Urticaria, commonly known as hives, is characterized by the development of wheals (raised, itchy bumps on the skin) and angioedema (swelling of deeper layers of skin). It can be classified as acute (lasting less than 6 weeks) or chronic (lasting more than 6 weeks). Chronic urticaria is further classified as chronic spontaneous urticaria or chronic inducible urticaria. Chronic inducible urticaria includes physical urticarias that are triggered by specific stimuli like pressure, cold exposure, vibration, etc. Mast cells play a key role in the pathogenesis of urticaria by releasing histamine and other inflammatory mediators upon activation. Autoimmune mechanisms and coagulation
Cutaneous lupus erythematosus (CLE) is a manifestation of the autoimmune disease systemic lupus erythematosus (SLE) that presents with diverse skin lesions. There are three main subtypes of CLE - acute (ACLE), subacute (SCLE), and chronic (CCLE, including discoid lupus erythematosus (DLE)). CLE results from a complex interplay between genetic susceptibility, environmental triggers like ultraviolet light, and dysregulated immune responses. Histopathology is useful but not definitive for diagnosis, which relies on clinical presentation and serological markers. CLE can range from limited skin involvement to systemic disease affecting major organs.
This document summarizes the mechanisms of atopic dermatitis (AD). It discusses the epidemiology of AD and notes that it commonly affects children under 5 years old. The pathophysiology involves genetic, environmental, immunological, and epidermal factors. Key aspects of the pathophysiology discussed include the role of skin barrier dysfunction and genes involved in barrier function like filaggrin. It also examines the role of the immune system in AD, focusing on the predominance of TH2 cytokines and immune cells like dendritic cells, T lymphocytes, mast cells, and eosinophils that perpetuate the inflammatory response in AD.
Steven-Johnson syndrome (SJS) is a severe skin reaction characterized by lesions and mucous membrane erosions. It is caused by an immune reaction, often to drugs. The symptoms include fever and pain followed by spreading rashes, blisters and sores in the mouth, eyes and genitals. SJS is diagnosed based on its symptoms and skin biopsy. Treatment focuses on supportive care, stopping the triggering drug, and preventing infections. With prompt treatment the prognosis is usually good, but it can be life-threatening in severe cases with extensive blistering over large body areas.
Atopic dermatitis is a chronic inflammatory skin disease associated with respiratory allergies. It is characterized by recurrent eczematous lesions and intense itch. Genetic factors like filaggrin mutations cause skin barrier defects allowing allergens and microbes to trigger immune responses. The disease involves type 2 immunity cytokines activating neurons to produce itch. Staphylococcus aureus colonization exacerbates inflammation. Clinical features include erythematous patches and plaques with lichenification in chronic cases.
This document provides information on urticaria (hives), including definitions, epidemiology, pathogenesis, classification, and specific types. Some key points:
- Wheals are central swellings surrounded by erythema that itch or burn and resolve within 24 hours. Angioedema causes swelling below the skin that takes longer to resolve.
- Urticaria prevalence is 15-25% lifetime and chronic urticaria affects 1% annually, more common in adults and women.
- Pathogenesis involves skin mast cell degranulation in response to triggers like allergens, autoantibodies, neuropeptides.
- Classification includes acute (<6 weeks), chronic (>6 weeks),
This document discusses atopic dermatitis (AD), also known as eczema. Some key points:
1. AD is a chronic, relapsing inflammatory skin disease that is most common in childhood. It affects 15-20% of children in industrialized nations.
2. Symptoms vary by age but commonly include itchy, red, scaly skin rashes. Lesions typically affect the face, neck, hands and skin folds.
3. AD results from a complex interaction between genetic and environmental factors. Triggers include wool, harsh soaps and emotional stress. Treatment focuses on reducing triggers and includes emollients, topical steroids and antihistamines.
Urticaria, commonly known as hives, is characterized by the development of wheals (raised, itchy bumps on the skin) and angioedema (swelling of deeper layers of skin). It can be classified as acute (lasting less than 6 weeks) or chronic (lasting more than 6 weeks). Chronic urticaria is further classified as chronic spontaneous urticaria or chronic inducible urticaria. Chronic inducible urticaria includes physical urticarias that are triggered by specific stimuli like pressure, cold exposure, vibration, etc. Mast cells play a key role in the pathogenesis of urticaria by releasing histamine and other inflammatory mediators upon activation. Autoimmune mechanisms and coagulation
Cutaneous lupus erythematosus (CLE) is a manifestation of the autoimmune disease systemic lupus erythematosus (SLE) that presents with diverse skin lesions. There are three main subtypes of CLE - acute (ACLE), subacute (SCLE), and chronic (CCLE, including discoid lupus erythematosus (DLE)). CLE results from a complex interplay between genetic susceptibility, environmental triggers like ultraviolet light, and dysregulated immune responses. Histopathology is useful but not definitive for diagnosis, which relies on clinical presentation and serological markers. CLE can range from limited skin involvement to systemic disease affecting major organs.
This document summarizes the mechanisms of atopic dermatitis (AD). It discusses the epidemiology of AD and notes that it commonly affects children under 5 years old. The pathophysiology involves genetic, environmental, immunological, and epidermal factors. Key aspects of the pathophysiology discussed include the role of skin barrier dysfunction and genes involved in barrier function like filaggrin. It also examines the role of the immune system in AD, focusing on the predominance of TH2 cytokines and immune cells like dendritic cells, T lymphocytes, mast cells, and eosinophils that perpetuate the inflammatory response in AD.
Steven-Johnson syndrome (SJS) is a severe skin reaction characterized by lesions and mucous membrane erosions. It is caused by an immune reaction, often to drugs. The symptoms include fever and pain followed by spreading rashes, blisters and sores in the mouth, eyes and genitals. SJS is diagnosed based on its symptoms and skin biopsy. Treatment focuses on supportive care, stopping the triggering drug, and preventing infections. With prompt treatment the prognosis is usually good, but it can be life-threatening in severe cases with extensive blistering over large body areas.
Atopic dermatitis is a chronic inflammatory skin disease associated with respiratory allergies. It is characterized by recurrent eczematous lesions and intense itch. Genetic factors like filaggrin mutations cause skin barrier defects allowing allergens and microbes to trigger immune responses. The disease involves type 2 immunity cytokines activating neurons to produce itch. Staphylococcus aureus colonization exacerbates inflammation. Clinical features include erythematous patches and plaques with lichenification in chronic cases.
This document provides information on urticaria (hives), including definitions, epidemiology, pathogenesis, classification, and specific types. Some key points:
- Wheals are central swellings surrounded by erythema that itch or burn and resolve within 24 hours. Angioedema causes swelling below the skin that takes longer to resolve.
- Urticaria prevalence is 15-25% lifetime and chronic urticaria affects 1% annually, more common in adults and women.
- Pathogenesis involves skin mast cell degranulation in response to triggers like allergens, autoantibodies, neuropeptides.
- Classification includes acute (<6 weeks), chronic (>6 weeks),
This document discusses atopic dermatitis (AD), also known as eczema. Some key points:
1. AD is a chronic, relapsing inflammatory skin disease that is most common in childhood. It affects 15-20% of children in industrialized nations.
2. Symptoms vary by age but commonly include itchy, red, scaly skin rashes. Lesions typically affect the face, neck, hands and skin folds.
3. AD results from a complex interaction between genetic and environmental factors. Triggers include wool, harsh soaps and emotional stress. Treatment focuses on reducing triggers and includes emollients, topical steroids and antihistamines.
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by dry, itchy skin lesions. It is associated with elevated IgE levels and a family history of atopic diseases. The causes involve genetic susceptibility and environmental triggers that disrupt the skin barrier and promote a TH2-mediated immune response. Treatment focuses on identifying and avoiding triggers while improving the skin barrier with emollients and controlling inflammation with topical corticosteroids and calcineurin inhibitors. New targeted therapies that block cytokines and immune cells involved in AD pathogenesis are under investigation.
1. Atopic dermatitis is the most common type of dermatitis, which is a chronic, pruritic inflammatory skin disease that varies in severity. It primarily causes intense itching.
2. The pathogenesis is multifactorial involving genetic predisposition, skin barrier dysfunction, and immune abnormalities.
3. Treatment focuses on managing flares with topical corticosteroids and infections, while remission involves long-term emollient use and trigger avoidance.
Allergic rhinitis is a hypersensitivity reaction of the nasal mucosa to allergens like pollen or dust mites. It causes sneezing, runny nose, nasal itching and congestion. Diagnosis involves assessing symptoms and examining the nose for swelling and discharge. Skin or blood tests can identify allergens. Treatment includes allergen avoidance, oral antihistamines like cetirizine or leukotriene inhibitors like montelukast, intranasal steroids, and immunotherapy for long term management.
This document discusses updates in the management of chronic urticaria. It begins with definitions of acute and chronic urticaria, noting that chronic urticaria is defined as symptoms lasting more than 6 weeks. It then discusses the classification of urticaria as either spontaneous or inducible. Mast cell activation and degranulation are identified as the key pathological mechanisms involved in urticaria symptoms. Autoimmune processes involving immunoglobulins such as IgG and IgE autoantibodies are also discussed as potential pathological factors in chronic urticaria. Guidelines for the treatment of urticaria have been updated.
