Specimen Collection
24 hr urine collected into acid (plastic 2 litre bottle containing 20 mL 6mol/L HCl).
(The same acidified sample can also be used for 24hr urine HIAA testing)
Casual urine samples are not acceptable.
Laboratory Notes:
Minimum volume: 10mls of acidified urine.
Store at 4°C
Transport by ice pack (no need to be frozen).
Sendaway address:
Royal Prince Alfred Hospital Pathology Specimen Reception
Central Specimen Reception, Level 5, Building 77
Royal Prince Alfred Hospital
Missenden Rd,
Camperdown 2050
N.S.W.
AUSTRALIA
Declined tests:
If a test is declined, the specimen will be held for a reasonable period (usually 3 weeks but dependant on the stability of the sample). Medical practitioners seeking approval for a declined test should email the on-call Chemical Pathologist, giving the patient's name and NHI number and the clinical justification for the test. If unable to email, call the on-call Chemical Pathologist via Lablink and identify yourself as a doctor.
Reference Intervals
Vitamin B3 - MCP = 25 - 110 umol/day
Vitamin B3 - NMN = 10 - 75 umol/day
NMN values below 9 umol/day are suggestive of Vitamin B3 deficiency. Pellagra is normally not observed with urinary NMN values > 6 umol/day.
Diagnostic Use and Interpretation:
Niacin (vitamin B3) includes nicotinic acid and nicotinamide (also called nicotinic acid amide or niacinamide). It is a product of Tryptophan metabolism. Niacin is a substrate for the synthesis of co-enzymes NAD (nicotinamide adenine dinucleotide) and NADP which are essential for normal bodily functions.
Niacin deficiency causes Pellagra - which has the classic triad of dermatitis, diarrhoea, and dementia. If the condition is severe, death can result. Pellagra itself further worsens niacin deficiency by inducing diarrhoea and malabsorption.
At risk groups for Niacin deficiency include:
- those on corn and maize (without lime treatment) as main staple food sources (found in some underdeveloped countries). Lime (alkali) treatment is needed release niacin from these sources
- protein malnourished subjects
- alcoholics
- patients with inflammatory bowel diseases (with or without use of azathioprine)
- Hartnup's disease and Carcinoid syndrome (where tryptophan levels can become depleted)
- certain medications, e.g. isoniazid, azathioprine, 6 mercaptopurine, and anticonvulsants like valproic acid can also predispose to niacin deficiency.
- Concomitant pyridoxine (vitamin B6) deficiency, as pyridoxine is required as a co-factor in one of the enzymes responsible for the conversion of Tryptophan to Niacin (see figure below).
It is not niacin itself, which is measured, but the two main metabolites, MCP (methyl carboxamide pyridone) and NMN (N-methylnicotinamide) (see figure below). However, urine excretion of NMN also tends to parallel creatinine excretion, so the ratio of NMN/creatinine excretion is an insensitive marker. Excretion of NMN and MCP also vary with age and other factors. In pregnancy, especially at the 2nd and 3rd trimester, there is a physiological rise in urinary NMN.
The metabolite ratio (MCP/NMN) is considered a useful index of niacin status. The MCP/NMN ratio bypasses the influence of both age and creatinine. Normally, 40-60% of niacin is excreted in form of MCP and 20-30% in form of NMN. However, in niacin deficiency, the urine excretion of MCP is reduced more than that for NMN.
Subjects with optimal to high intake of nicotinic acid and tryptophan have MCP/NMN ratio of 1.3 to 4; an MCP/NMN ratio of <1.0 is generally considered indicative of niacin deficiency. Alcoholics and cirrhotics can have low urinary MCP to NMN ratio due to delayed oxidation of NMN to MCP, likely due to liver damage. However, if well fed, the absolute value of their urinary niacin metabolites will be high as opposed to low in pellagra. Niacin toxicity is rare unless nicotinic acid intake is greater than 1000mg/day, and usually over 2000mg/day. Symptoms include flushing,