Itching, an unpleasant sensation leading to scratching.
Most common symptom in dermatology that may occur with or without visible skin lesions.
Reported as a symptom by patients with more than 7 million outpatient visits per year in the US, and 25% of such patients are 65 years or older.
May be localized or generalized in nature.
Incidence increases with age.
Affects nearly one third of nursing home patients.
In a Turkish study prevalence of chronic pruritus in a geriatric population in patients aged 65 years was 12% and nearly 20% for patients 85 years or older(Yalcin B et al ).
More common in women than men.
More common in Asians than whites.
Chronic pruritus can be categorized into neuropathic, inflammatory, or combination of neuropathic and inflammatory etiologies.
Many forms of purities were due to a combination of neuronal dysfunction and inflammatory dysregulation.
May be induced or altered by histamine, catecholamines, chemokines, interleukin 2, interleukin 31, endothelin, neuropathies, acetylcholine, kallikreins, prostaglandins, proteases, leukotriene B4 and opioids.
Chronic itch that occurs from infections, or systemic diseases and medications induce neural, and immunologic system abnormalities that result in pruritus.
Medications that can cause pruritus include Pemrolizumab,opioid pain medications and stimulants such as amphetamines.
The process may be acute or chronic, and if it lasts longer than 6 weeks it is referred to as chronic pruritus.
Acute disease is a physiologic symptom while chronic pruritus is a common symptom of a systemic or dermatological disorder.
Associated with a reduction in quality of life, as it may be as debilitating as chronic pain.
Severity of pruritus may range from very mild to severe and depends on the anatomical location, time of day, or season, as well as exacerbating factors, such as exposure to sunlight, water, physical pressure on the skin, or stress.
physical examination may indicate inflamed skin, suggesting a primary inflammatory or infectious ideology, or un inflamed, consisting of normal appearing skin with without secondary lesions, which suggest underlying systemic, neurogenic, neuropathic, or psychogenic causes.
Associated with impaired sleep patterns, mood disturbances, anxiety, depression.
Seevere chronic pruritus may impair quality of life and lead to social isolation.
All of the above symptoms may exacerbate itching.
Severe itching should prompt an evaluation for evidence of underlying kidney, liver, or thyroid disease, underlying malignancy and dermatitis herpetiformis.
Dry skin is a common cause.
Chronic disease classified as dermatologic, systemic, neurologic, psychogenic, mixed or of unknown etiology.
Chronic pruritus is defined as symptom of itch that last longer than six weeks and the accounts were approximately one percent of all physician visits and approximately 7 million visits annually in the US.
Lifetime prevalence of chronic purities is approximately 22%.
Older age increases the likelihood of chronic pruritus.
Only approximately half of patients with chronic pruritis seek medical attention.
Chronic pruritus is categorized into neuropathic, inflammatory, or a combination of these processes as an underlying etiology.
Neuropathic itch is caused by neuropathic or neurogenic signals, causing pathologic nerve impulses and can be caused by nerve impingement such as nostalgia paresthetica, and brachioradial pruritus.
Nerve impingement dysesthesia can result from cervical nerve impingement that can cause itching in the mid back and dorsal lateral arms.
Neuropathic itch can also be caused by damage to nerves such as postherpetic itch.
Neuropathic itch is typically due to local nerve damage, but there are systemic metabolic disorders, such as diabetes that can cause peripheral neuropathy that contribute to itch.
Inflammation, can precipitate itch by the immune system such as allergic contact dermatitis, atopic dermatitis, and urticaria.
Urticaria is mediated by direct effects of histamine on sensory nerves.
Pruritus due to allergic contact dermatitis is typically related to mast cell release via histamine independent biologic pathways.
Atopic dermatitis is mediated by cytokines IL-4, IL-13, and IL-31 which act as pruritogens, which are substances that stimulate itch when introduced into the skin and Janus Kinase 1 signaling within itch sensing nerves.
Cytokines can be released such as IL 33 and can contribute to pruritus in patients with other inflammatory diseases and dry skin.
