dermis, leading to the urticarial lesion. The intense pruritus (itchiness) of urticaria is a result of histamine released into the dermis. Histamine is the ligand for two membrane-bound receptors, the H1 and H2 receptors, which are present on many cell types. The activation of the H1 histamine receptors on endothelial and smooth muscle cells leads to increased capillary permeability. The activation of the H2 histamine receptors leads to arteriolar and venule vasodilation. […] This process is caused by several mechanisms. The type I allergic IgE response is initiated by antigen-mediated IgE immune complexes that bind and cross-link Fc receptors on the surface of mast cells and basophils, thus causing degranulation with histamine release. The type II allergic response is mediated by cytotoxic T cells, causing deposits of immunoglobulins, complement, and fibrin around blood vessels. This leads to urticarial vasculitis. The type III immune-complex disease is associated with systemic lupus erythematosus and other autoimmune diseases that cause urticaria.

• #6 Urticaria – Indian Journal of Dermatology, Venereology and Leprology

  https://ijdvl.com/urticaria/

  Activation of cutaneous mast cells liberates various mediators predominantly histamine which induces increased permeability of capillaries and venules which in turn produces uriticaria. The clinical response of urticaria to antihistamines proves this hypothesis. Mast cells may be activated by allergic or non-allergic mechanisms. Allergic mast cell activation occurs as a result of linkage of two adjacent a sub – units of high affinity eg. penicillin. As a result of this, preformed histamines, proteases, prostaglandin D2, LT4 and interleukin 4 (IL-4), IL – 8 and tumour necrosis factor (TNF – a) are released. Non allergic mast cell activation occurs with a variety of substances like neuropeptides (substance P), drugs like morphine, codeine, vancomycin, radio contrast media and some foods such as strawberries.

• #7 Eczema and Hives: Identifying and Managing Them Successfully

  https://www.dexeryl.com/en/your-skin/atopic-dermatitis/different-types-of-eczema/urticaria-eczema

  Urticaria results from a complex reaction involving mast cells, key immune system cells in the skin, and mucous membranes. These cells contain an inflammation molecule: histamine. When mast cells are activated, they release histamine, which causes blood vessel dilation and increased permeability. This reaction leads to fluid and cell infiltration into the surrounding tissues, causing oedema. This mechanism is at the root of urticaria patches. […] Chronic urticaria is characterised by persistent or recurrent outbreaks over at least six weeks. It’s a non-allergic skin inflammation, sensitising the skin’s mast cells to a variety of non-allergic stimuli. […] Understanding these triggers is essential for the prevention of urticaria.

• #8 Urticaria: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/762917-overview

  Urticaria (hives) results from the release of histamine, bradykinin, leukotriene C4, prostaglandin D2, and other vasoactive substances from mast cells and basophils in the dermis. These substances cause extravasation of fluid into the dermis, leading to the urticarial lesion. The intense pruritus (itchiness) of urticaria is a result of histamine released into the dermis. Histamine is the ligand for two membrane-bound receptors, the H1 and H2 receptors, which are present on many cell types. The activation of the H1 histamine receptors on endothelial and smooth muscle cells leads to increased capillary permeability. The activation of the H2 histamine receptors leads to arteriolar and venule vasodilation. […] This process is caused by several mechanisms. The type I allergic IgE response is initiated by antigen-mediated IgE immune complexes that bind and cross-link Fc receptors on the surface of mast cells and basophils, thus causing degranulation with histamine release. The type II allergic response is mediated by cytotoxic T cells, causing deposits of immunoglobulins, complement, and fibrin around blood vessels. This leads to urticarial vasculitis. The type III immune-complex disease is associated with systemic lupus erythematosus and other autoimmune diseases that cause urticaria.

• #9 Cold urticaria – What we know and what we do not know – PubMed

  https://pubmed.ncbi.nlm.nih.gov/33249577/

  Cold urticaria (ColdU) is a common form of chronic inducible urticaria characterized by the development of wheals, angioedema or both in response to cold exposure. […] Today, its pathophysiology is thought to involve the cold-induced formation of autoallergens and IgE to these autoallergens, which provoke a release of proinflammatory mediators from skin mast cells. […] The classification of ColdU includes typical and atypical subtypes. […] The management of ColdU includes cold avoidance, the regular use of nonsedating antihistamines and the off-label use of omalizumab. […] However, many questions regarding ColdU remain unanswered.

