Minocycline and generalized cutaneous pigmentation

Simons, James J.; Morales, Alejandro

doi:10.1016/s0190-9622(80)80186-1

Cited by 107 publications

(38 citation statements)

References 5 publications

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“…Diffuse muddy brown discolorations in sun-exposed areas of the skin (type III reaction) induced by minocyclin, a tetracycline-derivative, are well documented side-effects presumably resulting from increased melanin production by minocyclin-stimulated melanocytes that can lead, among other things, to deposits of melanin or minocyclin/melanincomplexes at the epidermal basal membrane and in the dermis [48]. Chemotherapeutics such as bleomycin, daunorubicin, doxorubicin, cyclophosphamide and 5-fluoruracil are able to cause hyperpigmentation, supposedly by stimulation of melanogenesis via direct toxic effects on melanocytes, although the underlying mechanisms are unknown.…”

Section: Induction Of Hyperpigmentation -Specific Mechanismsmentioning

confidence: 99%

Modifying skin pigmentation – approaches through intrinsic biochemistry and exogenous agents

Brenner

Hearing

2008

Drug Discovery Today: Disease Mechanisms

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Rates of skin cancer continue to increase despite the improved use of traditional sunscreens to minimize damage from ultraviolet radiation. The public perception of tanned skin as being healthy and desirable, combined with the rising demand for treatments to repair irregular skin pigmentation and the desire to increase or decrease constitutive skin pigmentation, arouses great interest pharmaceutically as well as cosmeceutically. This review discusses the intrinsic biochemistry of pigmentation, details mechanisms that lead to increased or decreased skin pigmentation, and summarizes established and potential hyper-and hypo-pigmenting agents and their modes of action.

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Section: Induction Of Hyperpigmentation -Specific Mechanismsmentioning

confidence: 99%

Modifying skin pigmentation – approaches through intrinsic biochemistry and exogenous agents

Brenner

Hearing

2008

Drug Discovery Today: Disease Mechanisms

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“…Our patients had high-performance liquid chromatography results and a histological picture consistent with type III minocycline-related pigmentation [11]. Type III pigmentation generally develops when patients have received a high cumulative dose of minocycline and corresponds to the formation of a minocycline-melanin complex [19]. …”

Section: Commentsmentioning

confidence: 99%

Minocycline-Induced DRESS: Evidence for Accumulation of the Culprit Drug

et al. 2008

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Background: Minocycline-induced drug rash with eosinophilia and systemic symptoms (DRESS) may have a prolonged course, especially in African and African-American patients. Objectives: To determine if a prolonged course of minocycline-induced DRESS was associated with an accumulation of the culprit drug. Patients and Methods: We determined plasma and skin levels of minocycline in patients with minocycline-induced DRESS. We investigated the genetic polymorphisms of enzymes potentially involved in the detoxification of the drug, glutathione S-transferases and UDP-glucuronosyltransferases. Results and Conclusions: We demonstrated the persistence of minocycline in the plasma and/or in the skin of 7 out of 9 patients with skin phototypes V–VI. As pigmented skin contains more melanin, this could promote the formation of a melanin-minocycline complex, which could explain the severe and prolonged DRESS which may occur in this subgroup of patients.

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“…Complexes of melanin and minocycline-melanin complex are theorized to cause the pigment and melanization of the basal layer [16]. Biopsy of a patient's sun-exposed neck demonstrated membrane-bound pigment in dermal macrophages as well as pigment deposition in extracellular collagen bundles [17].…”

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

confidence: 99%

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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Minocycline and generalized cutaneous pigmentation

Cited by 107 publications

References 5 publications

Modifying skin pigmentation – approaches through intrinsic biochemistry and exogenous agents

Modifying skin pigmentation – approaches through intrinsic biochemistry and exogenous agents

Minocycline-Induced DRESS: Evidence for Accumulation of the Culprit Drug

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

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