Pruritus is defined as an unpleasant sensation that provokes the desire to lớn scratch. Certain systemic diseases have long been known to cause pruritus that ranges in intensity from a mild annoyance khổng lồ an intractable, disabling condition. Generalized pruritus may be classified inkhổng lồ the following categories on the basis of the underlying causative sầu disease: renal pruritus, cholestatic pruritus, hematolô ghích pruritus, endocrine pruritus, pruritus related khổng lồ malignancy, & idiopathic generalized pruritus.

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Pruritus, or itch, is most commonly associated with a primary skin disorder such as xerosis, atopic dermatitis, drug eruption, urticaria, psoriasis, arthropod assault, mastocytosis, dermatitis herpetiformis, or pemphigoid. However, when a primary skin condition cannot be identified as the cause of pruritus, then a systemic or neuropathic cause must be sought. Patients without signs of a primary skin condition should undergo a thorough evaluation of potential systemic causes of itching.

The sensation of pruritus is transmitted through slow-conducting unmyelinated C-polymodal and possibly type A delta nociceptive sầu neurons with free nerve sầu endings located near the dermoepidermal junction or in the epidermis. These neurons appear to be located more superficially và are more sensitive sầu lớn pruritogenic substances than pain receptors. Activators of these nerves include histamine, neuropeptide substance P.., <1> serotonin, bradykinin, proteases (eg, mast cell tryptase), và endothelin (which stimulates the release of nitric oxide). Impulses are transmitted from the dorsal root ganglion to lớn the spinothalamic tract và eventually lớn the thalamus. <2>

Opioids are known to modulate the sensation of pruritus, both peripherally and centrally. Stimulation of opioid mu receptors accentuates pruritus, while stimulation of kappage authority receptors and blockage of mu receptors suppress pruritus.

In the mouse model that mimics atopic dermatitis in humans, the histamine (H4) receptor mediates both TH-2 inflammation & pruritus. <3> A variety of interleukins (ILs) and chemokines play a role in the pruritus of atopic dermatitis. IL-4 & IL-13, as well as TH2 chemokines CCL17, CCL22, và CCL26 play a pivotal role in the development of atopic dermatitis inflammation. <4> IL-33 induces IL-31, thereby promoting pruritus và scratching behavior. <5> IL-31 promotes growth, elongation, and branching of sensory nerves in atopic dermatitis. <6>

Renal pruritus

Renal pruritus can occur in patients with chronic renal failure (CRF) & is most often seen in patients receiving hemodialysis (HD). This term is synonymous with uremic pruritus; however, the condition is not due lớn elevated serum urea levels. The actual pruritogenic substance has yet khổng lồ be identified. Pruritus is relatively absent in persons with axinh tươi renal failure; therefore, serum mediators other than urea and creatinine are implicated.

Other theories include elevated levels of circulating histamine in patients receiving HD. Researchers have sầu found increased numbers of mast cells in various organ systems. However, antihistamines are, at best, marginal in the treatment of renal pruritus, suggesting other causative sầu factors.

Parathyroid hormone (PTH) levels are commonly elevated in persons with CRF. <1> Dramatic relief of renal pruritus after subtotal parathyroidectomy has been described, and findings from 1 study confirmed previous case reports. However, other studies have sầu shown no correlation between circulating PTH levels & the intensity of pruritus. Of note, a patient with a PTH-producing bronchogenic carcinoma was reported khổng lồ have sầu intractable pruritus as the presenting symptom. <7, 8, 9>

Elevated levels of divalent ions, such as calcium, magnesium, và phosphate, are thought to play a role. Marked improvement of pruritus resulting from low dialysate calcium & magnesium concentrations has been reported. <10, 11> Increased amounts of these ions are also seen in the skin of pruritic patients.

Decreased transepidermal elimination of pruritogenic substances, xerosis, elevated levels of serum bile acids, and increased epidermal Vi-Ta-Min A levels all may contribute khổng lồ the condition. Elevated serum levels of serotonin are seen in patients with CRF. Serotonin is important in the transmission of pain and may be a contributing factor.

Proliferation of nonspecific enolase-positive sầu sensory nerves in the epidermis has been documented in patients with uremia & may contribute; however, these results must be confirmed.