• #10

  https://link.springer.com/article/10.1007/s11882-024-01160-y

  It has also been proposed that de novo synthesized autoantigens (autoallergens) can be induced by physical or environmental triggers such as cold, and subsequently detected by IgE bound to skin mast cells (MCs) leading to degranulation in ColdU patients. […] Overexpression of the IgE receptor, FcRI, on basophils is observed in patients with CIndU independently of the subtype and is comparable to the expression found in CSU patients. […] Altogether, this evidence indicates that skin MC and IgE play an important role in the pathogenesis of CIndU. […] Moreover, there is direct and indirect evidence of histamine release by in vivo and in vitro analyses in all types of CIndU. […] ColdU is characterized by wheals, angioedema, or both, occurring rapidly in response to cooling. […] The pathogenesis of ColdA is not completely understood.

• #11 Physiopathology of cold urticaria, Centre de Preuves en Dermatologie

  https://reco.sfdermato.org/en/guidelines-cold-ulticaria/physiopathology

  The pathophysiology of cold urticaria (CU) is not well understood. Passive transfer experiments have shown that CU can be induced in healthy patients by intradermal injection of serum from patients with CU: serum from CU patients was injected intradermally, followed by a „passive sensitization” period of 2 to 48 hours before performing the ice cube test. […] Performing the ice cube test without this minimum 2-hour delay or cooling the skin before the serum injection did not trigger CU in healthy patients. Only neutralization of IgE prevented the urticarial reaction after a new intradermal injection of serum, which is why the involvement of an IgE was suggested. […] The involvement of an IgE-type cryoglobulin was ruled out because basophils sensitized with serum from CU patients were not stimulated by cooling in vitro. It has therefore been suggested that either cutaneous mast cells release mediators after a temperature change and binding of an abnormal IgE, or an abnormal IgE binds to an unknown thermosensitive cutaneous antigen that activates mast cell degranulation. An autoantigen (autoallergen) may therefore form de novo at a specific temperature and be detected by IgE bound to cutaneous mast cells. […] Mast cell degranulation may act as a protective mechanism to maintain blood circulation and prevent cellular damage.

• #12 Physiopathology of cold urticaria, Centre de Preuves en Dermatologie

  https://reco.sfdermato.org/en/guidelines-cold-ulticaria/physiopathology

  The pathophysiology of cold urticaria (CU) is not well understood. Passive transfer experiments have shown that CU can be induced in healthy patients by intradermal injection of serum from patients with CU: serum from CU patients was injected intradermally, followed by a „passive sensitization” period of 2 to 48 hours before performing the ice cube test. […] Performing the ice cube test without this minimum 2-hour delay or cooling the skin before the serum injection did not trigger CU in healthy patients. Only neutralization of IgE prevented the urticarial reaction after a new intradermal injection of serum, which is why the involvement of an IgE was suggested. […] The involvement of an IgE-type cryoglobulin was ruled out because basophils sensitized with serum from CU patients were not stimulated by cooling in vitro. It has therefore been suggested that either cutaneous mast cells release mediators after a temperature change and binding of an abnormal IgE, or an abnormal IgE binds to an unknown thermosensitive cutaneous antigen that activates mast cell degranulation. An autoantigen (autoallergen) may therefore form de novo at a specific temperature and be detected by IgE bound to cutaneous mast cells. […] Mast cell degranulation may act as a protective mechanism to maintain blood circulation and prevent cellular damage.

• #13 Urticaria – Kaplan AP (Updated 2019)

  https://www.worldallergy.org/component/content/article/urticaria-kaplan-ap-updated-2019?catid=16&Itemid=101

  Idiopathic cold urticaria is characterized by the rapid onset of pruritus, erythema, and swelling after exposure to a cold stimulus. The location of the swelling is confined to those parts of the body that have been exposed. […] One proposal to explain this phenomenon is that patients have an IgE autoantibody to a cold-induced skin antigen. […] The time course of this reaction (i.e., cold challenge followed by hive formation as the area returns to body temperature) demonstrates that a two-step reaction has occurred in which exposure to cold is a prerequisite, but hive formation actually occurs as the temperature increases. […] Patients with vasculitis and urticaria appear to be a separate sub-population in whom the cause and pathogenesis of hive formation probably involves immune complexes, complement activation, anaphylatoxin formation, histamine release, and neutrophil accumulation, activation, and degranulation.

