Hey everyone welcome back to another lesson. This lesson is on vitamin b3 or niacin side effects skin deficiency. So vitamin b3 or niacin is also known as nicotinic acid or nicotinamide.
So this is what vitamin b3 looks like vitamin b3 is a water-soluble vitamin. And it is actually one of eight b vitamins now niacin deficiency the condition.
We’re going to talk about in this lesson is also known as pellagra. We’re going to talk about the clinical features and some of the other ways of diagnosing and treating it later.
Why do We Need Vitamin B3 & Niacin
On in this lesson why do we need vitamin b3 or niacin. To begin, with we need it for several processes one of them is nutrient metabolism. So very important we require vitamin b3 for nutrient metabolism. Metabolism of proteins fats and carbohydrates. And we also need it for cholesterol and fatty acid synthesis.
What are some of the sources of vitamin b3 so the dietary sources of vitamin b3. Include the following fortified cereals and grains. So, cereals and grains that have had niacin added to them artificially.
We can also find it in meat and fish legumes and to a lesser extent in nuts tea. And coffee and we can also get niacin from endogenous synthesis. So endogenous synthesis means.
We are making it inside our own bodies. Actually do this through hepatic synthesis through synthesis in our liver. And what happens is niacin or vitamin b3 is synthesized in our liver.
From tryptophan and this process requires riboflavin. And the recommended daily intake of niacin is the following 16 milligrams per day for males. 14 milligrams per day for females and for pregnant individuals 18 milligrams per day.
So why do we need vitamin b3 or niacin to begin with well. We actually need it for the production of a couple of important cofactors.
And these include nicotinamide adenine dinucleotide or nad and nicotinamide adenine dinucleotide phosphate or nad. So, with regards to nad or nicotinamide adenine dinucleotide.
This is a carrier of chemical energy allowing generation of atp adenosine triphosphate. So the cell’s energy source. But it’s also required for other enzymes as well. The enzymes that require nad as a cofactor include the following enzymes in alcohol metabolism require nad. Alcohol dehydrogenase requires nad.
We also see it in glycolysis so glyceraldehyde 3 phosphate dehydrogenase. Requires it the krebs cycle so we can see it in enzymes like alpha ketoglutarate dehydrogenase. And we can also see in fat catabolism as well with regards to nadp.
This is involved in the pentose phosphate pathway. So, we can remember the p here nadp p for pentose phosphate pathway. It’s required for enzymes in the following processes. Generated in the pentosci pathway and it’s required for enzymes in fatty acid synthesis oxidative stress.
Homeostasis in cytochrome p450 system in the liver. So again very important nad and nadp required for all these processes. Again, a lot of processes here you might not need to know. But it’s important to recognize that. A lot of times nad is a carrier of chemical energy when it’s reduced to nadh.
It allows the generation of atp in the electron transport chain in the mitochondria. And it’s also involved in other processes as well alcohol metabolism being. One of them and then nadp generated in the pentose phosphate pathogen required for processes. Like fatty acid synthesis which is important as well.
So How is vitamin b3 absorbed
Now talked about those sources of vitamin b3 including dietary sources. And hepatic synthesis or synthesis in the liver. We need both of those processes to actually maintain proper adequate amounts of vitamin b3. So when we ingest it in our diet.
You ingest it it enters into our gastrointestinal tract. And if it’s in the form of nad or nadp. When we ingest it we have to actually process. It to allow the absorption of the vitamin b3. So it could be one of these forms.
Have to convert it into nicotinamide in order to absorb it most of the time. It’s absorbed in the small intestine although. Some can be absorbed from the stomach.
And again it’s absorbed in the forms of nicotinamide and niacin. So it becomes absorbed and it enters into the bloodstream and eventually it’ll lead to the kidneys.
Where it is excreted in the urine so that was a very brief explanation of the absorption and excretion of vitamin b3. So what causes vitamin b3 deficiency so we mentioned that. We get vitamin b3 from dietary sources but also liver synthesis from tryptophan.
Leading Vitamin D3
So as we’ll see here these two both play roles in leading to vitamin b3 deficiency. The first category of causes is poor dietary intake so this makes sense. If you’re not eating enough niacin and you’re not eating enough tryptophan make it in your liver from tryptophan.
You’re going to have low amounts of niacin or low amounts of vitamin b3. One of the states is alcoholism so chronic alcoholism a lot of times.
Individuals with chronic alcoholism don’t eat a whole lot in general. They’re going to have issues with getting enough niacin. And tryptophan malnutrition for the same reason vegan diet so.
Although we did talk about some fortified grains and cereals and legumes. We often get a lot of vitamin b3 from meats and fish. So certain vegan diets can lead to a vitamin b3 deficiency fasting and starvation.
Again due to similar reasons we talked about before and anorexia nervosa as well. The second category of causes decreased synthesis.
So we need both oral intake through our diet of niacin or vitamin b3. But you also need some of that synthesis from tryptophan to make enough niacin for adequate levels of vitamin b3.
If you don’t have enough synthesis you’re going to have some vitamin b3 deficiency as well. One of them liver disease because as we mentioned before tryptophan processed into niacin in the liver.
