Australasian Journal of Dermatology (2016) 57, e23–e25
doi: 10.1111/ajd.12262
BRIEF REPORT
Coloured sweat in two brothers: First report of familial chromhidrosis Daniel C Gaffney and Hywel L Cooper Department of Dermatology, St. Mary’s Hospital, Portsmouth Hospitals NHS Trust, Portsmouth, UK
ABSTRACT The uncommon diagnosis of chromhidrosis is most frequently made in young adults. This sweat gland disease, although benign, may impact significantly on the patient’s quality of life. We describe the first report of familial chromhidrosis of pseudo-eccrine type (pseudochromhidrosis) occurring in two brothers aged 9 and 12 years. The classification and causality of chromhidrosis is described and approaches to assessment and management are outlined. Key words: chromhidrosis, coloured sweat, pseudochromhidrosis, pseudo-eccrine chromhidrosis.
INTRODUCTION Noticeably coloured sweat is a rare phenomenon. The condition was first described in 1709 and there are numerous reports in the 19th century literature of what is thought to have been chromhidrosis of various types.1 Contemporary reports have highlighted new treatment options; however none of these have described the condition presenting in members of the same family. Like many skin conditions it can be embarrassing for patients and result in a degree of social dysfunction and emotional distress.2 It may affect patient’s clothing choices and lead to costly frequent washing or the replacement of clothing. The condition has not been linked to malignancy or to any other medical or dermatologic disease. We report two cases of brothers aged 12 and 9 years who attended dermatology clinics at different
Correspondence: Daniel C Gaffney, Department of Dermatology, St Mary’s Hospital, Milton Road, Portsmouth, Hampshire PO3 6AD, UK. Email: [email protected] Daniel C Gaffney, MRCS. Hywel L Cooper, MRCP. Conflict of interest: none Submitted 24 February 2014; accepted 10 September 2014. © 2015 The Australasian College of Dermatologists
times complaining of coloured sweat. We believe that these cases represent examples of pseudo-eccrine chromhidrosis (pseudochromhidrosis).
PATIENTS Patient one is a boy aged 12 who presented with a 6-month history of blue-green tinged sweat prominent in the axillae, neck, chest and arms, and on the face around the eyes and forehead. This had appeared a few weeks after starting a course of lymecycline for acne and had continued after the cessation of the drug. Three months prior to his presentation to dermatology he had commenced erythromycin 250 mg twice daily, also for acne treatment, which initially had no effect on his coloured sweat. His medical history included acne vulgaris, hypospadias, Gilles de la Tourette’s disorder and behavioural difficulties. His predilection for dark-coloured clothing initially raised the possibility of pseudo-eccrine chromhidrosis due to the staining of sweat by clothing dyes. However, the problem persisted even when he wore white shirts only and the blue-green discolouration of an alcohol wipe occurred when swabbed across normal looking skin, even if distant from sites of contact with dark clothing (Fig. 1). Investigations including a full blood count, urea and serum biochemistry and liver function tests were normal. On review 4 months later the discolouration of the sweat had apparently resolved. The condition recurred at some time after ceasing antibiotic treatment but he did not re-present immediately. Swabs from the skin taken at the time of initial presentation, and several further times two years later, grew skin flora including coagulase-negative staphylococci, coliforms, Enterococcus spp, diphtheroids, Candida spp. and Micrococcus spp. This case was attributed to suspected skin colonisation with chromogenic bacteria presumed to have been eliminated by the initial antibiotic treatment for acne. Our second case is the younger brother of patient one. He presented almost two years after his brother at the age of 9 with a short history of blue-green sweat most noticeable around the neck and ears and at the wrists and antecubital
Abbreviation: BTX-A
botulinum toxin type A
e24
DC Gaffney and HL Cooper
Figure 1 Handprint pattern blue-green discolouration of a white wipe after rubbing down skin of the arm of case 1.
fossae. There was no significant medical history or medications. This patient’s skin was swabbed for bacterial culture which demonstrated normal skin flora including Bacillus spp. staphylococci, coliforms, diphtheroids, Pseudomonas aeruginosa, candida spp. and Micrococcus spp. At this time it was noted that the first patient’s chromhidrosis had recurred after only a short remission and the repeat swabs were taken from patient one. An antimicrobial wash containing octenidine was prescribed for both patients to use every second day. After 6 months the younger brother’s condition had resolved but patient one continued to be affected although his condition was less noticeable.
