Mario Badescu Skincare Lawsuit: Undisclosed Steroids

Mario Badescu Skincare Inc. is a brand that beauty influencers swear by.  From the simplistic packaging, high end price tag, and delectable scents, who wouldn't feel like a million dollars starting and ending their day with a Badescu product? 

Mario Badescu (MB) has been charged with fraudulent concealment and gross negligence among others due to the undisclosed addition of potent steroids in their Control Cream and Healing Cream which was branded as safe for daily use.  The two steroids were hydrocortisone and triamcinolone acetonide where the latter was present in higher than prescription doses. Triamcinalone is an exogenous steroid, meaning it is not produced naturally by the body. Hydrocortisone is a corticosteroid secreted by the adrenal cortex.  There are four different strengths of topical steroids: mild, moderate, potent, and very potent. Triamcinalone is classified between moderate and potent, thus, is generally avoided for use on the face.(9)

The products were advertised to have active 'botanicals' only.  Individuals were using these creams for years (~up to 14 years).  They were experiencing painful withdrawal symptoms on days where they did not use the product.  Over time, the users began to experience steroid-related conditions such as, but not limited to, cataracts, glaucoma, mood disorders, cardiovascular problems, elevated cortisol levels, adrenal system suppression and Cushing's syndrome. 

This post aims to explain how and why these disorders can come about with long-term steroid cream use.  

N.B: Steroid creams should only be used when prescribed by your doctor.  Ensure you follow their medical advice on the product's usage for the most efficacy, safety, and prevention of unwanted side effects.  If you start to get any symptoms or signs, do call your doctor immediately.  This post does not aim to give medical advice, I am not a doctor.  I am a third year medical student with a BSc (Hons) in Molecular Medicine.

One of the main drivers in cortisol release is the Hypothalamic-Pituitary-Adrenal axis (HPA axis). This is a major neuroendocrine system of the body.  The hypothalamus sits above the brain stem and under the thalamus, making up part of the diencephalon.  To keep things simple, it contains nerve fibres that enable communication between the nervous system and the endocrine system.  This enables careful regulation and control of many body processes (immune system, stress, mood, emotion, and energy) via negative and positive feedback loops. (1) The paraventricular nuclei of the hypothalamus secretes Corticotropin Releasing Hormone (CRH).  The release of CRH is dependent on various factors such as stress, pregnancy, or medication. 

The CRH travels via blood vessels to the pituitary gland (a pea-shaped structure under the thalamus). CRH binds to CRH receptors in the pituitary which stimulates the release of Adrenocorticotropic Hormone (ACTH).  This is then secreted into the blood stream to act on the adrenal glands.  

Adrenal glands sit on top of each kidney (hence sometimes referred to as suprarenal glands).  The adrenal glands have a medulla and a cortex.  In this context, it is the adrenal cortex (specifically the adrenal fasciculata) that produces the major glucacorticoid, cortisol. When levels of cortisol reach a certain point in the blood, it signals to the hypothalamus and anterior pituitary to stop secretion of ACTH and CRH.  This ensures levels of cortisol do not get too high.  By applying corticosteroids topically, it will inform the hypothalamus and pituitary gland that we have too much and cause HPA axis suppression.

Given that the MB creams had steroids at higher than prescription doses, we have an increased likelihood of experiencing adverse reactions. 

The conditions mentioned by the users are chronic diseases that will require treatment, care, and follow-up appointments for a long period of time and potentially the rest of their life. Cushing's Syndrome, for example, occurs when the body is stimulated to produce too much cortisol via ACTH.  In addition, adrenal cortex pathology can lead to the over secretion and production of cortisol. In this case, the users are said to be suffering with hypercortisolism due to corticosteroid use over a long period of time at higher than prescription doses.

Hypercorticolism can present as hirsutism (facial hair on females), hyperglycemia resulting in diabetes mellitus (or mask any latent diabetes), moon-face, osteoporosis (brittle bones, bone loss), buffalo hump, visceral/abdominal fat and thin arms, and striae (purple stripes). Hydrocortisone has mineralcorticoid activity, meaning that it acts to stimulate aldosterone which retains water and sodium in the blood. Therefore, it can lead to edema, hypertension (high blood pressure), and hypocalcemia (decreased calcium levels). (4) We also get suppression of the immune system as cortisol is vital in the 'fight or flight' response of the body. This acts to protect ourselves from immediate danger and stresses such as running from lions. The suppressed immune system increases risk of mucocutaneous infections during treatment with topical steroids. The activation of our stress response also explains the mood disorders users were experiencing. (8)