• #14 Physiopathology of cold urticaria, Centre de Preuves en Dermatologie

  https://reco.sfdermato.org/en/guidelines-cold-ulticaria/physiopathology

  The pathophysiology of cold urticaria (CU) is not well understood. Passive transfer experiments have shown that CU can be induced in healthy patients by intradermal injection of serum from patients with CU: serum from CU patients was injected intradermally, followed by a „passive sensitization” period of 2 to 48 hours before performing the ice cube test. […] Performing the ice cube test without this minimum 2-hour delay or cooling the skin before the serum injection did not trigger CU in healthy patients. Only neutralization of IgE prevented the urticarial reaction after a new intradermal injection of serum, which is why the involvement of an IgE was suggested. […] The involvement of an IgE-type cryoglobulin was ruled out because basophils sensitized with serum from CU patients were not stimulated by cooling in vitro. It has therefore been suggested that either cutaneous mast cells release mediators after a temperature change and binding of an abnormal IgE, or an abnormal IgE binds to an unknown thermosensitive cutaneous antigen that activates mast cell degranulation. An autoantigen (autoallergen) may therefore form de novo at a specific temperature and be detected by IgE bound to cutaneous mast cells. […] Mast cell degranulation may act as a protective mechanism to maintain blood circulation and prevent cellular damage.

• #15 Urticaria – Kaplan AP (Updated 2019)

  https://www.worldallergy.org/component/content/article/urticaria-kaplan-ap-updated-2019?catid=16&Itemid=101

  Idiopathic cold urticaria is characterized by the rapid onset of pruritus, erythema, and swelling after exposure to a cold stimulus. The location of the swelling is confined to those parts of the body that have been exposed. […] One proposal to explain this phenomenon is that patients have an IgE autoantibody to a cold-induced skin antigen. […] The time course of this reaction (i.e., cold challenge followed by hive formation as the area returns to body temperature) demonstrates that a two-step reaction has occurred in which exposure to cold is a prerequisite, but hive formation actually occurs as the temperature increases. […] Patients with vasculitis and urticaria appear to be a separate sub-population in whom the cause and pathogenesis of hive formation probably involves immune complexes, complement activation, anaphylatoxin formation, histamine release, and neutrophil accumulation, activation, and degranulation.

• #16 AAIR :: Allergy, Asthma & Immunology Research

  https://e-aair.org/DOIx.php?id=10.4168/aair.2017.9.6.477

  Urticaria lasting greater than 6 weeks is divided into 2 general groups; namely, inducible or spontaneous. Inducible urticarias are, perhaps, more accurately described as intermittent urticarias because the frequency is dependent on the particular stimulus. In this category are physical urticarias e.g., cold urticaria and dermatographism. […] For an extensive discussion of our current knowledge and historical perspectives, review articles can be consulted. I will present a summary of current concepts including some areas that remain controversial. Since there is no exogenous stimulus or cause, neither foods, drugs, food additives, or other chemicals are relevant which is why routine food skin testing or radioallergosorbent test (RAST) is not recommended for evaluation. […] Among the possibilities for the etiology of CSU is that it is an autoimmune skin disease, or at least a subpopulation of patients could be considered as such. Depending on the authors, 35%-40% of patients have an IgG antibody to the subunit of the high affinity IgE receptor (IgG anti-FcRI) while an additional 5%-10% have IgG anti-IgE. These are functional and can be shown to induce histamine release from blood basophils or cutaneous mast cells.

