Jane Woods
Liverpool Hospital
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Publication
Featured researches published by Jane Woods.
Australasian Journal of Dermatology | 1994
Patricia M Lowe; Jane Woods; Anne Lewis; Alison Davies; Alan Cooper
A multicentre clinical trial has been conducted to assess the efficacy and safety of tretinoin 0.05% cream (Retin‐A®) in the treatment of photodamaged Australian skin. Subjects with cutaneous facial photodamage were randomised to treatment with tretinoin (62) or vehicle (63) cream. After an initial two week run‐in, all subjects applied the cream to the face, neck and left forearm/hand, once nightly for 24 weeks. Changes in clinical signs of photodamage and parameters of cutaneous irritation were assessed by investigators using a 7 point scale, whilst changes in signs of photodamage were rated by subjects using a 5 point scale. Changes in skin biopsies and silicone skin surface replicas were also assessed. Significant improvements in skin wrinkles, mottled hyperpigmentation, laxity, lentigines and roughness of tretinoin treated subjects were noted by investigators. Subjects receiving tretinoin noted significant improvements in skin wrinkles, tightness, colour and pores. Improvement in overall severity of photodamage was significantly greater for tretinoin treated subjects and was progressive over the study period. Histological findings included a significant increase in mean epidermal thickness. Significant topographical changes were not detected in skin surface replica sets. Cutaneous irritation, the most common side effect, was usually mild and transient. We conclude that tretinoin 0.05% cream significantly improved the appearance of photodamaged skin.
Experimental Dermatology | 2015
John W. Frew; Dunja Ana Vekic; Jane Woods; Geoffrey D. Cains
Summary of general pathogenic mechanisms Hidradenitis Suppurativa is a chronic inflammatory conditionmanifesting in recurrent painful deep-seated nodules and abscesseswith variable phenotypic presentations (1). Melnik and Plewig elo-quently describe the concept of HS as an autoinflammatory dis-ease with dysregulation of the gamma-secretase/Notch pathway(2); however, recent studies have identified ‘typical’ and ‘atypical’HS subtypes with differing morphology (nodules, comedones),lesion distribution (axillary, submammary and gluteal) and com-orbidity prevalence (1). The pathogenic hypothesis proposed byMelnik and Plewig (2) as well as reports of inconsistent responsesto systemic therapies (3,4) has led to suggestions that variablephenotypic presentations are suggestive of heterogeneous patho-genic inflammatory dysregulation within the gamma-secretase/Notch pathway paradigm (5). The complex interaction between metabolicsyndrome and HS Pascoe and Kimball describe the complex yet ‘established link’between metabolic syndrome and HS (6). Comorbidities includ-ing insulin resistance, glucose intolerance (7), dysregulated adipo-kine levels (8) (indirectly measured via BMI) (9) and bacterialsuperinfection (10) are all possible modulators of disease activity.These associations, however, have not taken into account the het-erogeneity of HS presentations and ensuing confounding relation-ships. The point prevalence of HS is quoted at 18% amongstbariatric surgery patients (11) with an odds ratio for metabolicsyndrome of 3.89 (95% CI 1.90–7.98) for a hospital HS cohort(12). However, analysis by Canoui-Poitrine et al. (1) shows statis-tically significant variation in BMI between ‘subtypes’ of HS, dis-crepancies which may confound existing results. Miller et al.(12), adjusting for BMI, revealed significant correlation betweendecreased HDL/elevated TG levels and HS in this cohort, suggest-ing an underlying metabolic disturbance independent of BMI.The role of adipose tissue as a dynamic endocrinological organacross all BMI ranges in HS requires further investigation (7).HS occurs in individuals with normal BMI (11), with 52.6% ofindividuals in Canoui-Poitrine’s analysis of BMI 25 or lower (1).The rates of metabolic derangements in this ‘atypical’ subtype areless well defined than their ‘typical’ counterparts. Hence, treat-ment focused on metabolic comorbidities may be appropriate in‘typical’ HS but their utility is as yet unclear in ‘atypical’ sub-types.