This document provides an overview of chronic spontaneous urticaria (CSU), including its epidemiology, pathophysiology, clinical presentation, investigations, and management. It discusses the diagnosis and classification of urticaria and focuses on the diagnosis and investigation of CSU. Routine diagnostic measures for CSU include CBC, ESR or CRP, and eliminating possible causes such as medications or foods. Extended diagnostic testing may include allergy testing, infections screening, autoantibody testing such as the autologous serum skin test, and screening for underlying conditions. The gold standard treatment for CSU is non-sedating H1 antihistamines as monotherapy or in increased doses. Refractory cases may require the addition
1) The document outlines an overview of chronic spontaneous urticaria (CSU), including its epidemiology, clinical presentation, natural history, and pathogenesis.
2) CSU affects approximately 0.5-1% of the general population and is more common in adults than children, with a peak age of onset between 20-40 years.
3) The pathogenesis of CSU is not fully understood but is believed to involve inappropriate activation of mast cells and basophils by autoantibodies, leading to the release of inflammatory mediators that cause wheals and angioedema.
This document provides information on atopic dermatitis (AD), including its definition, epidemiology, pathophysiology, clinical manifestations, and treatment. Some key points:
1. AD is a chronic inflammatory skin disease associated with other atopic disorders like asthma. It is characterized by dry skin and sensitization to allergens.
2. The prevalence of AD has increased in recent decades, commonly starting early in life. Genetic factors like mutations in the filaggrin gene contribute to impaired skin barrier function which increases allergen sensitization risk.
3. Clinical features include severe pruritus, chronic relapsing course, and characteristic rash typically located in flexural areas. Complications can include
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Hyper-IgE Syndrome, also known as Job's syndrome or Buckley's syndrome, is a rare primary immunodeficiency disorder characterized by elevated serum immunoglobulin E (IgE) levels, eczema, recurrent skin and lung infections, and a distinctive facial appearance. There are both autosomal dominant and recessive forms. The autosomal dominant form is caused by mutations in the STAT3 gene and is characterized by clinical features including newborn rash, boils, pneumonia, pneumatoceles, and elevated IgE levels above 2000 IU/mL. Patients often have a characteristic facial appearance, dental abnormalities, fractures from minimal trauma, and brain and vascular abnormalities. The disorder results from defects in the JAK
Chronic spontaneous urticaria (CSU) is characterized by the development of hives and angioedema for more than 6 weeks without triggering factors. It affects 1% of the population. CSU is diagnosed through patient history and physical exam. Treatment involves high dose antihistamines as first line, with omalizumab recommended for severe cases. Management aims to control symptoms and improve quality of life through a treatment plan evaluated every 3-6 months.
1) The patient, a 45-year-old female, presented with multiple fluid-filled itchy lesions over her limbs and face for the past week and developed oral lesions 3 days after admission.
2) A clinical diagnosis of bullous pemphigoid was made based on tense fluid-filled cutaneous lesions, involvement of oral mucosa, histopathology showing subepidermal blistering, and direct immunofluorescence demonstrating linear deposition of IgG and C3 along the basement membrane zone.
3) The patient was treated with systemic corticosteroids and immunosuppressants along with topical corticosteroids for oral lesions and advised long-term follow-up to manage the chronic autoimmune condition.
Hereditary angioedema (HAE) is a rare disease caused by C1 inhibitor deficiency and characterized by recurrent episodes of non-pruritic swelling in the skin, gastrointestinal tract, and airways. The disease has an autosomal dominant pattern of inheritance and is caused by mutations in the C1 inhibitor gene. Diagnosis involves evaluating family history, symptoms of recurrent non-pitting edema, and laboratory tests showing low C4 and C1 inhibitor levels. Proper diagnosis is important to distinguish it from other causes of angioedema and manage attacks.
Chronic urticaria lasts longer than 6 weeks and presents as recurrent hives and angioedema occurring more than 3 days a week. It can be classified as inducible or spontaneous. Inducible types are triggered by specific physical stimuli like pressure, cold, heat, or vibration. Chronic urticaria is considered after ruling out look-alike conditions such as urticarial vasculitis and other autoinflammatory syndromes. Its evaluation involves considering potential systemic triggers or underlying causes.
Dr Muhammad Raza's presentation provides information about atopic dermatitis (eczema), including its signs and symptoms, causes, diagnosis, and management. The key points are that it is a chronic skin condition causing red, itchy, cracked skin that is common in children; has genetic and immunological factors; and is typically diagnosed clinically and managed through moisturizers, topical steroids, and other topical or systemic treatments depending on severity. The goal is for participants to understand the basic concepts, diagnosis, management, and appropriate referrals for atopic dermatitis.
Psoriasis is a chronic, inflammatory skin condition that causes red scaly patches to appear on the skin. The most common form is plaque psoriasis, which accounts for 80-90% of cases, appearing as raised, red patches covered with silvery scales. Psoriasis occurs when skin cells multiply up to 10 times faster than normal. It is believed to be both a disorder of skin cell growth and an immune-mediated disease driven by T cells and cytokines. Psoriasis has no cure but can be managed with topical treatments and phototherapy. It affects the joints in 10-20% of cases (psoriatic arthritis).
Atopic dermatitis is a common inflammatory skin condition characterized by itchy, red lesions. It has a complex pathogenesis involving skin barrier dysfunction, immune dysregulation with Type 2 inflammation, and microbial dysbiosis. Genetic factors like filaggrin mutations contribute to impaired skin barrier function. Colonization by Staphylococcus aureus and Malassezia yeasts further damages the skin and promotes inflammation. Pruritus (itching) activates scratch responses that sustain the condition through additional skin damage and inflammation. Treatment involves managing symptoms, restoring skin barrier function, and controlling inflammation and infection.
Atopic dermatitis (eczema) is a condition that makes your skin red and itchy. It's common in children but can occur at any age. Atopic dermatitis is long lasting (chronic) and tends to flare periodically. It may be accompanied by asthma or hay fever.
This document provides an overview of physical urticarias. It defines physical urticarias as urticarias induced by physical stimuli like pressure, vibration, heat, cold, etc. It describes several types of physical urticarias in detail, including dermographism (pressure urticaria), delayed pressure urticaria, and vibratory angioedema. For each type, it covers epidemiology, clinical features, pathogenesis, diagnostic testing, and treatment approaches. The document is a comprehensive review and classification of physical urticaria subtypes.
This document provides an overview of various branches of medicine, including their definitions and focuses. It lists over 30 medical specialties ranging from Allergology to Urology. The specialties cover areas like internal organs, bodily systems, surgical procedures, and more. The document serves as a comprehensive reference for the different fields within the broader domain of medicine.
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by dry, itchy skin lesions. It is associated with elevated IgE levels and a family history of atopic diseases. The causes involve genetic susceptibility and environmental triggers that disrupt the skin barrier and promote a TH2-mediated immune response. Treatment focuses on identifying and avoiding triggers while improving the skin barrier with emollients and controlling inflammation with topical corticosteroids and calcineurin inhibitors. New targeted therapies that block cytokines and immune cells involved in AD pathogenesis are under investigation.
1. Atopic dermatitis is the most common type of dermatitis, which is a chronic, pruritic inflammatory skin disease that varies in severity. It primarily causes intense itching.
2. The pathogenesis is multifactorial involving genetic predisposition, skin barrier dysfunction, and immune abnormalities.
3. Treatment focuses on managing flares with topical corticosteroids and infections, while remission involves long-term emollient use and trigger avoidance.
Allergic rhinitis is a hypersensitivity reaction of the nasal mucosa to allergens like pollen or dust mites. It causes sneezing, runny nose, nasal itching and congestion. Diagnosis involves assessing symptoms and examining the nose for swelling and discharge. Skin or blood tests can identify allergens. Treatment includes allergen avoidance, oral antihistamines like cetirizine or leukotriene inhibitors like montelukast, intranasal steroids, and immunotherapy for long term management.
This document discusses updates in the management of chronic urticaria. It begins with definitions of acute and chronic urticaria, noting that chronic urticaria is defined as symptoms lasting more than 6 weeks. It then discusses the classification of urticaria as either spontaneous or inducible. Mast cell activation and degranulation are identified as the key pathological mechanisms involved in urticaria symptoms. Autoimmune processes involving immunoglobulins such as IgG and IgE autoantibodies are also discussed as potential pathological factors in chronic urticaria. Guidelines for the treatment of urticaria have been updated.
This document provides an overview of chronic spontaneous urticaria (CSU), including its epidemiology, pathophysiology, clinical presentation, investigations, and management. It discusses the diagnosis and classification of urticaria and focuses on the diagnosis and investigation of CSU. Routine diagnostic measures for CSU include CBC, ESR or CRP, and eliminating possible causes such as medications or foods. Extended diagnostic testing may include allergy testing, infections screening, autoantibody testing such as the autologous serum skin test, and screening for underlying conditions. The gold standard treatment for CSU is non-sedating H1 antihistamines as monotherapy or in increased doses. Refractory cases may require the addition
1) The document outlines an overview of chronic spontaneous urticaria (CSU), including its epidemiology, clinical presentation, natural history, and pathogenesis.
2) CSU affects approximately 0.5-1% of the general population and is more common in adults than children, with a peak age of onset between 20-40 years.
3) The pathogenesis of CSU is not fully understood but is believed to involve inappropriate activation of mast cells and basophils by autoantibodies, leading to the release of inflammatory mediators that cause wheals and angioedema.