• #17 Urticaria | Nature Reviews Disease Primers

  https://www.nature.com/articles/s41572-022-00389-z

  The pathogenesis of CSU consists of several interlinked events involving autoantibodies, complement and coagulation. […] In this study, IL-24 is a common, specific and functional autoantigen of IgE antibodies in patients with CSU, suggesting autoallergic mechanism in many patients with CSU. […] The role of coagulation and complement factors for mast cell activation in the pathogenesis of chronic spontaneous urticaria. […] This study involving more than 12,000 patients with CU points to a strong association between CU and major autoimmune diseases. […] In this report, functional histamine-releasing IgG autoantibodies to the -subunit of the high-affinity IgE receptor are detected in the circulation of some patients with CU, suggesting an involvement of these autoantibodies in the pathogenesis of CU.

• #18 Chronic Urticaria—Pathogenesis, Diagnostics, Therapy and Influence of Coexisting Angioedema

  https://www.mdpi.com/2077-0383/12/2/688

  Currently, two endotypes of CSU can be distinguished, which vary in terms of pathogenesis and markers of the disease, as well as clinical course and sensitivity to treatment applied: type I and IIb. Type I CSU is related to the occurrence of IgE antibodies to autoantigens such as TPO (thyroid peroxidase), TG (thyroglobulin), ds-DNA (double-stranded DNA) and Il-24. In type I, it is observed that the occurrence of allergic diseases and the total concentration of IgE are normal or even increased. Antihistamines and omalizumab used in this endotype therapy are usually effective. In type IIb CSU, IgG and IgM antibodies to IgE and high-affinity receptors for IgE (FceRI) are identified. Additionally, in the clinical course of this endotype, greater severity of symptoms and a prolonged duration of the disease, coexistence of autoimmune diseases, presence of ANA (antinuclear antibodies), elevated CRP levels, basopenia and eosinopenia in peripheral blood and reduced levels of total IgE occur.

• #19 The Role of Infection and Autoimmunity in Urticaria and Angioedema as a Common Entity – European Medical Journal

  https://www.emjreviews.com/allergy-immunology/article/the-role-of-infection-and-autoimmunity-in-urticaria-and-angioedema-as-a-common-entity-j010121/

  Although CSU is a multifactorial condition involving autoimmunity, coagulation, and inflammation, IgE-mediated autoimmunity, or autoallergy, is thought to play a major role. […] Histamine release likely occurs through cross-linking receptors by IgG-specific and specific auto-immune IgE autoantibodies derived against antigens, on mast cells and basophils. […] Anti-FcR1 antibodies are thought to be the more common of the two. […] Autoimmune mechanisms are contributing to the pathogenesis of chronic urticaria; different pathogenic autoantibodies, causing a release of histamine after reaction with IgE epitopes, or with the -chain of Fc epsilon RI receptors, are considered. […] This skin disease in a sub-group of patients is related to autoreactive IgE, but the nature of this autoreactive IgE is still poorly characterised. […] The author can hypothesise that the underlying lasting immune response to an infection, rather than infection itself, is the causative factor for persistence of urticaria, alongside autoimmune factors.

• #20

  https://link.springer.com/article/10.1007/s40521-024-00366-9

  Cold-induced anaphylaxis (ColdA) is a poorly understood form of anaphylaxis that occurs in patients with cold urticaria (ColdU). […] ColdA has been defined as acute cold-induced involvement of the skin and/or visible mucosal tissue accompanied by cardiovascular manifestations, difficulty breathing, or gastrointestinal symptoms, but a universally accepted definition is lacking. […] The pathophysiology of ColdA remains largely unexplored. […] We hypothesize that ColdA also predominantly involves MC and basophil activation. […] A study by Juhlin and Shelley in 1961 revealed histamine release in two patients with ColdA, with distinctive cytologic changes in tissue MCs and blood basophils. […] The hypothesis that cold exposure may trigger the formation of de novo autoallergens and subsequent IgE-mediated responses diverges from traditional views of anaphylaxis but could be crucial in understanding ColdA. […] TRPM8 (transient receptor potential cation channel subfamily M [melastatin] member 8) proteins, which form Ca2+-conducting cation channels activated by menthol or cold, have also been proposed as mediators of MC activation in ColdU.

