The histopathology of subcutaneous minocycline pigmentation

Bowen, Anneli R.; McCalmont, Timothy H.

doi:10.1016/j.jaad.2007.04.028

Cited by 55 publications

(40 citation statements)

References 10 publications

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“…Collective data from clinical application have revealed that skin pigmentation occurs in some rheumatoid patients with chronic minocycline administration (36,37). Although the underlying mechanism has not yet been elucidated, it has been observed that minocyclineinduced pigment deposit in papillary dermis but not in epidermis has been observed (38,39). Given the above, minocycline may be effective in promoting repigmentation in vitiligo patients.…”

Section: Discussionmentioning

confidence: 99%

Minocycline protects melanocytes against H2O2-inducedcell death via JNK and p38 MAPK pathways

Song

Xu²,

Pan³

et al. 2008

Int J Mol Med

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Abstract.Vitiligo is an acquired and progressive disorder manifested by the selective destruction of melanocytes in the skin. An extremely high level of hydrogen peroxide (H 2 O 2 ) in plasma as well as in lesional skin has been reported in vitiligo patients. High H 2 O 2 level has been suggested to be responsible for the disappearance of melanocytes in vitiligo. JNK and p38 MAPK are strongly induced by oxidative stress and related to neuron loss in neurodegenerative disorders. Minocycline, an antibiotic possessing antioxidant activity, is capable of attenuating oxidative stress-induced neurotoxicity. To investigate whether minocycline rescues melanocytes from H 2 O 2 -induced apoptosis, cultured mouse melanocytes (B10BR) were treated with H 2 O 2 in the presence or absence of minocycline. Our data showed that H 2 O 2 decreases cell viability in a concentration-dependent manner which is attenuated by minocycline. Also, H 2 O 2 treatment activates JNK and p38 MAPK, and executive caspase 3 in B10BR cells. Minocycline significantly inhibits H 2 O 2 -induced activation of JNK, p38 MAPK and caspase 3. Collectively, we concluded that minocycline protects melanocytes against H2O2-induced apoptosis in vitro. Its protective effect is associated with the inhibition of JNK and p38 MAPK. Our findings suggest that minocycline, a clinically well-tolerated, safe antibiotic, may be used to prevent melanocyte loss in the early stage of vitiligo.

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Section: Discussionmentioning

confidence: 99%

Minocycline protects melanocytes against H2O2-inducedcell death via JNK and p38 MAPK pathways

Song

Xu²,

Pan³

et al. 2008

Int J Mol Med

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“…Light and electron microscopy-analyzed tissue sections demonstrate pigment-laden granules within perivascular macrophages [12]. These pigments stain positively with Perls' stain, indicating the presence of iron and supporting the hypothesis that the granules contain minocycline metabolites complexed with iron [11,14].…”

Section: What Is the Clinical Spectrum Of Tetracycline-induced Skin Cmentioning

confidence: 65%

Minocycline Toxicity: Case Files of the University of Massachusetts Medical Toxicology Fellowship

2012

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A 61-year-old man was brought to the emergency department (ED) for shortness of breath, fatigue, frequent falls, and bluish discoloration of his skin. The primary care physician transferred the patient due to concern for cyanosis. On presentation to the ED, the patient was oriented but appeared fatigued. The patient was afebrile and had the following vital signs: blood pressure 161/88 mmHg, pulse 71/min, respiratory rate 16/min, and oxygen saturation 100 % on room air by fingertip pulse oximetry. On physical exam, pupils were 4 mm and reactive bilaterally, extraocular movements were intact, and there was no nystagmus. Anicteric sclerae were notable for blue pigmentation (Fig. 1). Heart sounds were regular, without murmurs, rubs, or gallops. Lung sounds were clear to auscultation bilaterally. Other than ataxia, the neurological exam was unremarkable. The skin had a generalized bluish tinge, especially on the arms, with darker pigmentation on the cheeks (Figs. 2, 3 and 4). There was acne on the back and facial rosacea. Bluish discoloration was also noted under the proximal nail beds (Fig. 5). When questioned about the skin discoloration, the patient and his family members described an insidious onset. Photographs of the patient from years ago confirmed that this was not congenital. Medical history included acne, orthostatic hypotension, and Parkinson's disease, for which a deep brain stimulator had been surgically implanted. A comprehensive medication list was not immediately available; however, the patient denied any recent medication additions or adjustments. The patient was unemployed, denied any recent travel, and no other members of his household were complaining of fatigue or similar blue skin discoloration.

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“…On hematoxylin and eosin stain, there were round green-gray globules of flocculent material in the subcutis that are non-polarizable and non-refractile, and range in diameter from 0.005 to 0.1 mm. They did not stain with Fontana or Perls' stains, but turned brown with the Fontana preparation [1].…”

Section: Introductionmentioning

confidence: 89%

“…Cutaneous hyperpigmentation is a well-documented, cosmetically bothersome complication of minocycline therapy [1] that may occur in 3-14% of the patients [2]. Pigment stains with Fontana Masson and Perls' stain, or both.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Resolution of blue minocycline pigmentation of the face after fractional photothermolysis

Izikson

Anderson

2008

Lasers Surg Med

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The histopathology of subcutaneous minocycline pigmentation

Cited by 55 publications

References 10 publications

Minocycline protects melanocytes against H2O2-inducedcell death via JNK and p38 MAPK pathways

Minocycline protects melanocytes against H2O2-inducedcell death via JNK and p38 MAPK pathways

Minocycline Toxicity: Case Files of the University of Massachusetts Medical Toxicology Fellowship

Resolution of blue minocycline pigmentation of the face after fractional photothermolysis

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