This document provides information on atopic dermatitis (AD), including its definition, epidemiology, pathophysiology, clinical manifestations, and treatment. Some key points:
1. AD is a chronic inflammatory skin disease associated with other atopic disorders like asthma. It is characterized by dry skin and sensitization to allergens.
2. The prevalence of AD has increased in recent decades, commonly starting early in life. Genetic factors like mutations in the filaggrin gene contribute to impaired skin barrier function which increases allergen sensitization risk.
3. Clinical features include severe pruritus, chronic relapsing course, and characteristic rash typically located in flexural areas. Complications can include
Searching for Psoriasis Natural Treatment. Peep In to get the best and natural psoriasis remedies that work. Here care my best home remedies for psoriasis that works best. take use of every natural psoriasis remedy you get.
Tags:
"psoriasis natural treatment"
"natural psoriasis treatment"
"Natural Psoriasis Remedies"
"psoriasis natural treatment scalp"
"psoriasis natural treatment options"
"psoriasis natural treatment diet"
"psoriasis natural treatments home remedies"
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Hyper-IgE Syndrome, also known as Job's syndrome or Buckley's syndrome, is a rare primary immunodeficiency disorder characterized by elevated serum immunoglobulin E (IgE) levels, eczema, recurrent skin and lung infections, and a distinctive facial appearance. There are both autosomal dominant and recessive forms. The autosomal dominant form is caused by mutations in the STAT3 gene and is characterized by clinical features including newborn rash, boils, pneumonia, pneumatoceles, and elevated IgE levels above 2000 IU/mL. Patients often have a characteristic facial appearance, dental abnormalities, fractures from minimal trauma, and brain and vascular abnormalities. The disorder results from defects in the JAK
Chronic spontaneous urticaria (CSU) is characterized by the development of hives and angioedema for more than 6 weeks without triggering factors. It affects 1% of the population. CSU is diagnosed through patient history and physical exam. Treatment involves high dose antihistamines as first line, with omalizumab recommended for severe cases. Management aims to control symptoms and improve quality of life through a treatment plan evaluated every 3-6 months.
1) The patient, a 45-year-old female, presented with multiple fluid-filled itchy lesions over her limbs and face for the past week and developed oral lesions 3 days after admission.
2) A clinical diagnosis of bullous pemphigoid was made based on tense fluid-filled cutaneous lesions, involvement of oral mucosa, histopathology showing subepidermal blistering, and direct immunofluorescence demonstrating linear deposition of IgG and C3 along the basement membrane zone.
3) The patient was treated with systemic corticosteroids and immunosuppressants along with topical corticosteroids for oral lesions and advised long-term follow-up to manage the chronic autoimmune condition.
Hereditary angioedema (HAE) is a rare disease caused by C1 inhibitor deficiency and characterized by recurrent episodes of non-pruritic swelling in the skin, gastrointestinal tract, and airways. The disease has an autosomal dominant pattern of inheritance and is caused by mutations in the C1 inhibitor gene. Diagnosis involves evaluating family history, symptoms of recurrent non-pitting edema, and laboratory tests showing low C4 and C1 inhibitor levels. Proper diagnosis is important to distinguish it from other causes of angioedema and manage attacks.
Chronic urticaria lasts longer than 6 weeks and presents as recurrent hives and angioedema occurring more than 3 days a week. It can be classified as inducible or spontaneous. Inducible types are triggered by specific physical stimuli like pressure, cold, heat, or vibration. Chronic urticaria is considered after ruling out look-alike conditions such as urticarial vasculitis and other autoinflammatory syndromes. Its evaluation involves considering potential systemic triggers or underlying causes.
Dr Muhammad Raza's presentation provides information about atopic dermatitis (eczema), including its signs and symptoms, causes, diagnosis, and management. The key points are that it is a chronic skin condition causing red, itchy, cracked skin that is common in children; has genetic and immunological factors; and is typically diagnosed clinically and managed through moisturizers, topical steroids, and other topical or systemic treatments depending on severity. The goal is for participants to understand the basic concepts, diagnosis, management, and appropriate referrals for atopic dermatitis.
Psoriasis is a chronic, inflammatory skin condition that causes red scaly patches to appear on the skin. The most common form is plaque psoriasis, which accounts for 80-90% of cases, appearing as raised, red patches covered with silvery scales. Psoriasis occurs when skin cells multiply up to 10 times faster than normal. It is believed to be both a disorder of skin cell growth and an immune-mediated disease driven by T cells and cytokines. Psoriasis has no cure but can be managed with topical treatments and phototherapy. It affects the joints in 10-20% of cases (psoriatic arthritis).
Atopic dermatitis is a common inflammatory skin condition characterized by itchy, red lesions. It has a complex pathogenesis involving skin barrier dysfunction, immune dysregulation with Type 2 inflammation, and microbial dysbiosis. Genetic factors like filaggrin mutations contribute to impaired skin barrier function. Colonization by Staphylococcus aureus and Malassezia yeasts further damages the skin and promotes inflammation. Pruritus (itching) activates scratch responses that sustain the condition through additional skin damage and inflammation. Treatment involves managing symptoms, restoring skin barrier function, and controlling inflammation and infection.
Atopic dermatitis (eczema) is a condition that makes your skin red and itchy. It's common in children but can occur at any age. Atopic dermatitis is long lasting (chronic) and tends to flare periodically. It may be accompanied by asthma or hay fever.
This document provides an overview of physical urticarias. It defines physical urticarias as urticarias induced by physical stimuli like pressure, vibration, heat, cold, etc. It describes several types of physical urticarias in detail, including dermographism (pressure urticaria), delayed pressure urticaria, and vibratory angioedema. For each type, it covers epidemiology, clinical features, pathogenesis, diagnostic testing, and treatment approaches. The document is a comprehensive review and classification of physical urticaria subtypes.
This document provides an overview of various branches of medicine, including their definitions and focuses. It lists over 30 medical specialties ranging from Allergology to Urology. The specialties cover areas like internal organs, bodily systems, surgical procedures, and more. The document serves as a comprehensive reference for the different fields within the broader domain of medicine.
Urticaria, commonly known as hives, is a skin rash with pale red, itchy bumps that appear and disappear quickly. It is characterized by transient wheals (swellings) and angioedema (swelling of deeper layers of skin). Urticaria can be caused by allergic reactions, infections, physical stimuli like heat, cold, pressure, or vibrations. It is classified as acute, chronic, physical or contact urticaria. Treatment involves identifying and avoiding triggers, and using antihistamines.
The document provides information about allergy diagnostics and testing. It discusses the different types of allergies including food, environmental, occupational and insect allergies. It describes the importance of taking a thorough case history and outlines different diagnostic methods used to identify allergens including skin prick tests, patch tests and allergen-specific IgE blood tests. Accurately identifying the specific allergens responsible for a patient's symptoms is key to successful management and treatment of their condition.
Guidelines for treatment of atopic eczemaLina Nuñez
Este documento presenta las guías para el tratamiento de la dermatitis atópica. Resume las recomendaciones para el diagnóstico, prevención y tratamiento de la enfermedad, incluyendo terapia emoliente, tratamiento tópico con corticosteroides e inhibidores de la calcineurina, y terapias antipruriginosas y antimicrobianas.
This document discusses various anthelmintic drugs used to treat helminth infections. It describes the classes of anthelmintics including benzimidazoles (e.g. mebendazole), imidazothiazoles (e.g. thiabendazole), avermectins (e.g. ivermectin), and praziquantel. It outlines their mechanisms of action, side effects, and uses in treating specific helminth infections like ascariasis, hookworm, and echinococcosis.
The document discusses urticaria (hives), including its definition, classification as acute or chronic, pathophysiology involving histamine release from mast cells, causes such as allergies, infections, and physical stimuli, associated conditions like angioedema, evaluation through patient history and physical exam, and treatment focusing on identification and avoidance of triggers as well as antihistamines.
Urticaria, also known as hives or wheals, is a common skin disorder that presents as raised, itchy bumps on the skin. It affects approximately one-fifth of the population at some point and can be acute (lasting less than 6 weeks) or chronic (lasting more than 6 weeks). Urticaria should be managed emergently as it can progress to life-threatening swelling and has many potential causes including drugs, foods, insect stings, and autoimmune diseases.
Night-time sedating H 1 -antihistamine increases daytime somnolence but not t...Georgi Daskalov
Night-time sedating H
1
-antihistamine increases daytime
somnolence but not treatment efficacy in chronic
spontaneous urticaria: a randomized controlled trial
The document discusses atopic dermatitis (AD), also known as eczema. It defines AD as a pruritic, chronic inflammatory skin condition characterized by dry skin and itchy rashes. AD is common in childhood and often runs in families with other allergic diseases. The pathogenesis involves genetic predisposition, skin barrier defects, and abnormal immune responses. Clinical manifestations vary depending on the stage of life, from facial rashes in infants to thickened plaques on flexural areas in older patients. Treatment focuses on moisturizing the skin, identifying trigger factors, and using topical corticosteroids or calcineurin inhibitors to control symptoms.
The document describes several studies related to chronic urticaria and solar urticaria. It summarizes:
1. A study that found increasing doses of levocetirizine and desloratadine up to 4 times the conventional dose improved symptoms in patients with difficult-to-treat chronic urticaria.
2. The case of a 16-year-old boy with solar urticaria that was refractory to oral antihistamines but partially improved with omalizumab treatment.
3. A study that treated 6 patients with severe chronic spontaneous urticaria resistant to other treatments with high-dose intravenous immunoglobulin, which improved symptoms.