International Journal of Dermatology | 2018
Dunja Ana Vekic; Jane Woods; Peter Lin; Geoffrey D. Cains
SAPHO (synovitis, acne, pustulosis, hyperostosis, and osteitis) syndrome is a rare inflammatory condition describing the combination of skin, bone, and joint manifestations that has a heterogeneous presentation. We report a case of severe SAPHO syndrome in association with hidradenitis suppurativa and pyoderma gangrenosum in a 27‐year‐old male. The patient had an initial migratory arthritis affecting the knees, ankles, metacarpophalangeal joints, proximal interphalangeal joints, wrists, shoulder, and lower back, which progressed to a persistent arthritis and swelling at the sternum, shoulders, wrists, hands, feet, and lower back. Radiographic changes were consistent with the diagnosis of SAPHO syndrome. Serum proinflammatory cytokine levels were significantly elevated and improved substantially after 3 months of therapy. Rationale for therapy in this patient was the observation that tumor necrosis alpha antagonists have been successfully used in SAPHO syndrome, and since arthropathy was so prominent in our patient, we elected to use adalimumab combined with methotrexate.
Australasian Journal of Dermatology | 2016
Dunja Ana Vekic; John W. Frew; Jane Woods; Geoffrey D. Cains
1. Herbst RA, Uter W, Pirker C et al. Allergic and non-allergic periorbital dermatitis: patch test results of the Information Network of the Departments of Dermatology during a 5-year period. Contact Dermatitis 2004; 51: 13–19. 2. Feser A, Plaza T, Vogelgsang L et al. Periorbital dermatitis – a recalcitrant disease: causes and differential diagnoses. Br. J. Dermatol. 2008; 159: 858–63. 3. Landeck L, John SM, Geier J. Topical ophthalmic agents as allergens in periorbital dermatitis. Br. J. Ophthalmol. 2014; 98: 259–62. 4. Kligman AM. Lanolin allergy: crisis or comedy. Contact Dermatitis 1983; 9: 99–107. 5. Ellis FA. Allergic contact dermatitis due to wool fat and cholesterol. Arch. Derm. Syphilol. 1947; 56: 801–6. 6. Eiermann HJ, Larsen W, Maibach HI et al. Prospective study of cosmetic reactions: 1977–1980. North American Contact Dermatitis Group. J. Am. Acad. Dermatol. 1982; 6: 909–17. 7. Landeck L, John SM, Geier J. Periorbital dermatitis in 4779 patients – patch test results during a 10-year period. Contact Dermatitis 2014; 70: 205–12. 8. Rietschel RL, Warshaw EM, Sasseville D et al. Common contact allergens associated with eyelid dermatitis: data from the North American Contact Dermatitis Group 2003–2004 study period. Dermatitis 2007; 18: 78–81. 9. Corazza M, Masieri LT, Virgili A. Doubtful value of patch testing for suspected contact allergy to ophthalmic products. Acta Derm. Venereol. 2005; 85: 70–1.
Australasian Journal of Dermatology | 2015
Samantha Cabrera; Niranthari Chinniah; Nannette Lock; Geoffrey D. Cains; Jane Woods
With the evolving emphasis on evidence‐based practice, the use of reliable clinical scales forms an important foundation for clinical assessment. The psoriasis area and severity index (PASI) is the most widely used tool for the measurement of psoriasis severity; however, there has been some debate over the potential reproducibility of PASI scoring.