Commonly associated with dermatological diseases including atopic eczema, psoriasis, lichen planus, and scabies.
May complicate systemic diseases, such as chronic renal failure, blood malignancies or liver disorders.
Pruritus is present at some point in the course of polycythemia Vera in approximately 65% of patients and is generally localized to the trunk and proximal extremities and classically occurs following a hot shower.
Biological processes contributing to itching includes loss of barrier function, immunosenescence and neuropathy.
Seen in 22-70% of hemodialysis patients.
Chronic pruritus associated with impaired quality of life, emotional distress and depression.
Aquagenic type refers to itching after exposure to water and is virtually pathognomonic for polycythemia rubra vera.
May be characterized as those with itching on primarily diseased skin or normal noninflamed skin, and chronic secondary scratch lesions.
The major symptom in atopic eczema, with essentially all patients suffering with this process sometime during the illness.
About 70% to 90% of patients with psoriasis suffer from pruritus.
Itching elicits secondary skin changes due to the scratching, rubbing, and picking.
The presence of secondary skin changes does not rule out a systemic disease.
Secondary skin changes of excoriation and nonspecific dermatitis can impair the diagnosis of cutaneous and non-cutaneous causes of itching.
Primary skin lesion suggest an underlying cutaneous disorder, including erythema, edema, vesiculation, scaling, bullar and atrophy.
The presence of the skin exanthem suggests an immunologic etiology: atopic dermatitis, or an infectious etiology, such as scabies.
Not all skin changes are associated with pruritus are red and scaled – xerosis, fibrosis and dyspigmentation may be associated with systemic sclerosis, dermatomyositis, and other connective tissue disorders.
A neuronal pathway for itch has been identified with stimuli transmitted mainly via small itch selective mechano-insensitive unmyelinated afferent C-fibers that have a particular low conduction velocity, large innervations territories and high transcutaneous electrical threshold.
Pruritic stimuli are transf2242ed via specific neurons of dorsal horns to the posterior part of the ventromedial thalamic nucleus, which projects to the dorsal insular cortex.
A number of mediators are involved in the sensation of itch and histamine triggered neurons and nonhistaminergic neurons may be involved.
Involves synapses of these neurons with secondary neurons cross to the contralateral spinothalamic tract and ascend to multiple sites in the brain that are involved with sensation, emotion, memory, reward and evaluation processes.
Chronic itch patients often have peripheral and central nervous system hypersensitization.
Itch stimuli induced predominantly in the left hemisphere.
Chronic pruritus frequently refractive to treatment.
With chronic pruritus without primary skin changes, secondary skin lesions, such as excoriations may be present.
These secondary skin lesions are manifestations of repeated, scratching, rubbing or picking.
With chronic pruritus without primary skin lesions neuropathic or mixed etiology lesions such as prurigo nodularis, or chronic pruritus of unknown origin are considered.
Chronic pruritus of unknown origin is a common diagnosis that counts for 15% of all patients with generalized chronic pruritus, in which no underlying cause is identified.
Patients with chronic pruritus of less than one year duration should be evaluated for systemic diseases, including certain malignancy: hematopoetic malignancies, such as non-Hodgkin’s lymphoma, liver and biliary malignancies colon carcinoma and pancreatic cancer are associated with chronic pruritus.
Chronic pruritus is associated with cholestasis, chronic kidney disease, hyperthyroidism, and neuroendocrine dysfunction.
Chronic pruritus exacerbated by sleep disturbances, and vice versa.
Can lead to frustration and depression.
Age associated changes that contribute to pruritus include a sensory neuropathy most commonly due to diabetes which can cause generalized itch, and neural impingement caused by localized pruritus commonly found in the genital area.
Treatment options for pruritus are based on the etiologic types, and considering if it inflammatory or infectious cause of chronic pruritus is present.
If an inflammatory or infectious cause of chronic pruritus is present, such as any form of eczema or scabies, the first line therapies treatment with immunomodulating or anti-infective medications.
Dry skin regimen should be recommended for patient with xerosis, including application of creams or ointment daily.