DISCUSSION Coloured sweat may occur to some extent in up to 10% of people; however it is rarely noticeable and so rarely comes to the attention of health care professionals.3 The modern classification was described by Cilliers and de Beer in 1999.4 Apocrine chromhidrosis is the most common endogenous form of the condition. It is most frequently noticed at the face and axillae but it has been noted at the areolae5–7 and has been reported to affect the perianal area only once.1 The patient, typically in the second to fourth decade of life, complains of sweat which is black, brown, green, blue or sometimes yellow in colour, most noticeable in situations where increased sweating is stimulated. One case has recently been reported in an infant.8 This form of chromhidrosis is thought to be due to the excess secretion of © 2015 The Australasian College of Dermatologists
lipofuscins in the apocrine sweat itself. More oxidized lipofuscins form a deep colour, while lighter coloured variants may fluoresce on fluorescence microscopy.1 Eccrine chromhidrosis rarely occurs physiologically and most reports follow the ingestion in sufficient quantities of a substance that has the ability to colour eccrine sweat. The patient may complain only of the staining of white clothing. In one case a 26-year-old woman with pink stained underwear was found to have consumed large amounts of a grain chip snack containing red pigment.4 A case of yellow eccrine chromhidrosis was attributed to the ingestion of an aperient tablet coated with the food colourant tartrazine.9 Conjugated hyperbilirubinaemia may cause green staining of keratin of the hands and feet following its excretion in eccrine sweat.10 Pseudo-eccrine chromhidrosis or pseudochromhidrosis occurs when colourless sweat becomes pigmented only at the skin surface. This is noticed on the skin and may also discolour clothing. It may occur in isolated sites or widely in almost any body region. It has been reported to be due to occupational exposure to metal salts3 or from contact with dyes, pigments or chromogenic microorganisms.11–14 Panagoulias and colleagues12 recently reported a case of localised brown pseudochromhidrosis due to Corynebacterium spp, while a case of localised red sweat on the cheeks of a 9-year-old girl in India11 was also thought to be due to bacterial overgrowth. Both patients were successfully treated with a combination of oral and topical erythromycin. In some cases, bacterial overgrowth resulting in pseudochromhidrosis appears to have followed the introduction of a new medicine presumed to cause an alteration to the normal acid mantle of the stratum corneum and thus to the balance of commensals.13,14 Our two patients are both thought to have had pseudo-eccrine chromhidrosis with an infective aetiology. Typical organisms include corynebacteria, Bacillus spp. or Piedraia.11–14 It is likely that close contact allowed the transmission of the organism between the brothers. Swabs from patient two demonstrated Pseudomonas aeruginosa, which may produce the green pigment pyocyanin, accounting for the presentation, although this organism was never found on swabs from patient one. Additionally, Bacillus spp. was colonised from patient two but not patient one. Both patients were colonised by diphtheroids (corynebacteria) although causation is extremely difficult to confirm. The antibiotic acne treatment used by patient one may have affected the culture results. During assessment, the colour of the sweat may be best appreciated by wiping the skin with an alcohol wipe or examining white clothing discoloured by sweat. Yellow, green or blue sweat derived from apocrine glands may fluoresce under a Wood’s lamp.1 Possible differential diagnoses include hyperbilirubinaemia and alkaptonuria and these should be considered during the work-up. Both may discolour the sclera and the rare diagnosis of alkaptonuria may be associated with back or joint pains. Note that ochronosis caused by drugs rather than by alkaptonuria discolours the skin but not the sweat. The diagnosis of chromhidrosis and subtypes may often be made clinically, avoiding the need for