Urticaria is characterized by WEALS (hives) or ANGIOEDEMA (swellings, in 10%) or both (in 40%). There are several types of urticaria
Spontaneous urticaria
Acute spontaneous urticaria Spontaneous wheals and/or angioedema <6 />6 wk
Urticarias induced by physical agents
dermographic urticaria Eliciting factor: mechanical shearing forces (wheals arising after 1–5 min)
Cold contact urticaria Eliciting factor: cold objects/air/fluids/wind
Solar urticaria Eliciting factor: UV and/or visible light
Delayed pressure urticaria Eliciting factor: vertical pressure (wheals arising with a 3–12 h latency)
Heat contact urticaria Eliciting factor: localized heat Hot water bottle Hot drink
Vibratory urticaria/angioedema Eliciting factor: vibratory forces, e.g. pneumatic hammer/Jack hammer
Other inducible urticarias
Contact urticaria Elicitation by contact with urticariogenic substance
Aquagenic urticaria Eliciting factor: water
Cholinergic urticaria Elicitation by increase of body core temperature due to physical exercises, spicy food, stress
Exercise-induced anaphylaxis/urticaria Eliciting factor: physical exercise
This document summarizes information on chronic urticaria, including its prevalence, causes, impact on quality of life, and treatment options. It notes that chronic urticaria affects approximately 1% of people with acute urticaria and has a significant negative impact on quality of life. First-line treatment includes non-sedating antihistamines, sometimes at higher off-label doses. If patients do not respond sufficiently to antihistamines alone, second-line options include doxepin, leukotriene antagonists, short-term corticosteroids, dapsone, sulfasalazine, and narrowband UVB phototherapy. The document reviews evidence on the efficacy and safety of these second-
Topic urticaria, angioedema and anaphylaxis finalBow Aya
This is a case of a 12-year-old Thai boy who developed lip swelling, rash and itching 5 minutes after receiving an intravenous injection of ceftriaxone for diarrhea. He has a history of rash after taking an antibiotic for a sore throat 1 year ago. The symptoms suggest he may have experienced anaphylaxis reaction to the antibiotic injection. Further evaluation and management are needed to confirm the diagnosis and treat the reaction.
The document discusses several intestinal protozoa and helminths including Ascaris lumbricoides, hookworms, Entamoeba histolytica, Giardia lamblia, and Cryptosporidium. It describes the morphology, life cycles, transmission routes, clinical manifestations, diagnosis, and treatment of each parasite. Prevention focuses on proper sanitation, hygiene practices like handwashing, water treatment, and health education.
- A 70 year old male presented with 10 years of dyspnea and white productive sputum without fever or other URI symptoms. Skin tests were positive for allergens.
- He has been prescribed several inhalers but was referred to determine if he has COPD or asthma.
- The document discusses the differences and similarities between the inflammation seen in COPD versus asthma. COPD typically involves neutrophilic inflammation in small airways and parenchyma while asthma usually shows eosinophilic inflammation, but there can be overlap between the conditions.
This document provides information on substance-related disorders including substance abuse, dependence, withdrawal, and intoxication. It defines substance abuse and dependence based on DSM-IV criteria. It describes the epidemiology, categories, and effects of commonly abused substances like stimulants, depressants, opiates, hallucinogens, inhalants, and caffeine. For each substance or class, it summarizes intoxication, withdrawal, treatment approaches, and diagnostic evaluation.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by autoantibodies directed against self-antigens. It can affect many different organs and tissues in the body. Kelsey, a 23-year-old woman, presented with fatigue, joint pain, and a rash. Laboratory tests showed positive ANA, anti-DNA, low complement levels, meeting criteria for SLE. SLE results from genetic and environmental factors interacting to cause immune system dysregulation and loss of self-tolerance. It commonly affects the skin, joints, kidneys, and cardiovascular and pulmonary systems. Timely diagnosis and treatment can help prevent organ damage and disease complications.
The study evaluated 195 patients with chronic idiopathic urticaria to determine the correlation between biomarkers of autoimmunity like ANA, ATA, and disease severity. It found that 46% of refractory patients tested positive for the CU Index compared to 30% of controlled patients. Combinations of biomarkers had slightly better sensitivity and negative predictive value than individual biomarkers for identifying refractory cases. The CU Index alone had the best specificity and positive predictive value.
Pearls in Allergy and Immunology, January 2014Juan Aldave
The purpose of this educational material is to provide updated knowledge for Allergy/Immunology Physicians. It summarizes recent articles from peer-reviewed journals. If there are any corrections needed, they should be sent directly to the authors by email.
The document summarizes several articles from recent issues of peer-reviewed journals, including:
1) A case report of anaphylaxis induced by streptomycin skin testing, highlighting the risks of systemic reactions from skin testing.
2) An overview of aspirin-exacerbated respiratory disease and approaches to aspirin desensitization, which can effectively improve asthma and sinusitis outcomes.
3) A discussion of the low adherence rates to asthma
The document summarizes guidelines from the British Society for Antimicrobial Chemotherapy (BSAC) on the treatment of infective endocarditis. It compares the 2004 guidelines, which were mostly based on expert opinion, to the 2012 guidelines which are now mostly evidence-based. The 2012 guidelines include recommendations for treatment of native valve endocarditis and prosthetic valve endocarditis. It also discusses evaluation, investigation, treatment considerations, and presentations of infective endocarditis. Monitoring of aminoglycoside and vancomycin levels is recommended due to their narrow therapeutic index and potential toxicity. Factors like penicillin allergy history and appropriate antibiotic substitutions are also covered.
Here are some key points in the differential diagnosis based on the information provided:
- Sepsis (given fever, hypotension, leukocytosis)
- Pneumonia (given fever, leukocytosis, back pain on exam)
- Urosepsis (given fever, hypotension, leukocytosis)
- Endocarditis (given fever, hypotension, family history of "social drinking")
- Myocarditis/pericarditis (given fever, back pain)
- Drug-related toxicity (given multiple comorbidities and medications)
- Adrenal crisis (given multiple comorbidities)
Given the acute onset of fever and hypotension requiring intubation and vasopressors, sepsis
This document discusses nonallergic rhinitis, specifically vasomotor rhinitis. It defines vasomotor rhinitis as chronic nasal symptoms that are not due to allergies or infections. Vasomotor rhinitis accounts for at least two-thirds of nonallergic rhinitis cases. Symptoms are triggered by factors like cold air, odors, and alcohol. While the nasal mucosa shows no inflammation, the condition involves increased reactivity to irritants and sensory nerve dysregulation. Symptoms include nasal obstruction and rhinorrhea. Treatment focuses on reducing triggers and using nasal irrigation, decongestants, and antihistamines.
Hypereosinophilic Syndrome (HES) is a rare condition characterized by elevated levels of eosinophils in the blood (eosinophilia) and tissue damage caused by eosinophils. The document discusses the historical background, definition, pathogenesis, epidemiology, classification, and clinical manifestations of HES. It defines HES based on eosinophilia greater than 1500 cells/microliter for more than 6 months with evidence of organ damage after ruling out other causes. HES can be classified into myeloproliferative and lymphocytic forms based on the underlying pathogenesis. The myeloproliferative form involves mutations in hematopoietic cells that drive eosinophil production while the lymphocy
Olivieri ignazio malattia di whipple torino gennaio 2011_14° convegno patolo...cmid
This document discusses the musculoskeletal manifestations of Whipple's disease, a rare infectious disease caused by the bacterium Tropheryma whipplei. It details that arthralgia and arthritis are among the most common extra-intestinal symptoms and may precede gastrointestinal complaints by many years. While spondyloarthritis has been reported in some cases of Whipple's disease, it is not considered to be part of the spondyloarthritis complex.
The document provides information on clinical diagnosis of periodontal disease. It discusses the importance of diagnosis and outlines the categories of periodontal diseases. It also describes the clinical examination process, including extraoral and intraoral soft tissue exams, periodontal probing, radiographs, casts, and photographs. The goal of diagnosis is to determine the type, extent, and severity of periodontal disease.
Familial Mediterranean Fever is an autosomal recessive disease characterized by recurrent fevers and inflammation localized to the peritoneum, pleura, joints, or skin. It is most common in people of Mediterranean descent and is caused by mutations in the MEFV gene. Symptoms include abdominal pain, fever, arthritis, and erysipelas-like lesions. If left untreated, it can lead to amyloidosis. Treatment involves lifelong colchicine to prevent inflammatory episodes and reduce amyloidosis risk. Some patients may be resistant to colchicine and require alternative treatments like interleukin-1 or tumor necrosis factor inhibitors.
1) The document discusses perioperative anaphylaxis, including its pathophysiology, clinical manifestations, differential diagnosis, investigation, and important causes.
2) Perioperative anaphylaxis is a potentially life-threatening reaction that can occur during or after surgery and anesthesia. The most common triggers include antibiotics, neuromuscular blocking agents, and latex.
3) Diagnosis is based on the timing and symptoms of the reaction. Investigations like skin testing and serum tryptase measurements are recommended 1-4 months later to identify culprit agents and safe alternatives for future procedures. Prompt recognition and management are important to prevent severe outcomes.
The document discusses Coccidioidomycosis (Valley Fever), providing information on the causative fungi, epidemiology, transmission, clinical disease in humans and animals, diagnosis and treatment. It causes respiratory illness in humans and can disseminate throughout the body, while many infections in animals are subclinical but can become serious; diagnosis involves direct visualization, culture and serology of the dimorphic fungi from body fluids or tissues.