Opioid accumulation may contribute to itching in persons with CRF và overexpression and activation of opioid mu receptors. Mixed results with the use of opioid antagonists in the treatment of renal pruritus have led to conflicting opinions about the role of opioids. A newer kappa-opioid receptor agonist, nalfurafine, has shown effectiveness in end-stage renal disease patients. Nalfurafine is only available for intravenous administration. <13, 14>

An immune hypothesis has also been suggested. In patients with CRF, a systemic inflammatory response involving overexpression of activated type 1 helper T lymphocytes (which secrete interleukin 2) may induce pruritus. UV-B, thalidomide, and tacrolimus all target mediators of this inflammation. Elevated ferritin & low transferrin và albumin levels have sầu been correlated with the severity of pruritus.

Cholestatic pruritus

Cholestasis, or a decrease or arrest in the flow of bile, is associated with pruritus. The deposition of bile salts in the skin was thought to directly cause a pruritogenic effect, but this theory has been proven incorrect. In addition, indirect hyperbilirubinemia does not induce pruritus. Pruritus is more comtháng with intraheptic cholestasis than extrahepatic cholestasis.

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Other theories implicate elevated venous histamine levels, retention of pruritogenic intermediates in bile salt synthesis, và high hepatic concentrations of bile salts resulting in hepatic injury và release of a pruritogenic substance. In tư vấn of the last point, rifampin & ursodeoxycholic acid decrease intrahepatic concentrations of bile salts and provide some relief of cholestatic pruritus.

One study has proposed that autotaxin, the enzyme that converts lysophosphatidylcholine into lysophosphatidic acid, may be a potential mediator of cholestatic pruritus. <15>

The accumulation of endogenous opioids, which modulate pruritus và increase opioidergic tone in the brain, is of recent interest because opioid antagonists have been shown khổng lồ partially relieve cholestatic pruritus. In tư vấn of this theory, treatment with opioid antagonists may induce an opioid withdrawal–lượt thích syndrome.

Perhaps some combination of the pruritogenic substances mentioned above (ie, bile salts, histamine, opioids) induces cholestatic pruritus.

Hematoxúc tích và ngắn gọn pruritus

Iron is a critical factor in many enzymatic reactions. Although iron deficiency has not been proved to be a cause of pruritus, it may contribute to lớn pruritus through a variety of metabolic paths. Patients with pruritus & iron deficiency may not be anemic; this observation suggests that pruritus may be related to lớn iron & not hemoglobin.

Patients with polycythemia vera have increased numbers of circulating basophils and skin mast cells, which have sầu been correlated with itching. The itch typically occurs during cooling after a hot shower. Mast cell prostaglandins và increased platelet degranulation, which lead to the release of serotonin & prostanoids, are thought to lớn be important mediators of itching, along with iron deficiency, which may be a contributing factor. The fact that aspirin & paroxetine alleviate this khung of pruritus suggests that serotonin from platelets may play a role. However, one study showed that the concentration of platelet serotonin was the same in polycythemic patients with và without pruritus. <16>

Endocrine pruritus

Hyperthyroidism has been associated with pruritus. Excess thyroid hooc môn may activate kinins from increased tissue metabolism or may reduce the itch threshold as a result of warmth và vasodilation.

Diabetes mellitus is another possible cause, but cause & effect remain unproven. Metabolic abnormalities, autonomic dysfunction, anhydrosis, và diabetic neuropathy all may contribute.

Pruritus và malignancy

Numerous reports have linked pruritus to lớn almost every type of malignancy. Release of toxins và the immune system have sầu been suggested lớn play roles in malignancy-related pruritus.

Chronic pruritus without associated skin changes is a risk factor for having undiagnosed hematoxúc tích và ngắn gọn & biliary tract malignancies, but not other malignancies. <17>

In patients with Hodgkin disease, leukopeptidase & bradykinin appear to be the pruritogenic mediators released as an autoimmune response is mounted against malignant lymphoid cells.

Cutaneous T-cell lymphoma may cause intractable pruritus and may have sầu the cytokine interleukin 31 as a mediator of itching. <18>



Renal pruritus occurs in patients with CRF, most often those receiving HD. The exact cause is not known, although toxic substances retained during HD, histamine, opioids, và neural proliferation have sầu been postulated as potential causes.

The exact mechanism of cholestatic pruritus is not known. However, bile salts, histamine, opioids, and an unknown pruritoren from damaged hepatocytes are postulated as potential causes. Cholestatic pruritus is particularly common with cholestasis caused by primary biliary cirrhosis, primary sclerosing cholangitis, chronic hepatitis C, choledocholithiasis, obstructive sầu carcinoma of the pancreas/biliary system, cholestasis of pregnancy, và end-stage liver disease of any cause. Drug-induced cholestasis may be caused by chlorpropamide, tolbutamide, phenothiazines, erythromycin, anabolic steroids, & oral contraceptives.

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