Australasian Journal of Dermatology | 2010
Veronica Preda; Christopher Henderson; Jane Woods
A 41‐year‐old Phillipino man presented with a 3‐year history of a relapsing and remitting generalized chronic pruritic erythematous papular and plaque‐like eruption. Investigations showed a persistently elevated eosinophil count. His disease was limited to cutaneous involvement with an absence of demonstrable internal organ involvement, despite extensive investigations and multidisciplinary review. Other causes of eosinophilia were excluded. A diagnosis of idiopathic hypereosinophilic syndrome was made. Our patients presentation raises a number of issues related to hypereosinophilic syndrome. In particular, relating to managing hypereosinophilic syndrome and the challenge of minimizing therapy side‐effects. Our case highlights the considerable morbidity of untreated isolated cutaneous disease, for which he was hospitalized with suicidal ideations. In a minority of reports, skin involvement is the only manifestation of hypereosinophilic syndrome.
Journal of The American Academy of Dermatology | 2018
John W. Frew; Dunja Ana Vekic; Jane Woods; Geoffrey D. Cains
2. Gooderham M, Papp K. The psychosocial impact of hidradenitis suppurativa. J Am Acad Dermatol. 2015;73(5 suppl 1): S19-22. 3. Tiplady B, Jackson SH, Maskrey VM, Swift CG. Validity and sensitivity of visual analogue scales in young and older healthy subjects. Age Ageing. 1998;27:63-66. 4. Flytstr€ om I, Stenberg B, Svensson A, Bergbrant IM. Patients’ visual analog scale: a useful method of assessing psoriasis severity. Acta Derm Venereol. 2012;92:347-348. 5. Tavakol M, Dennick R. Making sense of Cronbach’s alpha. Int J Med Educ. 2011;27:53-55.
JAAD case reports | 2018
Tevi Wain; Bonita Choy; Andrew C. Satchell; Jane Woods; John W. Frew
CLL: chronic lymphocytic leukemia IL: interleukin PRP: pityriasis rubra pilaris INTRODUCTION Pityriasis rubra pilaris (PRP) is a heterogeneous group of rare papulosquamous disorders characterized by folliculocentric keratinization. PRP has a bimodal incidence with equal gender predilection. It can be spontaneous in nature and associated with familial inheritance or as a paraneoplastic phenomenon. PRP has a variable clinical presentation with Griffiths criteria classifying PRP into 5 subtypes based on age of onset, clinical course, and prognosis. HIV-related PRP and paraneoplastic PRP have been proposed as additional subtypes. The pathophysiology of PRP remains unclear but is proposed to be triggered by a variety of as-yetunidentified triggers of chronic inflammation. Reported effective treatment with etanercept, adalimumab, ustekinumab, and secukinumab implicate tumor necrosis factor a, interleukin (IL)-12/IL-23, and IL-17 as involved in the downstream inflammatory cascade, although the variability in response indicates some degree of disease heterogeneity within Griffiths subtypes. Feldmeyer et al demonstrated upregulation of helper T cell 17 cytokines including IL-17A, IL-17F, and IL-22 in lesional skin of a patient with PRP who demonstrated a rapid resolution of disease with ustekinumab. Ustekinumab has also been reported as particularly beneficial in patients with CARD14 polymorphisms.
Australasian Journal of Dermatology | 2018
Dunja Ana Vekic; Jane Woods; Geoffrey D. Cains
We report the first case series of hidradenitis suppurativa in patients of Indigenous Australian heritage. The incidence and ethnicity of populations affected by this condition are not known. The high comorbid disease burden and socioeconomic disadvantage that is well recognised in the Indigenous Australian population poses significant challenges to therapeutic outcomes.
Internal Medicine Journal | 2016
Fiona Moghaddas; Roger Allen; Justine A. Ellis; Joanne Smart; Jane Munro; Alicia Oshlack; Angela Cox; Samar Ojaimi; Len Harrison; Sue Piper; Dianne E. Campbell; Melanie Wong; Dunja Ana Vekic; Jane Woods; Vanessa L. Bryant; Geoffrey D. Cains; Damien Chan; David Gillis; Paul Gray; Pravin Hissaria; Jonathan D. Akikusa; Peter Gowdie; Charlotte Slade; Constance H. Katelaris; Sam Mehr; Ian P. Wicks; Seth L. Masters