Patients with no skin changes that indicate an underlying primary skin ideology should be managed with topical anesthetics such as menthol or pramoxine.
First line therapy for patients with liver or kidney disease is the management of the underlying systemic condition.
For patients with no underlying disease process and chronic pruritus are prescribed neuropathic or mixed treatments.
Immunomodulatory topicalagents are preferred for patients with immune caused chronic pruritus such as atopic dermatitis or contact dermatitis.
These agents include high potency topicall corticosteroids, such as betasol or betamethasone and mid potency triamcinolone, and are effective for people with inflammatory skin conditions.
Calcineurin inhibitors-tacrolimus can reduce pruritus in patients with inflammatory skin conditions which include seborrheic dermatitis, psoriasis and types of eczema, such as atopic or contact dermatitis.
Newer agents approved for atopic dermatitis and psoriasis include JAK inhibitors, ruxolitinib, phosphodiesterase 4 inhibitors, roflumist, and arylhydrocarbanate.
Neuropathic topical therapies are effective for mild and localized pruritus with low rates of systemic adverse effects.
Neuropathic topical agents reduce nerve activity.
Commonly used anti-pruritic topical anesthetics include pramoxine, lidocaine,, and capsaicin, all of which are effective for neuropathic facial and anogenital itch.
Topical analgesic, such as menthol can be used for neuropathic itch.
Other topical neuropathic medications include amitriptyline, ketamine, and lidocaine and gabapentin are available.
Systemic oral has antihistamines are commonly used for chronic pruritus, but there’s no efficacy other than in patient with urticaria: oral antihistamines have limited benefit for chronic colitis.
Gabapentoids are effective for chronic puritus and in neuropathic conditions such as brachioradial pruritus or notalgia, paresthetica, chronic kidney disease, pruritus associated with burns, or cutaneous lymphoma.
The most frequent adverse effects of somnolence, dizziness, and leg swelling occur with gabapentoids.
Drugs affecting the neural system and reduce neural sensitization include: selective serotonin reuptake inhibitors, and elective serotonin, and neuroepinephrine inhibitors that can reduce generalized pruritus in patients with psychogenic pruritus, neuropathic etiologies, mixed etiologies, and generalized systemic causes such as lymphoma, kidney disease and liver disease.
Sertraline is the most commonly used of the selective serotonin reuptake inhibitors.
Tricyclic antidepressants such as doxepin and amitriptyline have efficacy for neuropathic pruritus , and intravenous ketamine has also been used in refractory cases.
Mu-opioid receptor antagonism and kappa-opioid receptor agonist activity can reduce neuropathic Pruritus: naltrexone, butorphanol, difelikeafalin, and antagonist/kappa agonists can reduce itch in patients with chronic kidney disease and notalgia paresthetica.
Systemic immunosuppressant antipruritic therapies consist of oral steroids, methotrexate, cyclosporine, azothiaprine, or thalidomide.
Phototherapy can be used for chronic pruritus of immunologic causes such as a atopic dermatitis and cutaneous T cell lymphoma as well as with chronic kidney disease.
Approximately 80% of patients treated with phototherapy for atopic, dermatitis and arthritis associated with chronic kidney disease can show improvement.
Dupilumab in anti-interleukin -4 receptor alpha antibody for atopic dermatitis and prurigo nodularis significantly reduce pruritus rating scores.
IL-31 receptor inhibitor nemolizumab reduced pruritus compared with placebo and oral JAK inhibitors are reported to significantly reduce itch.
Reducing stress/anxiety can reduce symptoms of chronic pruritus and techniques like cognitive behavior, therapy, progressive muscle relaxation, transcutaneous electrical, neurostimulation, acupuncture, are effective additions to pharmacotherapy.
The prognosis for chronic pruritus depends on the etiology, severity, and duration of the process, and the presence of coexisting medical conditions.
The presence of severe and prolonged pruritus can cause sensation of itch sensing nerves, where the nerves are chronically modified to present continued stimulation of itching symptoms, and may result in lichenification and other secondary skin changes from scratching:the itch-scratch cycle.
Itch-scratch cycle may require months or years to resolve.