Familial chromhidrosis Table 1 Suggested investigations for a patient with suspected chromhidrosis. Full blood count, liver function tests, split bilirubin, urea and electrolytes Skin swabs for culture or smear microscopy Skin biopsy Urinary homogentisic acid (alkaptonuria) Spectrophotometry tests
invasive investigations. If necessary, the investigations listed in Table 1 may be performed. In cases of apocrine chromhidrosis, a skin biopsy may be sent for H&E and fluorescence microscopy of unstained sections,15 or alternatively for a cytological examination of a secretion smear that may demonstrate apocrine gland cells with lipofuscin granules. This may be useful if a biopsy is contraindicated. In some patients, samples of sweat, urine, sebum, skin rubbings and even water-extraction samples from clothing have been subjected to spectrophotometer analysis to aid diagnosis.4 Treatment of chromhidrosis depends on the type and cause. If it is apocrine, manual pressure can deplete the contents of the glands and improve the appearance for 2–3 days.6 Most other treatments for apocrine chromhidrosis aim to reduce perspiration. This may be attempted with antiperspirants, particularly those containing aluminium chloride,15 with capsaicin creams5–7,16 or by injection of botulinum toxin type A (BTX-A).2,17,18 In some cases, treatment has been provided based on a presumptive diagnosis without first establishing the type and causality of chromhidrosis. A resolution of symptoms following treatment with BTX-A has been used to identify the eccrine origin of the disease as the effects are limited to these glands.2,16 However, despite this assumption, there are reports of both success17 and failure19 of treatment of suspected apocrine chromhidrosis with BTX-A. In cases of true eccrine chromhidrosis any causative agent being ingested should be sought and if possible stopped or replaced. Rifampicin may turn sweat orange or red, while levadopa may colour it red, brown or black. Food or drugs coated in food colourants may also be to blame. In pseudochromhidrosis the cause should be established, if possible, remembering that drugs may again be implicated. A trial of topical or systemic antimicrobial treatment may be reasonable with a view to eradicating the causative microorganism. It should be noted, however, that it may not be possible to permanently eradicate a chromogenic organism if it forms part of an individual’s normal skin flora.
psycho-socially problematic for patients and their relatives. A thorough assessment should be undertaken with a view to establishing the diagnosis, classification and causality. Treatment should be guided by final diagnosis and patient factors.
REFERENCES 1. 2.
3.
4. 5.
6. 7.
8. 9.
10.
11. 12.
13.
14.
15.
16. 17.
18.
CONCLUSION Chromhidrosis is a rarely encountered condition in routine dermatology practice. While it is not symptomatic it can be
e25
19.
Shelly WB, Hurley HJ. Localised chromidrosis a survey. Arch. Dermatol. Syphiligr. 1954; 69: 449–71. Beer K, Oakley H. Axillary chromhidrosis: report of a case, review of the literature and treatment considerations. J. Cosmet. Dermatol. 2010; 9: 318–20. Coulson IH. Disorders of sweat glands. In: Burns D, Breathnach S, Cox N et al. (eds). Rook’s Textbook of Dermatology, Vol. 2, 8th edn. Chichester: Wiley-Blackwell, 2010; 1–22. Cilliers J, de Beer C. The case of red lingerie: chromhidrosis revisited. Dermatology 1999; 199: 149–52. Saff DM, Owens R, Kahn TA. Apocrine chromhidrosis involving the areolae in a 15-year-old amateur figure skater. Pediatr. Dermatol. 