Anaphylaxis is a severe allergic reaction that is life-threatening. It involves two or more body systems and can cause low blood pressure, breathing difficulties, skin rash, and gastrointestinal issues. Common triggers include foods like peanuts, medications like antibiotics, and insect stings. Treatment involves epinephrine injection, oxygen, intravenous fluids, antihistamines, and steroids. Prevention focuses on avoidance of known allergens and always having epinephrine available for emergencies.
This document summarizes hyper IgE syndrome, a rare genetic disorder characterized by recurrent skin and lung infections and extremely high levels of IgE antibodies. It exists in two forms - autosomal dominant and autosomal recessive - caused by mutations in the STAT3, DOCK8, and TYK2 genes. The autosomal dominant form presents with eczema, lung infections, characteristic facial features, bone fractures, and serum IgE over 2000 IU/ml. The autosomal recessive forms, caused by DOCK8 and TYK2 mutations, present similarly but without bone or facial abnormalities. Diagnosis involves clinical features, genetic testing, and immunological abnormalities like low Th17 cells. Treatment focuses on long-
This document provides information on Behcet's syndrome and Sjogren's syndrome. It discusses the diagnostic criteria for Behcet's syndrome according to the 1990 International Study Group. It describes the common oral, skin, eye, neurological, and other manifestations of Behcet's syndrome. It also discusses the etiology, pathogenesis, epidemiology, and management of Sjogren's syndrome.
Celiac disease power point presentationdrbeenaMemon
Celiac disease is an immune-mediated enteropathy caused by a permanent sensitivity to gluten in genetically susceptible individuals. It can present with gastrointestinal and non-gastrointestinal symptoms, and some individuals are asymptomatic. The disease exists on a spectrum from symptomatic to silent to latent forms depending on the presence of symptoms and mucosal damage. Diagnosis requires serological testing followed by small intestinal biopsy showing damage. Treatment is a lifelong gluten-free diet, though adherence can be challenging. Left untreated, celiac disease can lead to complications.
NSAIDs hypersensitivity, in particular NERD (NSAIDs-exacerbated respiratory disease), can manifest as exacerbations of asthma and chronic rhinosinusitis symptoms after ingestion of NSAIDs. NERD is characterized by chronic eosinophilic inflammation of the upper and lower airways in patients with underlying asthma and/or rhinosinusitis with nasal polyps. Clinical features may include nasal congestion, wheezing, coughing, and shortness of breath within 30-180 minutes of NSAID intake. Diagnosis is typically made through an oral aspirin challenge demonstrating provocation of respiratory symptoms.
This document provides information on anaphylaxis, including its historical background, definitions, epidemiology, symptoms, causes, diagnosis, and treatment. It was discovered in 1902 by scientists attempting to immunize dogs to sea anemone venom. They unexpectedly sensitized the dogs, who reacted to a later nonlethal dose. Anaphylaxis is an immediate hypersensitivity reaction mediated by IgE or other non-IgE mechanisms, causing symptoms in multiple organ systems. Epinephrine is the first-line treatment and works through alpha and beta receptor agonism to reverse symptoms and prevent further mediator release.
Japanese encephalitis is a mosquito-borne viral disease that causes brain swelling. The virus was first isolated in Japan in the 1930s and spread to other parts of Asia. It is transmitted by Culex mosquitoes and affects pigs, birds, and humans. Common symptoms include fever, headache, vomiting and seizures. There is no treatment, so care is supportive. Prevention relies on vaccination programs and reducing mosquito habitats by eliminating standing water.
Similar to Chronic idiopathic urticaria part 2: investigation and management (20)
- Cat and dog allergens such as Fel d 1 and Can f 1 are major allergens found in fur, dander, and saliva that can become airborne and cause sensitization in a large percentage of allergic individuals.
- Lipocalins make up many mammalian allergens and show cross-reactivity between species due to structural similarities, explaining co-sensitizations between cats, dogs, horses, and other animals.
- Higher levels of IgE antibodies to specific dog lipocalins are associated with more severe asthma in children with dog allergy.
1) DRESS syndrome is a severe cutaneous drug reaction characterized by fever, lymphadenopathy, hematologic abnormalities, multisystem involvement, and viral reactivation. It has a delayed onset of 2-3 weeks after starting the culprit drug.
2) The skin manifestations are typically a polymorphous maculopapular eruption and facial edema. Systemic involvement can include the liver, kidneys, lungs and other organs.
3) Diagnosis is based on clinical criteria including the RegiSCAR scoring system which evaluates morphology, timing of onset, organ involvement, hematologic abnormalities and viral reactivation.
Wheat is one of the most important global food sources and wheat allergy prevalence varies from 0.4-4% depending on age and region. Several wheat proteins have been identified as major allergens, including omega-5-gliadin, alpha-amylase inhibitors, and glutenins. Studies have found that serum testing for IgE antibodies to specific wheat allergens, such as omega-5-gliadin, glutenins, and alpha-amylase inhibitors, can help diagnose wheat allergy and distinguish between mild and severe cases. Sensitization to different wheat allergens is associated with wheat-dependent exercise-induced anaphylaxis versus occupational baker's asthma. Proper diagnosis and
Major indoor allergens include dust mites, domestic animals like cats and dogs, insects like cockroaches, mice, and fungi. Dust mites thrive in warm, humid environments like mattresses, bedding, and upholstered furniture, where they feed on human skin scales and excrete allergenic fecal particles. Cat allergens like Fel d 1 accumulate in fur and can become airborne, causing worse asthma outcomes in sensitized individuals. Minimizing exposure involves removing carpets, frequent washing of bedding, humidity control, HEPA filtration and ventilation.
This document provides information on Hymenoptera, focusing on the families Apidae and Vespidae. It discusses the epidemiology and prevalence of insect venom allergy. It also covers the taxonomy, venom composition, and clinical manifestations of common stinging insects like honeybees, hornets, wasps and yellow jackets. Key allergens are identified for different species.
- NSAIDs hypersensitivity can present with distinct clinical phenotypes based on organ system involvement and timing of symptoms. It is estimated that less than 20% of reported adverse reactions to NSAIDs are true hypersensitivities.
- AERD/NERD involves eosinophilic rhinosinusitis, asthma, and nasal polyps. Exposure to aspirin or other NSAIDs exacerbates bronchospasms and rhinitis. Management involves lifelong avoidance of culprit and cross-reacting NSAIDs.
- Various phenotypes are described beyond the EAACI classification, including blended reactions involving multiple organs, food-dependent NSAID-induced anaphylaxis, and NSAID-selective immediate reactions. Proper diagnosis relies
The document discusses food immunotherapy for treating food allergies. It provides definitions and outlines immune mechanisms and efficacy evidence from studies on peanut, cow's milk, egg, and wheat oral immunotherapy (OIT). Peanut OIT studies showed 67-78% of children achieved desensitization and 21-46% achieved sustained unresponsiveness. Cow's milk and egg OIT also demonstrated desensitization in 50-75% of children. Wheat OIT studies found 52-69% achieved desensitization. OIT was effective at increasing tolerance but also increased rates of adverse events during treatment.
This document summarizes X-linked agammaglobulinemia (XLA), an inherited primary immunodeficiency caused by mutations in the Bruton's tyrosine kinase (Btk) gene. XLA is characterized by absent B cells and low immunoglobulin levels, leading to recurrent bacterial infections starting in infancy. Management involves immunoglobulin replacement and antibiotic therapy. With treatment, life expectancy has improved dramatically though complications can include lung disease. The document also briefly discusses other forms of agammaglobulinemia caused by defects in genes important for early B cell development.
This document discusses histamine and anti-histamines. It provides information on:
1. The structure and function of histamine and its receptors in immune response regulation. Histamine plays a role in processes like antigen presentation and influencing T and B cell responses.
2. The classification and structures of different types of anti-histamines, including first and second generation anti-histamines from different chemical classes.
3. Some anti-histamines have the potential to cause hypersensitivity in rare cases, even those from different chemical classes with no structural similarity.
The document discusses beta-lactam allergy, including penicillin and cephalosporin allergies. It covers the epidemiology, classifications, structures, mechanisms, and investigations of beta-lactam allergies. Specifically, it notes that penicillin is the most commonly reported antibiotic allergy. It describes the hapten concept of small molecules like beta-lactams binding covalently to proteins to form antigen complexes. Skin testing and in vitro tests are used to investigate immediate IgE-mediated allergies, while patch testing is used for delayed reactions.
This document provides an overview of intravenous immunoglobulin (IVIG) therapy. It discusses the structure and classes of immunoglobulins, mechanisms of action including neutralization, opsonization, and modulation of immune cells. It also covers the manufacturing process, pharmacokinetics, indications for use in primary immunodeficiencies and autoimmune diseases, dosing, administration, and adverse effects. The differences between IVIG products are also reviewed.
More from Chulalongkorn Allergy and Clinical Immunology Research Group (20)
The skin is the largest organ and its health plays a vital role among the other sense organs. The skin concerns like acne breakout, psoriasis, or anything similar along the lines, finding a qualified and experienced dermatologist becomes paramount.
