The use of intermittent itraconazole therapy for superficial mycotic infections: a review and update on the ‘one week’ approach

Rosso, J.Q. Del; Gupta, Aditya K.; Frcp,

doi:10.1046/j.1365-4362.1999.00011.x

Cited by 10 publications

(4 citation statements)

References 110 publications

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“…Itraconazole is effective at a dosage of 200 mg/d, 190 when taken for either 5 or 7 days. The minimum cumulative dose for itraconazole is 1000 mg, although an improved efficacy is more likely to occur with the regimen of 200 mg/d for 7 days 196 Table 2. summarizes the randomized clinical trials that have been conducted using itraconazole to treat pityriasis versicolor 197–211 …”

Section: Treatmentmentioning

confidence: 99%

Pityriasis versicolor

Gupta

Bluhm

Summerbell

2002

Acad Dermatol Venereol

151

168

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Section: Treatmentmentioning

confidence: 99%

Pityriasis versicolor

Gupta

Bluhm

Summerbell

2002

Acad Dermatol Venereol

151

168

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“…Current concepts suggest that clinical trigger factors of rosacea such as ultraviolet (UV) radiation, heat, cold, psychological stress, spicy food, skin irritants, microbes (Demodex folliculorum) and others modulate TLR signalling, induce ROS and enhance antimicrobial peptide and neuropeptide production (20)(21)(22)(23)(24)(25). At the molecular level, all clinical rosacea triggers may represent ER stressors:…”

Section: Rosacea Trigger Factors Induce Er Stressmentioning

confidence: 99%

Endoplasmic reticulum stress: key promoter of rosacea pathogenesis

Melnik

2014

Experimental Dermatology

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Recent scientific interest in the pathogenesis of rosacea focuses on abnormally high facial skin levels of cathelicidin and the trypsin-like serine protease kallikrein 5 (KLK5) that cleaves the cathelicidin precursor protein into the bioactive fragment LL-37, which exerts crucial proinflammatory, angiogenic and antimicrobial activities. Furthermore, increased expression of tolllike receptor 2 (TLR2) has been identified in rosacea skin supporting the participation of the innate immune system. Notably, TLRs are expressed on sensory neurons and increase neuronal excitability linking TLR signalling to the transmission of neuroinflammatory responses. It is the intention of this viewpoint to present a unifying concept that links all known clinical trigger factors of rosacea such as UV irradiation, heat, skin irritants and special foods to one converging point: enhanced endoplasmic reticulum (ER) stress that activates the unfolded protein response (UPR). ER stress via upregulation of transcription factor ATF4 increases TLR2 expression, resulting in enhanced production of cathelicidin and KLK5 mediating downstream proinflammatory, angiogenic and antimicrobial signalling. The presented concept identifies rosacea trigger factors as environmental stressors that enhance the skin's ER stress response. Exaggerated cutaneous ER stress that stimulates the TLR2-driven inflammatory response may involve sebocytes, keratinocytes, monocyte-macrophages and sensory cutaneous neurons. Finally, all antirosacea drugs are proposed to attenuate the ER stress signalling cascade at some point. Overstimulated ER stress signalling may have evolutionarily evolved as a compensatory mechanism to balance impaired vitamin D-driven LL-37-mediated antimicrobial defenses due to lower exposure of UV-B irradiation of the northern Celtic population.Abbreviations: AGE, advanced glycation end product; AMP, antimicrobial peptide; ASK1, apoptosis signal regulating kinase-1; ATF4, activating transcription factor 4; ATF6, activating transcription factor 6; ATRA, all-trans-retinoic acid; AzA, azelaic acid; BiP, immunoglobulin heavy chain-binding protein (=heat-shock 70 kD protein 5); C/EBPa, CCAAT/enhancer-binding protein alpha; CAMP, cathelicidin antimicrobial peptide (hCAP18); CD14, monocyte differentiation antigen CD14; CHOP, C/EBP-homologous protein; COL1A1, collagen type 1; eIF2a, eukaryotic translation initiation factor 2-alpha; ER, endoplasmic reticulum; HSP70, heat-shock protein 70 kD; IRE1, inositol-requiring 1a; KLK5, kallikrein 5; LL-37, cathelicidin C-terminal fragment; mTORC1, mechanistic target of rapamycin complex 1; NFjKB, nuclear factor kappa B; PERK, doublestranded RNA-dependent protein kinase (PKR)-like ER kinase; RAGE, receptor for advanced glycation end products; ROS, reactive oxygen species; RXR, retinoid X receptor; S1P, sphingosine-1-phosphate; SPHK1, sphingosine kinase 1 isoform; SREBP, sterol regulatory element-binding transcription factor; TGFb1, transforming growth factor beta 1; TLR, tolllike receptor; TRPV, transient rece...