1995; 12: 48–50. Griffith JR. Isolated areolar apocrine chromhidrosis. Pediatrics 2005; 115: e239–41. Gandhi V, Vij A, Bhattacharya SN. Apocrine chromhidrosis localized to the areola in an Indian female treated with topical capsaicin. Indian J. Dermatol. Venereol. Leprol. 2006; 72: 382–3. Carman KB, Aydogdu SD, Sabuncu I et al. Infant with chromhidrosis. Paediatr. Int. 2011; 53: 283–4. Krishnaram AS, Bharathi S, Krishnan S. An interesting case of bisacodyl (dulcolax)-induced chromhidrosis. Indian J. Dermatol. Venereol. Leprol. 2012; 78: 756–8. Triwongwaranat D, Kasemsarn P, Boonchai W. Green pigmentation on the palms and soles. JAMA Dermatol. 2013; 149: 1339– 40. Thami GP, Kanwar AJ. Red facial pseudochromhidrosis. Br. J. Dermatol. 2000; 142: 1219–20. Panagoulias GS, St. Basagiannis C, Tentolouris N. Coloured sweat caused by pseudochromhidrosis. Ann. Intern. Med. 2010; 152: 198–9. Hill S, Duffill M, Lamont D et al. Pseudochromhidrosis: blue discolouration of the head and neck. Australas. J. Dermatol. 2007; 48: 239–41. Castela E, Thomas P, Bronsard V et al. Blue pseudochromhidrosis secondary to topiramate treatment. Acta Dermatol. Venerol. 2009; 89: 538–9. Cox NH, Popple AW, Large DM. Autofluoresence of clothing as an adjunct in the diagnosis of apocrine chromhidrosis. Arch. Dermatol. 1992; 128: 275–6. Marks JG Jr. Treatment of apocrine chromhidrosis with topical capsaicin. J. Am. Acad. Dermatol. 1989; 21: 418–20. Wu JM, Mamelak AJ, Nussbaum R et al. Botulinum toxin A in the treatment of chromhidrosis. Dermatol. Surg. 2005; 31: 963–5. Matarasso SL. Treatment of facial chromhidrosis with botulinum toxin type A. J. Am. Acad. Dermatol. 2005; 52: 89– 91. Barankin B, Alanen K, Ting PT et al. Bilateral facial apocrine chromhidrosis. J. Drugs Dermatol. 2004; 3: 184–6.
© 2015 The Australasian College of Dermatologists
doi: 10.1111/ajd.12262
BRIEF REPORT
Coloured sweat in two brothers: First report of familial chromhidrosis Daniel C Gaffney and Hywel L Cooper Department of Dermatology, St. Mary’s Hospital, Portsmouth Hospitals NHS Trust, Portsmouth, UK
ABSTRACT The uncommon diagnosis of chromhidrosis is most frequently made in young adults. This sweat gland disease, although benign, may impact significantly on the patient’s quality of life. We describe the first report of familial chromhidrosis of pseudo-eccrine type (pseudochromhidrosis) occurring in two brothers aged 9 and 12 years. The classification and causality of chromhidrosis is described and approaches to assessment and management are outlined. Key words: chromhidrosis, coloured sweat, pseudochromhidrosis, pseudo-eccrine chromhidrosis.
INTRODUCTION Noticeably coloured sweat is a rare phenomenon. The condition was first described in 1709 and there are numerous reports in the 19th century literature of what is thought to have been chromhidrosis of various types.1 Contemporary reports have highlighted new treatment options; however none of these have described the condition presenting in members of the same family. Like many skin conditions it can be embarrassing for patients and result in a degree of social dysfunction and emotional distress.2 It may affect patient’s clothing choices and lead to costly frequent washing or the replacement of clothing. The condition has not been linked to malignancy or to any other medical or dermatologic disease. We report two cases of brothers aged 12 and 9 years who attended dermatology clinics at different
Correspondence: Daniel C Gaffney, Department of Dermatology, St Mary’s Hospital, Milton Road, Portsmouth, Hampshire PO3 6AD, UK. Email: [email protected] Daniel C Gaffney, MRCS. Hywel L Cooper, MRCP. Conflict of interest: none Submitted 24 February 2014; accepted 10 September 2014. © 2015 The Australasian College of Dermatologists
times complaining of coloured sweat. We believe that these cases represent examples of pseudo-eccrine chromhidrosis (pseudochromhidrosis).