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
Kosmoderma Academy, a leading institution in the field of dermatology and aesthetics, offers comprehensive courses in cosmetology and trichology. Our specialized courses on PRP (Hair), DR+Growth Factor, GFC, and Qr678 are designed to equip practitioners with advanced skills and knowledge to excel in hair restoration and growth treatments.
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Test bank for karp s cell and molecular biology 9th edition by gerald karp.pdfrightmanforbloodline
Test bank for karp s cell and molecular biology 9th edition by gerald karp.pdf
Test bank for karp s cell and molecular biology 9th edition by gerald karp.pdf
Test bank for karp s cell and molecular biology 9th edition by gerald karp.pdf
How to Control Your Asthma Tips by gokuldas hospital.Gokuldas Hospital
Respiratory issues like asthma are the most sensitive issue that is affecting millions worldwide. It hampers the daily activities leaving the body tired and breathless.
The key to a good grip on asthma is proper knowledge and management strategies. Understanding the patient-specific symptoms and carving out an effective treatment likewise is the best way to keep asthma under control.
Travel Clinic Cardiff: Health Advice for International TravelersNX Healthcare
Travel Clinic Cardiff offers comprehensive travel health services, including vaccinations, travel advice, and preventive care for international travelers. Our expert team ensures you are well-prepared and protected for your journey, providing personalized consultations tailored to your destination. Conveniently located in Cardiff, we help you travel with confidence and peace of mind. Visit us: www.nxhealthcare.co.uk
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Co-Chairs, Val J. Lowe, MD, and Cyrus A. Raji, MD, PhD, prepared useful Practice Aids pertaining to Alzheimer’s disease for this CME/AAPA activity titled “Alzheimer’s Disease Case Conference: Gearing Up for the Expanding Role of Neuroradiology in Diagnosis and Treatment.” For the full presentation, downloadable Practice Aids, and complete CME/AAPA information, and to apply for credit, please visit us at https://bit.ly/3PvVY25. CME/AAPA credit will be available until June 28, 2025.
Chronic idiopathic urticaria part 2: investigation and management
1. Chronic Idiopathic
Urticaria
Episode 2:
Gathering information,
investigation and management
Wat Mitthamsiri, M.D.
Allergy and Clinical Immunology Unit
Department of Medicine
King Chulalongkorn Memorial Hospital
2. Outline
• Gathering information
– History
– Remarkable notes about PE
– Assessment
• Recommended investigations
• Management in general population
• Management in special population
(children and pregnant woman
5. History taking
• Time of onset of disease
• Frequency and duration of wheals
• Diurnal variation
• Occurrence in relation to weekends,
holidays, and foreign travel
• Shape, size, and distribution of wheals
• Associated angioedema
• Associated subjective symptoms of
lesion, e.g. itch, pain
Torsten Z, A Summary of the New International EAACI/GA2LEN/EDF/WAO Guidelines in Urticaria, WAO Journal 2012; 5:S1–S5.
6. History taking
• Family+personal Hx of urticaria & atopy
• Previous or current allergies, infections,
internal diseases, or other possible causes
• Psychosomatic/psychiatric diseases
• Surgical implantations and events during
surgery
• Gastric/intestinal problems (stool,
flatulence)
• Induction by physical agents or exercise
Torsten Z, A Summary of the New International EAACI/GA2LEN/EDF/WAO Guidelines in Urticaria, WAO Journal 2012; 5:S1–S5.
7. History taking
• Use of drugs
– NSAIDs
– Injections
– Immunizations
– Hormones
– Laxatives
– Suppositories
– Ear and eye drops
– Alternative remedies
Torsten Z, A Summary of the New International EAACI/GA2LEN/EDF/WAO Guidelines in Urticaria, WAO Journal 2012; 5:S1–S5.
8. History taking
• Observed correlation to food
• Relationship to the menstrual cycle
• Smoking habits
• Type of work
• Hobbies
• Stress
• Quality of life related to urticaria and
emotional impact
• Previous Rx and response to Rx
Torsten Z, A Summary of the New International EAACI/GA2LEN/EDF/WAO Guidelines in Urticaria, WAO Journal 2012; 5:S1–S5.
10. Muckle–Wells syndrome
• A rare autosomal dominant disease
• Comprises of
– Sensorineural deafness
– Recurrent hives
– Amyloidosis
• Other possible symptoms: episodic
fever, chills, and painful joints.
• Caused by a defect in the CIAS1 gene
which creates the protein cryopyrin
Mukle T, et al., Q J Med. 1962 Apr;31:235-48.
Lieberman A. et al., J Am Acad Dermatol. 1998 Aug;39(2 Pt 1):290-1.
11. Schnitzler Syndrome
• Characteristics
– Chronic urticaria
– Intermittent fever
– Osteosclerotic bone lesions
– Monoclonal gammopathy
• Sometimes also: joint
pain/inflammation, weight loss,
malaise, fatigue, swollen lymph
nodess and hepato/splenomegaly
• Unknown cause
Oren S, et al., IMAJ 2002;4:466±467
Koning H, et al., Seminars in arthritis and rheumatism 37, 2007, (3): 137–48.
12. Gleich's Syndrome
• A rare disease with
– Angioedema
– Increased IgM Ab
– Eosinophilia
• First described in 1984
• Unknown cause
Gleich G, et al., N Engl J Med. 1984 Jun 21;310(25):1621-6.
13. Wells Syndrome
• A rare disease with pruritic or tender
cellulitis-like eruption
• Typical histologic features:
– Edema
– Flame figures
– Marked eosinophils infiltration in the
dermis
• Unknown cause
Wells G, et al., Trans St Johns Hosp Dermatol Soc. 1971;57(1):46-56
Brehmer-Andersson E, et al. Acta Derm Venereol. 1986;66(3):213-9.
14. History taking
Michihiro H. et al., Japanese Guidelines for Diagnosis and Treatment of Urticaria in Comparison with Other Countries, Allergology International. 2012;61:517-527
15. History taking
Michihiro H. et al., Japanese Guidelines for Diagnosis and Treatment of Urticaria in Comparison with Other Countries, Allergology International. 2012;61:517-527
16. Physical examination
Remarkable note:
• Test for dermographism where
indicated by history
• Antihistamine should be discontinued
for at least 2–3 days
EAACI/GA2LEN/EDF/WAO guideline: definition, classification and diagnosis of urticaria, Allergy 2009: 64: 1417–1426.
17. Assessment
• Disease activity assessment
– Urticaria activity score
• Effects on patient’s quality of life
– Health Related Quality of Life (HRQL)
• General HRQL
• Disease-specific HRQL: Chronic Urticaria
Quality of Life Questionnaire (CU-Q2oL)
EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
19. Assessment: Japanese
Michihiro H. et al., Japanese Guidelines for Diagnosis and Treatment of Urticaria in Comparison with Other Countries, Allergology International. 2012;61:517-527
20. HRQL
Centers for Disease Control and Prevention. Measuring Healthy Days. Atlanta, Georgia: CDC, November 2000.
• http://www.cdc.gov/hrqol/hrqol14_measure.htm
21. HRQL
Murphy B, et al. Australian WHOQoL instruments: User’s manual and interpretation guide. World Health Organization (1993).
WHOQoL Study Protocol. WHO (MNH7PSF/93.9).
27. Recommended Tests
Torsten Z, A Summary of the New International EAACI/GA2LEN/EDF/WAO Guidelines in Urticaria, WAO Journal 2012; 5:S1–S5.
28. Recommended Tests
Torsten Z, A Summary of the New International EAACI/GA2LEN/EDF/WAO Guidelines in Urticaria, WAO Journal 2012; 5:S1–S5.
29. Recommended Tests
Torsten Z, A Summary of the New International EAACI/GA2LEN/EDF/WAO Guidelines in Urticaria, WAO Journal 2012; 5:S1–S5.
30. Recommended Tests
Torsten Z, A Summary of the New International EAACI/GA2LEN/EDF/WAO Guidelines in Urticaria, WAO Journal 2012; 5:S1–S5.
31. Infection
• H. pylori
• Streptococci
• Staphylococci
• Yersinia
• Giardia lamblia
• Mycoplasma pneumonia
EAACI/GA2LEN/EDF/WAO guideline: definition, classification and diagnosis of urticaria, Allergy 2009: 64: 1417–1426.
32. Infection
• Hepatitis virus
• Norovirus
• Parvovirus B19
• Anisakis simplex
• Entamoeba spp
• Blastocystis spp
• Dental or ENT infections
EAACI/GA2LEN/EDF/WAO guideline: definition, classification and diagnosis of urticaria, Allergy 2009: 64: 1417–1426.
33. Infection
• Hepatitis virus
• Norovirus
• Parvovirus B19
• Anisakis simplex
• Entamoeba spp
• Blastocystis spp
• Dental or ENT infections
EAACI/GA2LEN/EDF/WAO guideline: definition, classification and diagnosis of urticaria, Allergy 2009: 64: 1417–1426.
•Norwalk virus
•Feco-oral and contact
transmission
•Most common cause of
viral gastroenteritis in
humans
•Affect people of all ages
34. Infection
• Hepatitis virus
• Norovirus
• Parvovirus B19
• Anisakis simplex
• Entamoeba spp
• Blastocystis spp
• Dental or ENT infections
EAACI/GA2LEN/EDF/WAO guideline: definition, classification and diagnosis of urticaria, Allergy 2009: 64: 1417–1426.