• #21

  https://link.springer.com/article/10.1007/s11882-024-01160-y

  It has also been proposed that de novo synthesized autoantigens (autoallergens) can be induced by physical or environmental triggers such as cold, and subsequently detected by IgE bound to skin mast cells (MCs) leading to degranulation in ColdU patients. […] Overexpression of the IgE receptor, FcRI, on basophils is observed in patients with CIndU independently of the subtype and is comparable to the expression found in CSU patients. […] Altogether, this evidence indicates that skin MC and IgE play an important role in the pathogenesis of CIndU. […] Moreover, there is direct and indirect evidence of histamine release by in vivo and in vitro analyses in all types of CIndU. […] ColdU is characterized by wheals, angioedema, or both, occurring rapidly in response to cooling. […] The pathogenesis of ColdA is not completely understood.

• #22 Chronic Urticaria: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1050052-overview

  The mast cell is the primary agent in the pathogenesis of urticaria. Dermal mast cell stimulation results in the release of both preformed (histamine) and newly formed (prostaglandin) mediators, as well as cytokines (interleukin [IL]1, tumor necrosis factor- [TNF-]) from cytoplasmic granules, which cause wheal formation, vasodilatation, and erythema. Mast cells also release chemoattractants for other cells (eg, neutrophils) involved in wheal formation. A complex interplay of varied proinflammarory cytokines, chemokines, and adhesion molecules that regulate vasoactivity and the dynamics of cellular infiltration ultimately evolves to form a lymphocyte- and granulocyte-mediated hypersensitivity reaction in the skin. […] This response may be augmented by complement activation and production of C5a. Unlike pulmonary mast cells, cutaneous mast cells have C5a receptors. C5a not only brings about mast cell activation, but is also a neutrophil and eosinophil chemoattractant, leading to accumulation of these cells in lesional skin.

• #23 Chronic urticaria: a focus on pathogenesis | F1000Research

  https://f1000research.com/articles/6-1095

  Following the first observation on skin reactivity to autologous serum that remains a cornerstone in urticaria research, the second important step in the definition of the pathogenic mechanism was the demonstration of histamine-releasing autoantibodies about 20 years ago, suggesting an autoimmune origin. […] The finding that at least a proportion of chronic urticaria patients show autoimmune phenomena targeting mast cells and basophils has led to the investigation of the diagnostic accuracy of basophil-based in vitro tests aiming to diagnose autoimmunity. […] The observation that the autologous plasma skin test (APST) may score positive in some ASST-negative patients has prompted investigation of the coagulation system in patients with chronic urticaria. […] The activation of the coagulation cascade might potentially play a relevant pathogenic role if one considers that thrombin can markedly increase the vascular permeability and is a potent inducer of mast cell degranulation in experimental models.

• #24 Urticaria – Dermatologic Disorders – MSD Manual Professional Edition

  https://www.msdmanuals.com/professional/dermatologic-disorders/approach-to-the-dermatologic-patient/urticaria

  Urticaria results from the release of histamine, bradykinin, kallikrein, and other vasoactive substances from mast cells and basophils in the superficial dermis, resulting in intradermal edema caused by capillary and venous vasodilation and occasionally caused by leukocyte infiltration. […] The process can be immune mediated or nonimmune mediated. […] Immune-mediated mast cell activation includes Type I hypersensitivity reactions, in which allergen-bound IgE antibodies bind to high-affinity cell surface receptors on mast cells and basophils. […] Nonimmune-mediated mast cell activation includes direct nonallergic activation of mast cells by certain medications or substances. […] Activation by physical or emotional stimuli; mechanism is poorly understood but possibly involves the release of neuropeptides that interact with mast cells. […] Cold-Induced Urticaria. […] This photo shows a positive ice cube test in a patient with idiopathic cold-induced urticaria.

• #25 Hives – Wikipedia

  https://en.wikipedia.org/wiki/Hives

  Mechanisms other than allergen-antibody interactions are known to cause histamine release from mast cells. Many drugs, for example morphine, can induce direct histamine release not involving any immunoglobulin molecule. Also, a diverse group of signaling substances called neuropeptides, have been found to be involved in emotionally induced hives. […] The skin lesions of urticarial disease are caused by an inflammatory reaction in the skin, causing leakage of capillaries in the dermis, and resulting in an edema which persists until the interstitial fluid is absorbed into the surrounding cells.