PATIENTS Patient one is a boy aged 12 who presented with a 6-month history of blue-green tinged sweat prominent in the axillae, neck, chest and arms, and on the face around the eyes and forehead. This had appeared a few weeks after starting a course of lymecycline for acne and had continued after the cessation of the drug. Three months prior to his presentation to dermatology he had commenced erythromycin 250 mg twice daily, also for acne treatment, which initially had no effect on his coloured sweat. His medical history included acne vulgaris, hypospadias, Gilles de la Tourette’s disorder and behavioural difficulties. His predilection for dark-coloured clothing initially raised the possibility of pseudo-eccrine chromhidrosis due to the staining of sweat by clothing dyes. However, the problem persisted even when he wore white shirts only and the blue-green discolouration of an alcohol wipe occurred when swabbed across normal looking skin, even if distant from sites of contact with dark clothing (Fig. 1). Investigations including a full blood count, urea and serum biochemistry and liver function tests were normal. On review 4 months later the discolouration of the sweat had apparently resolved. The condition recurred at some time after ceasing antibiotic treatment but he did not re-present immediately. Swabs from the skin taken at the time of initial presentation, and several further times two years later, grew skin flora including coagulase-negative staphylococci, coliforms, Enterococcus spp, diphtheroids, Candida spp. and Micrococcus spp. This case was attributed to suspected skin colonisation with chromogenic bacteria presumed to have been eliminated by the initial antibiotic treatment for acne. Our second case is the younger brother of patient one. He presented almost two years after his brother at the age of 9 with a short history of blue-green sweat most noticeable around the neck and ears and at the wrists and antecubital
Abbreviation: BTX-A
botulinum toxin type A
e24
DC Gaffney and HL Cooper
Figure 1 Handprint pattern blue-green discolouration of a white wipe after rubbing down skin of the arm of case 1.
fossae. There was no significant medical history or medications. This patient’s skin was swabbed for bacterial culture which demonstrated normal skin flora including Bacillus spp. staphylococci, coliforms, diphtheroids, Pseudomonas aeruginosa, candida spp. and Micrococcus spp. At this time it was noted that the first patient’s chromhidrosis had recurred after only a short remission and the repeat swabs were taken from patient one. An antimicrobial wash containing octenidine was prescribed for both patients to use every second day. After 6 months the younger brother’s condition had resolved but patient one continued to be affected although his condition was less noticeable.
DISCUSSION Coloured sweat may occur to some extent in up to 10% of people; however it is rarely noticeable and so rarely comes to the attention of health care professionals.3 The modern classification was described by Cilliers and de Beer in 1999.4 Apocrine chromhidrosis is the most common endogenous form of the condition. It is most frequently noticed at the face and axillae but it has been noted at the areolae5–7 and has been reported to affect the perianal area only once.1 The patient, typically in the second to fourth decade of life, complains of sweat which is black, brown, green, blue or sometimes yellow in colour, most noticeable in situations where increased sweating is stimulated. One case has recently been reported in an infant.8 This form of chromhidrosis is thought to be due to the excess secretion of © 2015 The Australasian College of Dermatologists
lipofuscins in the apocrine sweat itself. More oxidized lipofuscins form a deep colour, while lighter coloured variants may fluoresce on fluorescence microscopy.1 Eccrine chromhidrosis rarely occurs physiologically and most reports follow the ingestion in sufficient quantities of a substance that has the ability to colour eccrine sweat. The patient may complain only of the staining of white clothing. In one case a 26-year-old woman with pink stained underwear was found to have consumed large amounts of a grain chip snack containing red pigment.4 A case of yellow eccrine chromhidrosis was attributed to the ingestion of an aperient tablet coated with the food colourant tartrazine.9 Conjugated hyperbilirubinaemia may cause green staining of keratin of the hands and feet following its excretion in eccrine sweat.10 Pseudo-eccrine chromhidrosis or pseudochromhidrosis occurs when colourless sweat becomes pigmented only at the skin surface. This is noticed on the skin and may also discolour clothing. It may occur in isolated sites or widely in almost any body region. It has been reported to be due to occupational exposure to