Furthermore, chronic use of steroids on the skin will result in skin atrophy and hypopigmentation by suppression of melanocytes (the cells which provide pigment or skin color). Triamcinalone is more likely to result in hypopigmentation due to its molecular size and density. On top of this, comedonal acne is a very common side effect of excess steroid use. (2) Rosacea and nodular acne with haemorrhagic crusting and pustulation can also occur. (3)

Atrophic changes in the dermis and epidermis (top layers) of the skin can be seen within 3-14 days of steroid use. (6) This causes thinning, transparency, and prominance of underlying veins. In turn, we lose connective tissue support for the dermal vasculature which causes erythema (red flushed skin), telangiectasia (red thread-like patterns), and purpura (blood spots or skin haemorrhages). This is due to suppression of collagen synthesis (collagen 1 and 3) and cell proliferation (division). (7) To add, we get inhibition of keritinocyte production, fibroblasts, and hyaluronic acid which further weakens the skin's extracellular matrix.(16)

The painful withdrawal symptoms users were experiencing can be explained by HPA axis suppression. This is due to abruptly stopping chronic steroid use, in this case, the creams. This can also be coined as secondary adrenal insufficency. Without the exogenous steroids, we get low cortisol, androgen, and ACTH levels in the individual as the body has adapted to recieving steroids from an outside source. These symptoms can present on the skin as vitiligo (depigmented patches of skin), depression, salt-cravings, headaches, chills, diarrhoea, vomiting, and other flu-like symptoms. The list of symptoms the users experienced are outlined in the full case linked below. (3) In the case of topical steroids, continued use can result in local immunosuppression, resulting in increase risk of infection as aforementioned, and rebound flares of itching, redness, and scaliness. (7)

All in all, it is difficult to say whether or not the problems these plaintiffs obtained were directly from the creams. There could be many other confounding factors in their life that could've lead them to having similar outcomes or predisposed them to such diseases, disorders, and syndromes. However, there is a clear biological explanation as to how they could've obtained these symptoms from the MB creams which justifies the lawsuit. Nonetheless, the use of undisclosed steroids, especially at these concentrations, is unacceptable by any means. The key to safe steroid use is an appropriate potency. On top of this, steroids can interact with other medications in such a way that it can lead to deterimental effects for the patient. Thus, informing doctors of your steroid usage is vital so they can prescribe, manage, and treat other conditions appropriately. This is difficult to do if your creams have steroids that you didn't know of. If the skin's condition is left unchanged or worsened, prolonged steroid use is not advised. (16)


1. Selye, Hans (1974). Stress without distress. Philadelphia: Lippincott. ISBN 978-0-397-01026-4.




5.Adverse effects of topical glucocorticosteroids. Hengge UR, Ruzicka T, Schwartz RA, Cork MJ J Am Acad Dermatol. 2006 Jan; 54(1):1-15; quiz 16-8.

6. Berth-Jones J. Topical therapy. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rooks Textbook of Dermatology. 8th ed. 73. Vol.1 UK: Blackwell Science Ltd; 2010. pp. 1–73.

7. Srinivas CR, Lakshmi C. Principles of topical therapy in dermatology. In: Valia RG, Valia AR, editors. IADVL Textbook of Dermatology. 3rd ed. Vol. 2. Mumbai, India: Bhalani Publishing House; 2008. pp. 1591–618

8. Topical steroid-induced tinea pseudoimbricata: a striking form of tinea incognito. Verma S, Hay RJ Int J Dermatol. 2015; 54(5):e192-3.



11. eczema#:~:text=With%20long%2Dterm%20use%20of,acne%2C%20rosacea%20and%20perioral%20dermatitis.






17. Brazzini B, Pimpinelli N. New and established topical corticosteroids in dermatology: Clinical pharmacology and therapeutic use. Am J Clin Dermatol. 2002;3:47–58.

18. Fisher DA. Adverse effects of topical corticosteroid use. West J Med. 1995;162:123–6.

19. Rapaport MJ, Lebwohl M. Corticosteroid addiction and withdrawal in the atopic: The red burning skin syndrome. Clin Dermatol. 2003;21:201–14.

20. Hengge UR, Ruzicka T, Schwartz RA, Cork MJ. Adverse effects of topical glucocorticosteroids. J Am Acad Dermatol. 2006;54:1–18.

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