• #26 Cold urticaria in tropics: A clinico-epidemiological study from North India – Indian Journal of Dermatology, Venereology and Leprology

  https://ijdvl.com/cold-urticaria-in-tropics-a-clinico-epidemiological-study-from-north-india/

  Cold urticaria (ColdU) is classified as a subtype of chronic inducible urticaria characterised by recurring pruritic wheals and/or angioedema upon exposure to cold stimuli. […] The pathogenesis of ColdU involves various mechanisms, including aberrant temperature sensing, autoimmunity, autoallergy, and neurogenic pathways. Exposure to cold may trigger the formation of autoantigens, leading to an IgE-mediated immune response and subsequent mast cell degranulation. […] ColdU can also give rise to severe complications, like respiratory distress, disorientation and even shock with some studies reporting rates of up to 20%. […] Management of ColdU involves measures to protect against cold exposure and the use of anti-histamines to alleviate symptoms. […] In conclusion, this retrospective study sheds light on the clinical characteristics, epidemiology, and treatment response of North Indian patients with ColdU. Further research with larger and diverse populations, prospective, and exploration of genetic and environmental factors is needed to deepen our understanding of this condition in tropical regions.

• #27 Review of cold-induced urticaria characteristics, diagnosis and management in a Western Canadian allergy practice | Allergy, Asthma & Clinical Immunology | Full Text

  https://aacijournal.biomedcentral.com/articles/10.1186/s13223-018-0310-5

  Cold-induced urticaria is a significant condition, especially among young females. […] It results in pruritic wheals with or without angioedema secondary to the release of leukotrienes, histamine and pro-inflammatory mast cell mediators after exposure of the skin to cold air, liquid or cold objects. […] Cold-induced urticaria is divided into primary and secondary forms and there have been many associations reported in the literature. Primary forms are defined when a secondary, or triggering, etiology cannot be determined. Secondary cold-induced urticaria has been reported to be associated with both bacterial and viral infections, medications, Hymenoptera stings, hematological malignancies and immunotherapy, largely based on various case reports. […] The most common cause of secondary acquired cold-induced urticaria is primary and secondary cryoglobulinemia based on case reports. Infectious diseases are the second most common type of secondary acquired cold-induced urticaria.

• #28 Review of cold-induced urticaria characteristics, diagnosis and management in a Western Canadian allergy practice | Allergy, Asthma & Clinical Immunology | Full Text

  https://aacijournal.biomedcentral.com/articles/10.1186/s13223-018-0310-5

  Cold-induced urticaria is a significant condition, especially among young females. […] It results in pruritic wheals with or without angioedema secondary to the release of leukotrienes, histamine and pro-inflammatory mast cell mediators after exposure of the skin to cold air, liquid or cold objects. […] Cold-induced urticaria is divided into primary and secondary forms and there have been many associations reported in the literature. Primary forms are defined when a secondary, or triggering, etiology cannot be determined. Secondary cold-induced urticaria has been reported to be associated with both bacterial and viral infections, medications, Hymenoptera stings, hematological malignancies and immunotherapy, largely based on various case reports. […] The most common cause of secondary acquired cold-induced urticaria is primary and secondary cryoglobulinemia based on case reports. Infectious diseases are the second most common type of secondary acquired cold-induced urticaria.

• #29 Cold urticaria and infectious mononucleosis in children | Allergologia et Immunopathologia

  https://www.elsevier.es/en-revista-allergologia-et-immunopathologia-105-articulo-cold-urticaria-infectious-mononucleosis-in-13069705

  Cold urticaria, first described by Bourdon in 1866, is characterised by the development of urticaria and/or angioedema after exposition to cold (aquatic activities, cold air, rain, snow, ingestion of cold food or drink or contact with cold objects). […] The mechanism, through which infectious mononucleosis triggers cold urticaria, is unknown. Cold cryoglobulins and agglutinins can appear during infectious mononucleosis and have been pointed as eventual causing factors. […] Secondary acquired cold urticaria is a rare form and it is diagnosed in presence of suggestive clinical history, positive cold stimulation test and evidence of a causal pathology. Malignancies, systemic leukocytoclastic vasculitis and infectious diseases, such as syphilis and infectious mononucleosis, have been implicated in the aetiology of cold urticaria.