•Fifth disease (Slapped
cheek syndrome)
•Anemia in AIDS
•Reactive arthritis
•Hydrop fetalis
•Aplastic crisis
35. Infection
• Hepatitis virus
• Norovirus
• Parvovirus B19
• Anisakis simplex
• Entamoeba spp
• Blastocystis spp
• Dental or ENT infections
EAACI/GA2LEN/EDF/WAO guideline: definition, classification and diagnosis of urticaria, Allergy 2009: 64: 1417–1426.
•Nematodes parasite
•Host: fish and marine
mammals
•possible cause of recurrent
acute spontaneous urticaria
Foti C, et al. Acta Derm Venereol 2002;82:121–123
36. Infection
• Hepatitis virus
• Norovirus
• Parvovirus B19
• Anisakis simplex
• Entamoeba spp
• Blastocystis spp
• Dental or ENT infections
EAACI/GA2LEN/EDF/WAO guideline: definition, classification and diagnosis of urticaria, Allergy 2009: 64: 1417–1426.
37. Malignancy?
• No longer suggested
• No evidence available for a correlation
of urticaria with neoplastic diseases
EAACI/GA2LEN/EDF/WAO guideline: definition, classification and diagnosis of urticaria, Allergy 2009: 64: 1417–1426.
38. Thyroid diseases
• Autoimmune hypothyroidism
(Hashimoto’s thyroiditis)
– Association found with the presence of
peroxidase or thyroglobulin Ab.
– Incidence: 12–14%
– 24% incidence of antithyroglobulin Ab or
antimicrosomal Ab or both, found in
patients with chronic urticaria
Kikuchi Y, et al. J Allergy Clin Immunol 2003; 112(1):218.
Leznoff A, et al. Arch Dermatol 1983; 119(8):636–640.
Leznoff A, et al. J Allergy Clin Immunol 1989; 84(1):66–71.
39. Thyroid diseases
• Autoimmune hypothyroidism
(Hashimoto’s thyroiditis)
But…
– Thyroid status did not relate to the
occurrence of urticaria
– Hives persist even with euthyroid
achievement
Allen P Kaplan, Middleton’s Allergy: Principles and Practice 7th edition, 2009: 1063-1081.
40. Thyroid diseases
• A case-controlled study (140 vs 181)
found that CIU was associated with
• Hashimoto’s thyroiditis > Graves’
disease
• Female > male
Filliz C. et al., Eur J Dermatol 2006; 16 (4): 402-5
41. Thyroid diseases
• A study trying to figure out the
pathophysiologic relationship of anti-
thyroid and anti-FceRIa Ab reported
negative finding:
– Incubation of patient sera with FceRIa:
decreased ability to detect anti-FceRIa Ab
– But not thyroglobulin or thyroid
peroxidase
– Incubation with thyroid antigens did not
activation of mast cells
Jonathan DM., et al. Journal of Investigative Dermatology (2010) 130, 1860–1865.
42. Thyroid diseases
• So…epitopic cross-reactivity does not
explain the increased prevalence of
Hashimoto’s thyroiditis in CIU patients
• The frequent concurrence of
Hashimoto’s thyroiditis and CIU likely
reflects a genetic tendency toward
autoimmune diseases
Jonathan DM., et al. Journal of Investigative Dermatology (2010) 130, 1860–1865.
43. Thyroid diseases
• A recent case-controlled study of 115
patient found that
– Patients with CIU and autoimmune
thyroid disease had greater risk of
angioedema (16.2 times)
• Odds ratio
– Hypothyroidism: 4.6 (CI = 1.00-21.54)
– Hyperthyroidism: 3.3 (CI = 0.38-28.36).
Ruy FBGM., et al., Sao Paulo Med J. 2012; 130(5):294-8
44. Other autoantibodies
• Autologous Serum Skin Test (ASST)
• in vitro histamine release from
basophils: Histamine releasing assay
EAACI/GA2LEN/EDF/WAO guideline: definition, classification and diagnosis of urticaria, Allergy 2009: 64: 1417–1426.
45. ASST
• In-vivo test detecting functional
autoantibody
• Sensitivity about 70%
• Specificity about 80%
• Positive in about 40% of CIU patients
(30-50% in previous literature)
M Abd El-Azim, et al., J Investig Allergol Clin Immunol 2011; Vol. 21(7): 546-550
Sabroe R., et al. J Am Acad Dermatol. 1999;40:443-50.
46. ASST
• A small report found that positive
ASST patients tend to have
– Less inflammatory process than the ASST
negative patient
• Less TNF-alpha
• Less chemokines
• Less expression of adhesion molecules
• ASST negative patients might be more
refractory to Rx
Stefania P., et al., Int Arch Allergy Immunol 2002;128:59–66
47. ASST
• But newer study reported that patients
with ASST positive tend to have:
– More frequent urticaria attacks
– Higher urticaria activity score
– Lower absolute eosinophil count
– Lower serum IgE titer
– Significantly higher antithyroid Ab titer
– Significantly higher B-cell percentage
M Abd El-Azim, et al., J Investig Allergol Clin Immunol 2011; Vol. 21(7): 546-550
48. ASST
• Another report found that patients with
positive ASST…
– No significantly different clinical variables:
• Disease severity, duration, attack frequency
• Presence of angioedema
• Family history of urticaria
• Family/personal history of atopy
• Family/personal history of autoimmune (eg.
thyroid disease, DM, vitiligo, and rheumatoid)
– Significantly associated with distribution of
wheals on the face and extremities
Hayder R. ISRN Dermatology Volume 2013, Article ID 291524, 4
49. ASST in Thai
• Only 1 study of 85 patient during 2002-
2003
– 24.7% of patients had a positive ASST
• There was no significant difference
between patients with positive ASST
and negative ASST in these variables:
– Severity (wheal no., wheal size, itching
scores and body area involvement)
– Duration of the disease
Kanokvalai K. et al., Asian Pac J Allergy Immunol. 2006 Dec;24(4):201-6.
50. ASST: Teniques
• ID injection of 50 μL at volar forearm of:
– Autologous serum
– histamine
– Sterile physiological saline
• Avoid areas known to have had
spontaneous wheals in previous 48 hours
– Mast cells may be refractory to further
activation (local tachyphylaxis)
M Abd El-Azim, et al., J Investig Allergol Clin Immunol 2011; Vol. 21(7): 546-550
51. ASST: Teniques
• Measure the wheal after 30 minutes
(15 minutes for histamine)
– At its 2 longest perpendicular diameters
– Calculate the average value
• A positive ASST result was defined as:
– Serum-induced wheal diameter was
larger than saline-induced wheal
diameter ≥1.5 mm, at 30 minutes
M Abd El-Azim, et al., J Investig Allergol Clin Immunol 2011; Vol. 21(7): 546-550
52. Histamine releasing assay
• Gold standard of detecting functional
autoantibodies
• Time-consuming procedure
• Difficult to standardize
• Requires fresh basophils from healthy
donors
Grattan CE, et al. J Am Acad Dermatol. 2002;46:645-57,
53. Other tests
• Blood basophil count
• Skin biopsy
• Skin biopsy
– Histologic pattern does not correlate with
the severity of urticaria
– And can’t be used as a guide to Rx
EAACI/GA2LEN/EDF/WAO guideline: definition, classification and diagnosis of urticaria, Allergy 2009: 64: 1417–1426.
Allen P Kaplan, Middleton’s Allergy: Principles and Practice 7th edition, 2009: 1063-1081.
54. Other tests
D-dimer: There are reports about
• Positive autologus plasma skin testing
(APST) is higher than that of positive
autologus serum skin testing (ASST)
(80% vs. 50%)
• This difference suggested that
coagulation cascade is possibly
involved in the pathogenesis of CIU
Asero R, et al., J Allergy Clin Immunol 2006;117:1113-7.
55. Other tests
D-dimer: There are reports about
• Increased level of D-dimer in chronic
urticaria patient
– 10-35% in previous study
– 48.3% in a Thai study
• Positive correlation between plasma
D-dimer level and disease severity
Daranporn T. Asia Pac Allergy 2013;3:100-105.
56. Other tests
D-dimer: There are reports about
• No statistically significant difference in
plasma D-dimer level between:
– APST positive and negative groups
– ASST positive and negative groups.
• This may be an alternative way to
evaluate disease severity in patients
with CIU
Daranporn T. Asia Pac Allergy 2013;3:100-105.
57. Other tests
• There are potential tests that may be
useful in the future
• But they still need to be validated
– Western blotting
– ELISA
– Flow cytometry using chimeric cell lines
expressing the human FcεRIα
Grattan CE, et al., J Am Acad Dermatol 2002; 46: 645-57; quiz 57-60
58. In Japanese guideline
Michihiro H. et al., Japanese Guidelines for Diagnosis and Treatment of Urticaria in Comparison with Other Countries, Allergology International. 2012;61:517-527
59. In Japanese guideline
Michihiro H. et al., Japanese Guidelines for Diagnosis and Treatment of Urticaria in Comparison with Other Countries, Allergology International. 2012;61:517-527
60. In Japanese guideline
Michihiro H. et al., Japanese Guidelines for Diagnosis and Treatment of Urticaria in Comparison with Other Countries, Allergology International. 2012;61:517-527
70. Goal of Rx
• 1st stage: Symptom free
Michihiro H. et al., Japanese Guidelines for Diagnosis and Treatment of Urticaria in Comparison with Other Countries, Allergology International. 2012;61:517-527
71. Goal of Rx
• 1st stage: Symptom free
• Final stage: Drug free
Michihiro H. et al., Japanese Guidelines for Diagnosis and Treatment of Urticaria in Comparison with Other Countries, Allergology International. 2012;61:517-527
79. recommendations
EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
Patients with cellular infiltration
•May be refractory to antihistamines
•May respond completely to a brief burst of
corticosteroid
81. recommendations
EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
•Medium to high cost
•Moderate safety profile
•Moderate level of evidence for efficacy
•Recommended only for patients with severe
disease refractory to antihistamine
•Far better risk/benefit ratio compared with
steroids.