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“…It is characterized by flushing/transient erythema, persistent erythema, papules, pustules and telangiectasia. [1,2] Characteristic vascular changes in rosacea skin include enlarged, dilated vessels of the upper dermis and blood flow increase. [3][4][5] Although the pathophysiology of rosacea is yet not fully understood, it is suggested that neurovascular overstimulation may contribute to the transient erythema and flushing.…”

Section: Introductionmentioning

confidence: 99%

“…[5,[7][8][9] The resulting chronic vasodilation and angiogenesis might ultimately progress to fixed changes in the vasculature, leading to persistent erythema. [1,5,10] Vascular remodelling is also a hallmark of many inflammatory diseases associated with hyperpermeability and changes in adhesion molecules. [11] In addition to vascular and neuroimmune dysregulation, innate and adaptive immune systems may also be involved in the development of rosacea.…”

Section: Introductionmentioning

confidence: 99%

Brimonidine displays anti‐inflammatory properties in the skin through the modulation of the vascular barrier function

Bertino

Blanchet‐Réthoré

Ménonville

et al. 2018

Experimental Dermatology

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Background Rosacea is a chronic inflammatory skin disease. Characteristic vascular changes in rosacea skin include enlarged, dilated vessels of the upper dermis and blood flow increase. Brimonidine is approved for symptomatic relief of the erythema of rosacea. It acts by selectively binding to α2‐adrenergic receptors present on smooth muscle in the peripheral vasculature, resulting in transient local vasoconstriction. Objectives To provide further evidence of the anti‐inflammatory potential of brimonidine across preclinical models of skin inflammation and its ability to decrease the neutrophil infiltration in human skin after ultraviolet light exposure. Methods The anti‐inflammatory properties of brimonidine through modulation of the vascular barrier function were assessed using in vivo neurogenic vasodilation and acute inflammatory models and a well‐described in vitro transmigration assay. A clinical study assessed the neutrophil infiltration in human skin after exposure to UV in 37 healthy Caucasian male subjects. Results In vitro, brimonidine affects the transmigration of human neutrophils through the endothelial barrier by modulating adhesion molecules. In vivo, in the mouse, topical treatment with brimonidine, used at a vasoconstrictive dose, confirmed its anti‐inflammatory properties and prevented leucocyte recruitment (rolling and adhesion) mediated by endothelial cells. Topical pretreatment with brimonidine tartrate 0.33% gel once a day for 4 days significantly prevented neutrophil infiltration by 53.9% in human skin after exposure to UV light. Conclusion Results from in vitro, in vivo and from a clinical study indicate that brimonidine impacts acute inflammation of the skin by interfering with neurogenic activation and/or recruitment of neutrophils.

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The use of intermittent itraconazole therapy for superficial mycotic infections: a review and update on the ‘one week’ approach

Cited by 10 publications

References 110 publications

Pityriasis versicolor

Pityriasis versicolor

Endoplasmic reticulum stress: key promoter of rosacea pathogenesis

Brimonidine displays anti‐inflammatory properties in the skin through the modulation of the vascular barrier function

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