• #30 Cold urticaria and infectious mononucleosis in children | Allergologia et Immunopathologia

  https://www.elsevier.es/en-revista-allergologia-et-immunopathologia-105-articulo-cold-urticaria-infectious-mononucleosis-in-13069705

  Autoimmunity mechanisms could explain the association between Epstein-Barr virus, as well as other infectious agents, and the appearance of cold urticaria. […] The clinical diagnosis of cold urticaria was confirmed by the ice cube test, which was strongly positive, with induction of response after one minute of stimulus. […] Several studies indicate that severe systemic reaction (type III) occurs more frequently in patients with positive ice cube test for three minute or shorter stimuli, such as in the presented case. […] The presence of cold urticaria was confirmed by a positive response to the ice cube test: a 28 mm x 33 mm wheal appeared after application of cold stimulus (0 to 4 C) during 1 minute on the child’s forearm.

• #31

  https://link.springer.com/article/10.1007/s11882-024-01160-y

  Recent findings from the multicenter COLD-CE study show that patients with ColdA are more likely to experience cold-induced angioedema, oropharyngeal/laryngeal symptoms, and itchy earlobes compared to ColdU patients without systemic manifestations. […] ColdU is mostly acquired; however, rare hereditary autoinflammatory diseases that are interleukin-1 and factor XII mediated have been reported.

• #32 Cold urticaria – Wikipedia

  https://en.wikipedia.org/wiki/Cold_urticaria

  Cold urticaria is a disorder in which large red welts called hives (urticaria) form on the skin after exposure to a cold stimulus. […] The hives are a histamine reaction in response to cold stimuli, including a drastic drop in temperature, cold air, and cold water. […] Scientists from the USA National Institutes of Health have identified a genetic mutation in three unrelated families that causes a rare immune disorder characterized by excessive and impaired immune function: immune deficiency, autoimmunity, inflammatory skin disorders and cold-induced hives (cold urticaria). […] The mutation discovered occurs in a gene for phospholipase C-gamma2 (PLCG2), an enzyme involved in the activation of immune cells.

• #33 Cold urticaria – Wikipedia

  https://en.wikipedia.org/wiki/Cold_urticaria

  Cold urticaria is a disorder in which large red welts called hives (urticaria) form on the skin after exposure to a cold stimulus. […] The hives are a histamine reaction in response to cold stimuli, including a drastic drop in temperature, cold air, and cold water. […] Scientists from the USA National Institutes of Health have identified a genetic mutation in three unrelated families that causes a rare immune disorder characterized by excessive and impaired immune function: immune deficiency, autoimmunity, inflammatory skin disorders and cold-induced hives (cold urticaria). […] The mutation discovered occurs in a gene for phospholipase C-gamma2 (PLCG2), an enzyme involved in the activation of immune cells.

• #34 Acquired Cold Urticaria vs. Autoinflammatory Diseases, Genetic and Clinical Profile and Differential Diagnosis: Study of a Cohort of Patients in a Tertiary Reference Centre | HTML | Acta Dermato-Venereologica

  https://www.medicaljournals.se/acta/content/html/10.2340/00015555-3292

  Acquired cold urticaria (ACU) is characterized by the development of itchy wheals after cold exposure. […] In conclusion, ACU is not related to post-zygotic or germline pathogenic variants in the NLRP3, NLRP12, NLRC4 and PLCG2 genes. […] The pathophysiology of cold urticaria is yet to be fully elucidated, but the activation and degranulation of tissue-resident mast cells and circulating basophils with the subsequent release of inflammatory mediators have been shown to play key roles. […] The most supported hypothesis is that different autoantigens, the expression of which might be induced by the appropriate environmental triggers, bind to IgE on the surface of mast cells and basophils through the high-affinity IgE receptor (FcRI), resulting in the activation of these cells and the release of the inflammatory mediators.

• #35 Chronic urticaria: a focus on pathogenesis | F1000Research

  https://f1000research.com/articles/6-1095

  Quite recently, we were able to show that sera from patients with chronic urticaria induce significant activation of mast cells lacking the high-affinity IgE receptor, irrespective of the autoreactivity status or of the presence/absence of circulating autoantibodies. […] The pathogenesis of chronic urticaria is probably characterized by a multiplicity of mechanisms, including autoimmunity, auto-allergy, and coagulation, each of which may carry different weight in each patient.