metal salts3 or from contact with dyes, pigments or chromogenic microorganisms.11–14 Panagoulias and colleagues12 recently reported a case of localised brown pseudochromhidrosis due to Corynebacterium spp, while a case of localised red sweat on the cheeks of a 9-year-old girl in India11 was also thought to be due to bacterial overgrowth. Both patients were successfully treated with a combination of oral and topical erythromycin. In some cases, bacterial overgrowth resulting in pseudochromhidrosis appears to have followed the introduction of a new medicine presumed to cause an alteration to the normal acid mantle of the stratum corneum and thus to the balance of commensals.13,14 Our two patients are both thought to have had pseudo-eccrine chromhidrosis with an infective aetiology. Typical organisms include corynebacteria, Bacillus spp. or Piedraia.11–14 It is likely that close contact allowed the transmission of the organism between the brothers. Swabs from patient two demonstrated Pseudomonas aeruginosa, which may produce the green pigment pyocyanin, accounting for the presentation, although this organism was never found on swabs from patient one. Additionally, Bacillus spp. was colonised from patient two but not patient one. Both patients were colonised by diphtheroids (corynebacteria) although causation is extremely difficult to confirm. The antibiotic acne treatment used by patient one may have affected the culture results. During assessment, the colour of the sweat may be best appreciated by wiping the skin with an alcohol wipe or examining white clothing discoloured by sweat. Yellow, green or blue sweat derived from apocrine glands may fluoresce under a Wood’s lamp.1 Possible differential diagnoses include hyperbilirubinaemia and alkaptonuria and these should be considered during the work-up. Both may discolour the sclera and the rare diagnosis of alkaptonuria may be associated with back or joint pains. Note that ochronosis caused by drugs rather than by alkaptonuria discolours the skin but not the sweat. The diagnosis of chromhidrosis and subtypes may often be made clinically, avoiding the need for
Familial chromhidrosis Table 1 Suggested investigations for a patient with suspected chromhidrosis. Full blood count, liver function tests, split bilirubin, urea and electrolytes Skin swabs for culture or smear microscopy Skin biopsy Urinary homogentisic acid (alkaptonuria) Spectrophotometry tests
invasive investigations. If necessary, the investigations listed in Table 1 may be performed. In cases of apocrine chromhidrosis, a skin biopsy may be sent for H&E and fluorescence microscopy of unstained sections,15 or alternatively for a cytological examination of a secretion smear that may demonstrate apocrine gland cells with lipofuscin granules. This may be useful if a biopsy is contraindicated. In some patients, samples of sweat, urine, sebum, skin rubbings and even water-extraction samples from clothing have been subjected to spectrophotometer analysis to aid diagnosis.4 Treatment of chromhidrosis depends on the type and cause. If it is apocrine, manual pressure can deplete the contents of the glands and improve the appearance for 2–3 days.6 Most other treatments for apocrine chromhidrosis aim to reduce perspiration. This may be attempted with antiperspirants, particularly those containing aluminium chloride,15 with capsaicin creams5–7,16 or by injection of botulinum toxin type A (BTX-A).2,17,18 In some cases, treatment has been provided based on a presumptive diagnosis without first establishing the type and causality of chromhidrosis. A resolution of symptoms following treatment with BTX-A has been used to identify the eccrine origin of the disease as the effects are limited to these glands.2,16 However, despite this assumption, there are reports of both success17 and failure19 of treatment of suspected apocrine chromhidrosis with BTX-A. In cases of true eccrine chromhidrosis any causative agent being ingested should be sought and if possible stopped or replaced. Rifampicin may turn sweat orange or red, while levadopa may colour it red, brown or black. Food or drugs coated in food colourants may also be to blame. In pseudochromhidrosis the cause should be established, if possible, remembering that drugs may again be implicated. A trial of topical or systemic antimicrobial treatment may be reasonable with a view to eradicating the causative microorganism. It should be noted, however, that it may not be possible to permanently eradicate a chromogenic organism if it forms part of an individual’s normal skin flora.
psycho-socially problematic for patients and their relatives. A thorough assessment should be undertaken with a view to establishing the diagnosis, classification and causality. Treatment should be guided by final diagnosis and patient factors.
