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Acne Scarring and Patients of African Descent
Published in Antonella Tosti, Maria Pia De Padova, Gabriella Fabbrocini, Kenneth R. Beer, Acne Scars, 2018
Aldo D. Galvez, Amy J. McMichael
Hydroquinone reduces the production of melanin by inhibiting tyrosinase, which is responsible for converting L-3,4-dihydroxyphenylalanine (DOPA) to melanin. Other mechanisms of action, including destruction of melanocytes, degradation of melanosomes, and inhibition of deoxyribose nucleic acid and ribonucleic acid synthesis, have been attributed to hydroquinone. It is available in over-the-counter concentrations of 1%–2%, with a prescription strength of 3%–4% and compounded at 5%–10%. It is recommended to begin treatment after the acne is under control, or even after 2–4 weeks of acne treatment and should be applied after application of topical acne medication. Treatment can be used as spot treatment or diffusely once to twice a day. Results may be noticed within 8–12 weeks [6]. Adverse effects include irritant and allergic dermatitis, temporary hypopigmentation of surrounding normal skin, giving a halo appearance, and the much-debated exogenous ochronosis with prolonged use. Instruction on how to apply the hydroquinone product over an entire cosmetic unit will help to avoid the localized halo side effect. Various formulations are available; some with additives such as glycolic acid, tretinoin, vitamin C, steroids, sunscreens, and microsponges enhance delivery and efficacy of hydroquinone [29].
Musculoskeletal
Published in Vincent Helyar, Aidan Shaw, The Final FRCR, 2017
A rare autosomal recessive enzyme defect (homogentisic acid oxidase) resulting in homogentisic acid deposition, particularly in the joints. This leads to joint degeneration and inflammation, known as ‘ochronosis’. Ochronosis tends to affect large joints. It may also affect the eye and can cause urinary calculi, renal failure and cardiac failure.
Histopathology
Published in Dimitris Rigopoulos, Alexander C. Katoulis, Hyperpigmentation, 2017
Exogenous ochronosis is a disease of patients with darker skin types. It develops after prolonged usage of skin bleaching products that contain hydroquinone. Patchy grayish hyperpigmentation develops in the affected areas. On histopatholgy, the picture is very similar to that seen in alkaptonuria. Orange fibers of bizarre configuration are seen in the dermis (Figure 23.20).47 The exact pathomechanism is unknown, but it is assumed that hydroquinone inhibits the homogentisic acid oxygenase.
Cosmetic skin lightening use and side effects
Published in Journal of Dermatological Treatment, 2022
Natasha Masub, Amor Khachemoune
Hydroquinone is the gold standard skin lightening agent in the United States, albeit controversial. Hydroquinone is a phenol known to competitively inhibit melanin production by acting as a tyrosinase substrate. Through the release of semiquinone free radicals, melanocyte melanin production is damaged. With prolonged application, hydroquinone can result in exogenous ochronosis characterized by progressive pigmentation of the area to which the agent is applied (Figure 2). While the mechanism behind this is unknown, it is hypothesized that hydroquinone may inhibit homogentisic acid oxidase in the dermis leading to accumulation and polymerization of homogentisic acid (32). Histologically, exogenous ochronosis is characterized by banana-shaped yellow-brown deposits in the dermis (Figure 3). While several treatments have been reported in the literature for hydroquinone-induced ochronosis, results are mixed. Topical therapies including retinoic acid and trichloroacetic acid have not demonstrated efficacy. Light therapies including Q-switched alexandrite laser (755 nm) and oral tetracycline have demonstrated encouraging results (39,40). Other reported complications of hydroquinone include dermatitis, nail discoloration, and ocular symptoms such as conjunctival pigmentation and corneal degeneration (41–43).
Inflammatory rheumatic diseases in patients with ochronotic arthropathy
Published in Modern Rheumatology, 2021
Tuba Yuce Inel, Pelin Teke Kisa, Ali Balci, Sadettin Uslu, Zumrut Arslan, Burcu Ozturk Hismi, Ulku Ucar, Nur Arslan, Fatos Onen, Ismail Sari
Alkaptonuria (AKU) is an autosomal recessive metabolic disease caused by mutations in the homogentisate 1, 2-dioxygenase (HGD) gene. The prevalence of AKU is rare, which is estimated at 1 in 250000 to 1000000 individuals [1]. The defect in the HGD enzyme leads to the accumulation of homogentisic acid (HGA) and its products in the connective tissues (ochronosis) [2]. Patients with ochronosis tend to be asymptomatic in early adulthood and become symptomatic during the second and third decades of life [2,3]. The involvement of the musculoskeletal (MSK) system, which is known as ochronotic arthropathy (OcA), mainly affects weight-bearing peripheral joints such as the knee and hip, spine, and soft tissues. Premature osteoarthritis, osteopenia, and fractures, rupture of the tendons, muscles, or ligaments due to the altered tissues could be seen in the course of the OcA [4,5].
The potential of nitisinone for the treatment of alkaptonuria
Published in Expert Opinion on Orphan Drugs, 2019
There are still challenges and research to be done to understand the variability in the presentation of tyrosinemia and ocular pathologies associated with nitisinone administration in AKU patients, it is likely there are other variable factors within individuals that are responsible for these variations given that the dose of nitisinone administered in trials affects some but not others. The validation of Raman spectroscopy as a technique that has the ability to identify differing spectra of tissues with and without ochronosis is an exciting proposition particularly as it has already been validated as being able to detect pathological matrix in other osteoarticular tissues. This may prove useful for monitoring the absence/presence of ochronosis and enable the therapy to be targeted to an individuals presentation of ochronosis in tissues, given there is variability within an individual’s connective tissues (different tissues pigment at different rates) and across affected individuals. This may also mean that there is a reduced requirement for younger populations needing the administration of nitisinone, which still requires further research in AKU populations. AKU may also benefit from future advances in gene replacement or enzyme replacement therapies, only time will tell. The fact that this disease is the result of a single enzyme defect that causes an elevation in a single tyrosine metabolite suggests that it may be a useful model to look at gene therapies for more complex conditions where some of this information is yet to be clarified.