Water-soluble vitamin deficiency and toxicity: B1-B7: Pathology review

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Water-soluble vitamin deficiency and toxicity: B1-B7: Pathology review

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A 25-year-old woman comes to the clinic due to myalgia, loss of appetite and a skin rash.  She noticed a progressively worsening skin rash around her eyes, nose and mouth over the course of the last 4 weeks. She has not had a fever, and the rash is not painful or pruritic. Five months ago, she began an intense fitness regimen with a strict diet, which includes eating multiple egg whites everyday, as well as a protein shake every morning, in which she puts several raw eggs. Temperature is 37.0°C (98.6°F), pulse is 80/min, respirations are 20/min, and blood pressure is 125/85 mmHg. BMI is 19 kg/m2. Physical examination reveals macular patches around her eyes, nose and mouth. The physician suspects a nutritional deficiency. The cause of this patient’s symptoms is determined to be a vitamin deficiency that acts as a cofactor for the enzyme acetyl-CoA carboxylase. Which of the following additional biochemical processes uses the deficient vitamin as a cofactor? 


82 year old Henry presents to the clinic with his daughter, who is really worried that he is not eating proper meals, but he refuses any help. She mentions that Henry has been living alone since his wife died, about two years ago. Upon physical examination, you notice that Henry is severely underweight; in addition, his tongue is swollen, and he has some scaling and painful lesions on his lips and at the corners of his mouth.

Next to him, 60 year old Beth is brought to the clinic by her son because she’s had several episodes of diarrhea for the past few weeks. Her son also mentions that Beth has started forgetting things, and that she has a history of chronic alcohol abuse. On physical examination, you notice multiple rough and scaly skin lesions in Beth's face, neck, and limbs.

Based on the initial presentation, both Henry and Beth seem to have some form of water- soluble vitamin deficiency or toxicity. Water-soluble vitamins include the B-complex vitamins and vitamin C. And just like all vitamins, they need to be derived from food, and inadequate dietary consumption can result in deficiency. So, in a test question, look for individuals who come from lower income countries, are at an advanced age, engage in chronic alcohol abuse, or have an eating disorder like anorexia nervosa.

Okay, now, another high yield fact is that water-soluble vitamins get easily excreted in the urine. On the other hand, fat-soluble vitamins get stored in fat cells. And that’s why the water-soluble vitamin toxicity, also known as hypervitaminosis, is much less common than that of fat-soluble vitamins. Keep in mind that hypervitaminosis can indeed occur when there’s excess intake of vitamin supplements, highly fortified foods, or medications containing a vitamin derivative.

Okay, now in this video, we’re gonna be focusing on the water-soluble vitamins B1 through B7! Let’s start with vitamin B1, also known as thiamine, which is mainly found in whole grain cereals and legumes. The active form of B1 is thiamine pyrophosphate or TPP, which acts as a cofactor for four important enzymes.

These include pyruvate dehydrogenase, which converts pyruvate coming from glycolysis into acetyl-CoA, which can then be used in the Krebs cycle, also known as the tricarboxylic acid or TCA cycle. Then, there’s α-ketoglutarate dehydrogenase, which is an enzyme of the Krebs cycle that converts α-ketoglutarate to succinyl-CoA. The third enzyme is branched-chain alpha ketoacid dehydrogenase, which is involved in the breakdown of branched chain amino acids.


Water-soluble vitamin deficiencies are mainly caused by insufficient dietary intake and chronic alcohol abuse. Their toxicities or hypervitaminosis can be caused by excess intake of supplements, fortified foods, or vitamin derivative-containing medications, but this is rare. Various types of vitamin B deficiencies can result in distinct health issues. Vitamin B1, or thiamine deficiency can cause Wernicke encephalopathy and beriberi. Vitamin B2, or riboflavin, deficiency can lead to angular cheilosis, glossitis, and corneal neovascularization.

Vitamin B3, or niacin, deficiency can cause pellagra, which presents with diarrhea, dementia, and dermatitis. Vitamin B5, or pantothenic acid deficiency can cause enteritis, adrenal insufficiency, dermatitis, alopecia, and burning feet syndrome. � Vitamin B6, or pyridoxine deficiency can lead to peripheral neuropathy and sideroblastic anemia. Vitamin B7, or biotin, deficiency can cause alopecia, dermatitis, and enteritis.


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  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Guidelines on Food Fortification with Micronutrients" WHO (2006)
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  5. "Veterinary Medicine" Saunders Limited. (2016)
  6. "Krause's Food, Nutrition, & Diet Therapy" Saunders (2000)
  7. "Does Long-Term Furosemide Therapy Cause Thiamine Deficiency in Patients with Heart Failure? A Focused Review" The American Journal of Medicine (2016)
  8. "The Discovery and Characterization of Riboflavin" Annals of Nutrition and Metabolism (2012)
  9. "Riboflavin Deficiency in Man (Ariboflavinosis)" Public Health Reports (1896-1970) (1939)
  10. "Deficiencies of essential and conditionally essential nutrients" The American Journal of Clinical Nutrition (1982)

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