82. recommendations
EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
•Moderate, direct effect on mast cell mediator release
•Only agent to inhibit basophil histamine release
Zuberbier T, et al. Acta Derm Venereol 1996;76:295–297.
85. recommendations
EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
•High cost
•Good safety profile
•Low level of evidence for efficacy
•Dramatically effective in selected patient
Spector SL, et al., Ann Allergy Asthma Immunol 2007;99:190–193
86. recommendations
• There is a strong recommendation
against the long-term use of
corticosteroids outside specialist
clinics
• If there is no special indication, we
recommend against the routine use of
old sedating first generation
antihistamines
EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
87. recommendations
• We recommend against the use of
astemizole and terfenadine
– Pro-drugs requiring hepatic metabolism
to become fully active
– Cardiotoxic if this metabolism was
blocked by concomitant administration of
ketoconazole or erythromycin
EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
88. recommendations
• Suggest the same first line treatment
and up-dosing for children (weight
adjusted)
• Suggest the same first line treatment in
pregnant or lactating women
– (but safety data in a large meta-analysis is
limited to loratadine)
EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
89. EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
Autoantibody reduction
• Plasmapheresis
– Benefit in severely affected patients
– High costs
– AutoAb-positive patients who are
unresponsive to all other treatment.
91. EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
Hannuksela M, et al., Acta Derm Venereol 1985;65:449–450.
Borzova E, et al., J Am Acad Dermatol 2008;59:752–757.
Other Rx
• Phototherapy
– UV-A and UV-B Rx for 1–3 months can be
added to antihistamine treatment
• These agents were just case reports
and only be used in large centers as
last options
93. EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
Other Rx: Monotherapy
• There are reports but poor evidence of…
– Ketotifen
– Montelukast
– Warfarin
– Hydroxychloroquine
– Oxatomide
– Doxepin
– Nifedipine
– Autologs whole blood Injection
94. EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
Other Rx
• Monotherapy: Only case-control
report, no RCT about…
– Dapsone
– Sulfasalazine
– Methotrexate
– Interferon
– Plasmapheresis
– IVIG
95. EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
F/U evaluation
• Re-evaluate the necessity for
continued or alternative drug
treatment every 3–6 months.
96. recommendations
EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
These agents might be added in
some patients
•Hydroxyzine or diphenhydramine
•Doxepin
•Prednisone
Allen P Kaplan, Middleton’s Allergy: Principles and Practice 7th edition, 2009: 1063-1081.
97. Adjusting medication
• Sometimes, sedating antihistamine
might be needed
– Hydroxyzine or diphenhydramine
200mg/day divided into 3 or 4 doses
• Or sometimes, Doxepin
– It can interact with H1 receptors
– And also possesses some H2 receptor
activity
• But beware of sedation
Allen P Kaplan, Middleton’s Allergy: Principles and Practice 7th edition, 2009: 1063-1081.
98. Adjusting medication
• Drugs must be taken as prescribed and
not just as needed
– Daily administration minimizes or prevents
outbreaks
– Use of antihistamines after the onset of
lesions occurs is too late
– Ratio of histamine vs antihistamine at the
cutaneous endothelial cell H1 receptor
determines the response
– If histamine level exceeds antihistamine
level, Rx will be ineffective
Allen P Kaplan, Middleton’s Allergy: Principles and Practice 7th edition, 2009: 1063-1081.
99. Adjusting steroid
Allen P Kaplan, Middleton’s Allergy: Principles and Practice 7th edition, 2009: 1063-1081.
Day 1 2 3 4 5 6 7
Dose (mg) 40 40 40 35 30 25 20
• Start with prednisone 40 mg/d
100. Adjusting steroid
Allen P Kaplan, Middleton’s Allergy: Principles and Practice 7th edition, 2009: 1063-1081.
Day 1 2 3 4 5 6 7
Dose (mg) 40 40 40 35 30 25 20
• Start with prednisone 40 mg/d
Day 8 9 10 11 12 13 14
Dose (mg) 15 20 10 20 5 20 -
101. Adjusting steroid
Allen P Kaplan, Middleton’s Allergy: Principles and Practice 7th edition, 2009: 1063-1081.
Day 1 2 3 4 5 6 7
Dose (mg) 40 40 40 35 30 25 20
• Start with prednisone 40 mg/d
Day 8 9 10 11 12 13 14
Dose (mg) 15 20 10 20 5 20 -
Day 15 16 17 18 19 20 21
Dose (mg) 20 - 20 - 20 - 20
102. Adjusting steroid
• Then taper steroid dosage by 2.5–5.0
mg every 2-3 weeks
• Nearly 3 months would be needed to
discontinue the steroid
• Sometimes, steroid cannot be tapered
below a certain dosage
– That dosage may be maintained for 1-2
month
– Then try tapering again
Allen P Kaplan, Middleton’s Allergy: Principles and Practice 7th edition, 2009: 1063-1081.
103. Adjusting steroid
• Common problem
– Good control of on the steroid ‘on’ day
– Prominent exacerbation on the ‘off’ day
• Solution
– Separate prednisone into b.i.d. dosage
– After good control, try tapering the
evening dosage first
– Or daily dosage might be used
Allen P Kaplan, Middleton’s Allergy: Principles and Practice 7th edition, 2009: 1063-1081.
104. Adjusting steroid
• Some patient unable to metabolize
prednisone to prednisolone
– Low dosage of methylprednisolone is
often effective
• Antihistamines :continued and should
not be tapered until steroid is no
longer required
Allen P Kaplan, Middleton’s Allergy: Principles and Practice 7th edition, 2009: 1063-1081.
105. EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
Rx associated condition
• Rx of associated infection
• Rx of inflammatory processes
– Gastritis
– Reflux esophagitis
– Inflammation of the bile duct or gall
bladder
106. EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
Rx associated condition
• Rx of food and drug intolerance
– Diet containing only low levels
pseudoallergens : instituted and
maintained for at least 3–6 month
– In pseudoallergy, a diet must be
maintained for a minimum of 3 weeks
before beneficial effects are observed.
107. EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
Rx associated condition
• Rx psychological factors
• Symptomatic relief should be offered
while searching for causes
109. In Japanese guideline
Michihiro H. et al., Japanese Guidelines for Diagnosis and Treatment of Urticaria in Comparison with Other Countries, Allergology International. 2012;61:517-527
110. In Japanese guideline
Michihiro H. et al., Japanese Guidelines for Diagnosis and Treatment of Urticaria in Comparison with Other Countries, Allergology International. 2012;61:517-527
111. In Japanese guideline
Michihiro H. et al., Japanese Guidelines for Diagnosis and Treatment of Urticaria in Comparison with Other Countries, Allergology International. 2012;61:517-527
112. In Japanese guideline
Michihiro H. et al., Japanese Guidelines for Diagnosis and Treatment of Urticaria in Comparison with Other Countries, Allergology International. 2012;61:517-527
113. In Japanese guideline
Michihiro H. et al., Japanese Guidelines for Diagnosis and Treatment of Urticaria in Comparison with Other Countries, Allergology International. 2012;61:517-527
114. In Japanese guideline
Michihiro H. et al., Japanese Guidelines for Diagnosis and Treatment of Urticaria in Comparison with Other Countries, Allergology International. 2012;61:517-527
116. EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
Children
• Same first line treatment and up-dosing
(weight adjusted) is recommended as in
adults
• But…
• Nonsedating H1-antihistamines is not
licensed for use in children <6 months
of age
117. EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
Pregnant woman
General concept:
• Systemic Rx should generally be
avoided in pregnant women, especially
in the 1st trimester
• But pregnant women have the right to
best possible Rx
118. EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
Pregnant woman
Evidence?
• No systematic study on safety of Rx in
pregnant women with urticaria
• No study on negative effects of
increased levels of histamine occurring
in pregnant woman with urticaria, too.
• No reports of birth defects in women
having used 2nd generation
antihistamines during pregnancy
119. EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
Pregnant woman
In real world
• 2nd generation antihistamines can be
bought over-the-counter and widely
used in self-Rx
• So… many women might have used
these drugs at the beginning of
pregnancy before the pregnancy was
confirmed
120. EAACI/GA2LEN/EDF/WAO guideline: management of urticaria, Allergy 2009: 64: 1427–1443.
Pregnant woman
For highest safety possible, the current
suggestion is that:
• Use of 2nd generation antihistamines
should be limited to loratadine
• With the possible extrapolation to
desloratadine
121. Take Home Message
• History is the most important
diagnostic tool
• Investigations is for cause searching
• ASST is the best in-vivo test for
autoreactivity but basophil histamine
release assay is the gold standard
122. Take Home Message
• Non-sedating H1-receptor antagonist
antihistamine is the 1st line and
mainstay of treatment
• Treatment in children use the same
principle as normal adult
• In pregnant woman, available data
limited only to loratadine
• Other potential agents need more
study