Why doesn’t excessive ingestion of carrots cause yellow discoloration of the sclera?

Great question! “Carotenoderma” refers to the yellow discoloration of the skin caused by increased serum carotenoids1.  Carotenoids are absorbed by passive diffusion from the gastrointestinal tract which are partially metabolized in the intestinal mucosa and liver to vitamin A, and then transported in the plasma into the intercellular lipids of stratum corneum of the skin which has a high affinity for carotene1,2.

The maximal accumulation of carotenoids occurs in areas with an abundance of sweat glands (eg, the palms, soles, nasolabial folds). In the absence of strateum corneum, the sclera is spared!

Of note, there are many causes of carotenoderma besides excessive ingestion of carrots.  Among foods, increased ingestion of tomatoes, tangerines, red palm oil, and squash may also be responsible1,2

Systemic diseases associated with increase in serum carotenoids (possibly related to decreased conversion to vitamin A, hyperlipidemia, or other factors) include hypothyroidism, diabetes mellitus, anorexia nervosa, nephrotic syndrome, and liver disease.

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References 

  1. Horev L, Ramot Y, Klapholz L. Yellow feet in a patient with breast and thyroid carcinoma, due to oral intake of turmeric. Drug Saf-Case Rep 2015;2:4.https://link.springer.com/article/10.1007/s40800-015-0006-4
  2. Maharshak N, Shapiro J, Trau H. Carotenoderma-a review of the literature. Int J Dermatol 2003;42:178-181. http://onlinelibrary.wiley.com/doi/10.1046/j.1365-4362.2003.01657.x/epdf

 

Contributed by Clara Yang, Medical Student, Harvard Medical School

 

Why doesn’t excessive ingestion of carrots cause yellow discoloration of the sclera?

What is an abnormal post-void residual (PVR) volume?

Although measurement of PVR is a common everyday occurrence in hospitalized patients, the threshold of what constitutes an abnormal value is often poorly defined and not standardized. However, most urologists consider volumes of 50 ml to 100 ml to constitute the lower threshold of abnormal PVR (1).

Large PVRs are associated with urinary tract infections, especially in persons at risk (e.g. diabetes, spinal cord injury), while very large PVRs (>300 ml) may be associated with an increased risk of upper urinary tract dilatation and renal insufficiency.

Chronic urinary retention is often defined as a PVR > 300 ml (2).

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References

1. Kelly CE. Evaluation of voiding dysfunction and measurement of bladder volume. Rev Urol 2004;6 (suppl 1):S32-S37. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472847

 

2. Kaplan SA, Wein AJ, Staskin DR, Roehrborn CG, Steers WD. Urinary retention and post-void residual urine in men: separating truth from tradition. J Urology 2008;180:47–54. https://www.ncbi.nlm.nih.gov/pubmed/18485378

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

What is an abnormal post-void residual (PVR) volume?

Can oral candidiasis be symptomatic without actual pseudomembranes or “thrush”?

Yes!  Although we often associate oral candidiasis with thrush or pseudomembranous white plaques, another common form of oral candidiasis seen in hospitalized patients is “acute atrophic candidiasis” (AAC), also referred to as “antibiotic sore mouth” because of its association with use of broad spectrum antibiotics (1,2). 

Despite the absence of thrush, patients with AAC often have erythematous patches on the palate, buccal mucosa and dorsum of the tongue. Common symptoms include burning sensation in the mouth (especially with carbonated drinks in my experience), dry mouth and taste buds “being off” (2).  

Aside from antibiotics, other predisposing factors for AAC include corticosteroids, HIV disease, uncontrolled diabetes mellitus, iron deficiency anemia, and vitamin B12 deficiency.

So next time you see a hospitalized patient with new onset sore, burning mouth that wasn’t present on admission, think of antibiotic sore mouth!

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References

1. Stoopler ET, Sollecito TP. Oral mucosal diseases. Med Clin N Am 2014;98:1323-1352. https://www.ncbi.nlm.nih.gov/pubmed/25443679

2. Millsop JW, Fazel N. Oral candidiasis. Clin Derm 2016;34:487-94. https://www.ncbi.nlm.nih.gov/pubmed/27343964

Can oral candidiasis be symptomatic without actual pseudomembranes or “thrush”?