• #36 Azthena logo with the word Azthena

  https://www.news-medical.net/news/20240716/Chronic-Urticaria-Addressing-unmet-needs-emerging-therapies-and-advances-in-personalized-treatment-approaches.aspx

  CIU’s pathogenesis remains unclear and is often linked to specific neoallergen production in the skin. Identifying relevant triggers is crucial for management but can be challenging. […] CSU is considered a type 2 chronic inflammatory disease, particularly in patients with T-helper 2 (Th2) (a subset of T-helper cells)-skewed cutaneous inflammation. Cytokines such as Interleukin (IL)-4, IL-5, IL-13, and IL-31 play significant roles in the disease’s pathogenesis. […] There is a critical need for disease-modifying treatments that address the underlying mechanisms of chronic urticaria. Such therapies should aim to induce long-term remission or cure after withdrawal.

• #37 Cold urticaria in tropics: A clinico-epidemiological study from North India – Indian Journal of Dermatology, Venereology and Leprology

  https://ijdvl.com/cold-urticaria-in-tropics-a-clinico-epidemiological-study-from-north-india/

  Cold urticaria (ColdU) is classified as a subtype of chronic inducible urticaria characterised by recurring pruritic wheals and/or angioedema upon exposure to cold stimuli. […] The pathogenesis of ColdU involves various mechanisms, including aberrant temperature sensing, autoimmunity, autoallergy, and neurogenic pathways. Exposure to cold may trigger the formation of autoantigens, leading to an IgE-mediated immune response and subsequent mast cell degranulation. […] ColdU can also give rise to severe complications, like respiratory distress, disorientation and even shock with some studies reporting rates of up to 20%. […] Management of ColdU involves measures to protect against cold exposure and the use of anti-histamines to alleviate symptoms. […] In conclusion, this retrospective study sheds light on the clinical characteristics, epidemiology, and treatment response of North Indian patients with ColdU. Further research with larger and diverse populations, prospective, and exploration of genetic and environmental factors is needed to deepen our understanding of this condition in tropical regions.

• #38

  https://link.springer.com/article/10.1007/s40521-024-00366-9

  Cold-induced anaphylaxis (ColdA) is a poorly understood form of anaphylaxis that occurs in patients with cold urticaria (ColdU). […] ColdA has been defined as acute cold-induced involvement of the skin and/or visible mucosal tissue accompanied by cardiovascular manifestations, difficulty breathing, or gastrointestinal symptoms, but a universally accepted definition is lacking. […] The pathophysiology of ColdA remains largely unexplored. […] We hypothesize that ColdA also predominantly involves MC and basophil activation. […] A study by Juhlin and Shelley in 1961 revealed histamine release in two patients with ColdA, with distinctive cytologic changes in tissue MCs and blood basophils. […] The hypothesis that cold exposure may trigger the formation of de novo autoallergens and subsequent IgE-mediated responses diverges from traditional views of anaphylaxis but could be crucial in understanding ColdA. […] TRPM8 (transient receptor potential cation channel subfamily M [melastatin] member 8) proteins, which form Ca2+-conducting cation channels activated by menthol or cold, have also been proposed as mediators of MC activation in ColdU.

• #39 Azthena logo with the word Azthena

  https://www.news-medical.net/news/20240716/Chronic-Urticaria-Addressing-unmet-needs-emerging-therapies-and-advances-in-personalized-treatment-approaches.aspx

  CIU’s pathogenesis remains unclear and is often linked to specific neoallergen production in the skin. Identifying relevant triggers is crucial for management but can be challenging. […] CSU is considered a type 2 chronic inflammatory disease, particularly in patients with T-helper 2 (Th2) (a subset of T-helper cells)-skewed cutaneous inflammation. Cytokines such as Interleukin (IL)-4, IL-5, IL-13, and IL-31 play significant roles in the disease’s pathogenesis. […] There is a critical need for disease-modifying treatments that address the underlying mechanisms of chronic urticaria. Such therapies should aim to induce long-term remission or cure after withdrawal.

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