REFERENCES 1. 2.
3.
4. 5.
6. 7.
8. 9.
10.
11. 12.
13.
14.
15.
16. 17.
18.
CONCLUSION Chromhidrosis is a rarely encountered condition in routine dermatology practice. While it is not symptomatic it can be
e25
19.
Shelly WB, Hurley HJ. Localised chromidrosis a survey. Arch. Dermatol. Syphiligr. 1954; 69: 449–71. Beer K, Oakley H. Axillary chromhidrosis: report of a case, review of the literature and treatment considerations. J. Cosmet. Dermatol. 2010; 9: 318–20. Coulson IH. Disorders of sweat glands. In: Burns D, Breathnach S, Cox N et al. (eds). Rook’s Textbook of Dermatology, Vol. 2, 8th edn. Chichester: Wiley-Blackwell, 2010; 1–22. Cilliers J, de Beer C. The case of red lingerie: chromhidrosis revisited. Dermatology 1999; 199: 149–52. Saff DM, Owens R, Kahn TA. Apocrine chromhidrosis involving the areolae in a 15-year-old amateur figure skater. Pediatr. Dermatol. 1995; 12: 48–50. Griffith JR. Isolated areolar apocrine chromhidrosis. Pediatrics 2005; 115: e239–41. Gandhi V, Vij A, Bhattacharya SN. Apocrine chromhidrosis localized to the areola in an Indian female treated with topical capsaicin. Indian J. Dermatol. Venereol. Leprol. 2006; 72: 382–3. Carman KB, Aydogdu SD, Sabuncu I et al. Infant with chromhidrosis. Paediatr. Int. 2011; 53: 283–4. Krishnaram AS, Bharathi S, Krishnan S. An interesting case of bisacodyl (dulcolax)-induced chromhidrosis. Indian J. Dermatol. Venereol. Leprol. 2012; 78: 756–8. Triwongwaranat D, Kasemsarn P, Boonchai W. Green pigmentation on the palms and soles. JAMA Dermatol. 2013; 149: 1339– 40. Thami GP, Kanwar AJ. Red facial pseudochromhidrosis. Br. J. Dermatol. 2000; 142: 1219–20. Panagoulias GS, St. Basagiannis C, Tentolouris N. Coloured sweat caused by pseudochromhidrosis. Ann. Intern. Med. 2010; 152: 198–9. Hill S, Duffill M, Lamont D et al. Pseudochromhidrosis: blue discolouration of the head and neck. Australas. J. Dermatol. 2007; 48: 239–41. Castela E, Thomas P, Bronsard V et al. Blue pseudochromhidrosis secondary to topiramate treatment. Acta Dermatol. Venerol. 2009; 89: 538–9. Cox NH, Popple AW, Large DM. Autofluoresence of clothing as an adjunct in the diagnosis of apocrine chromhidrosis. Arch. Dermatol. 1992; 128: 275–6. Marks JG Jr. Treatment of apocrine chromhidrosis with topical capsaicin. J. Am. Acad. Dermatol. 1989; 21: 418–20. Wu JM, Mamelak AJ, Nussbaum R et al. Botulinum toxin A in the treatment of chromhidrosis. Dermatol. Surg. 2005; 31: 963–5. Matarasso SL. Treatment of facial chromhidrosis with botulinum toxin type A. J. Am. Acad. Dermatol. 2005; 52: 89– 91. Barankin B, Alanen K, Ting PT et al. Bilateral facial apocrine chromhidrosis. J. Drugs Dermatol. 2004; 3: 184–6.
© 2015 The Australasian College of Dermatologists