There’s any issue with the liver this process might disrupted. Another cause of decreased synthesis is carcinoid syndrome. So carcinoid syndrome is a perineo plastic syndrome. And it’s really due to a carcinoid cancer that is producing excessive amounts of serotonin.
What happens that excessive amounts of serotonin produced from tryptophan. So it consumes tryptophan so we don’t have enough tryptophan to make vitamin b3. And another cause of decreased synthesis of vitamin b3 is deficiency of riboflavin and iron.
I don’t know if you remember me mentioning it before. But i talked about hepatic synthesis requires tryptophan. We use tryptophan to produce niacin but we also need riboflavin for this process as well.
And we also need iron i didn’t mention that before but we also need iron for this process as well.
You’re deficient in riboflavin and iron you can have a niacin deficiency or vitamin b3 deficiency. Another category of causes decreased absorption. So we just talked about absorption if you’re not absorbing it.
From your small intestine you can have issues actually having enough vitamin b3. Some of these include inflammatory bowel disease. So there’s inflammation due to crohn’s for instance. That’s affecting parts of the small intestine. This can lead to decreased absorption of vitamins in general partner disease is another cause.
This is actually an autosomal recessive condition that leads to reduced tryptophan absorption. So it is a genetic cause. But it really is a decreased absorption but really decreased synthesis as well.
So it can fit into multiple categories so reduced tryptophan absorption. You don’t have enough tryptophan to produce vitamin b3 in the liver. And then gi surgery in general if there’s large amounts of the gastrointestinal system that removed.
Then you won’t have that surface area to actually absorb vitamin b3 and then finally the last category here.
We’re going to talk about is medications so the medications. That can cause vitamin b3 deficiency especially. If they used for long periods of time include the following one of them oniazid.
So this is the one that you’re actually going to see. That most often talked about with regards to causing vitamin b3 deficiency. But we can also see with 5 fluorouracil isothioprine pyrazinamide and phenylbarbitol use as well.
Now let’s talk about pellagra or niacin deficiency. So what are the clinical features of pellagra so pellegra is the term. We use for niacin deficiency and it has a particular mnemonic. That helps remember the clinical features.
It known as the four d’s diarrhea dermatitis dementia and death. So you going to see this mnemonic used for these to help. Remember the clinical features of pellagra.
We’re going to talk about the signs and symptoms. In more detail here as well so the first is gastrointestinal. So the first d diarrhea so diary we’re going to see in plaggar. But we can also see vomiting as well.
We’re now going to look at the integumentary system. So the integumentary system is your skin. And this the second d dermatitis more specifically though the dermatitis pigmented or hyper pigmented.
So it can look often times like this so you can see here. It hyper pigmented it’s often due to photosensitivity so areas of the body. That exposed to the sun go to get this hyper pigmented dermatitis. And it’s also symmetric so as you can see in these images here.
It’s on both sides it’s bilateral it’s symmetric. So we can see it a symmetric pigmented. Or hyperpigmented dermatitis and it’s due to photosensitivity you can see it here as well.
Then we can also see something known as casel’s necklace and sorry again for the pronunciation. So you can see something like this on a patient’s neck. Who has pellagra so you can see this type of a hyperpigmented skin lesion. And again this is due to sun exposure in that area.
We can also see glossitis so in inflammation of the tongue. So it can be a red tongue and we can see alopecia so hair loss as well being a sign of pellagra.
There are also neurological findings in pellagra as well. These include anxiety peripheral neuropathy delusions. So fixed false beliefs disorientation so, patients are not sure about their surroundings depression encephalopathy. An altered mental status and can lead to dementia, and ultimately into a coma and can progress to death.
These also talk about the third d here dementia and then the fourth d would be death. And some other clinical features of plaguery include headache. Fatigue and these can also tie in with these neurological findings as well.
As you can see the clinical features of plaggar are the four d’s diarrhea dermatitis dementia and death. But we can see there’s a lot of other little details here with regards to the symptomatology.
Now again it affects gastrointestinal system integumentary system and neurological system so how plagra evaluated.
The side effects of niacin usually mild and can managed. By taking breaks from niacin or by lowering your dosage. If you experience severe side effects, consult with your healthcare provider immediately.
This is a common side effect that occurs when you take high doses of niacin (over 1g). When this happens, you should lower your dosage or take a break from taking niacin altogether.
There are many reasons. Why people might cough while taking niacin, including allergies to preservatives in the supplement or dust in the air.
How it treated
The evaluation of pellagra involves measuring niacin metabolites in the urine. So these metabolites excreted in urine and can measured.
And if the urinary excretion rate of these metabolites is less than 5.8 micromoles per day. That indicates niacin deficiency and how it treated.
Quite simply if an individual is low in niacin. We give them niacin so niacin given niacin supplementation. And it can be given by mouth, or i am so an im injection an intramuscular injection.
Again measure nice and metabolize in urine. If it’s less than 5.8 micromoles per day that. indicates deficiency. And niacin supplementation is often used and a lot of times because these individuals. May be, deficient in other b vitamins a b complex vitamin will also be oftentimes used for these individuals.