icd 10 code for high homocysteine level

What causes high homocysteine?

Some common conditions associated with high homocysteine are:

• osteoporosis, or bone thinning
• atherosclerosis, or a buildup of fats and other substances in the arterial walls
• thrombosis, a blood vessel blood clot
• venous thrombosis, a blood clot in the veins
• heart attack
• coronary artery disease
• stroke
• dementia
• Alzheimer’s disease

What raises homocysteine levels?

Other risk factors include:

• low thyroid hormone levels
• psoriasis
• kidney disease
• certain medications
• genetics

What does a high homocysteine level mean?

Homocysteine is an amino acid produced when proteins are broken down. A high homocysteine level, also called hyperhomocysteinemia, can contribute to arterial damage and blood clots in your blood vessels. High homocysteine levels usually indicate a deficiency in vitamin B-12 or folate.

How to lower your homocysteine level?

• Low protein intake: need to make sure you are eating adequate protein. ...
• Low sulfur intake: if one does not consume enough sulfur-containing foods, homocysteine will break down in order to provide much needed cysteine for the body. ...
• Poor digestion and absorption of protein: eating protein is step one. ...

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What ICD 10 code will cover homocysteine?

ICD-10-CM Codes that Support Medical Necessity The service must be reasonable and necessary in the specific case and must meet the criteria specified in the Homocysteine Level, Serum L34419 LCD.

What is the ICD-10-CM code for homocystinuria?

ICD-10-CM Code for Homocystinuria E72. 11.

What is a high homocysteine level?

A high homocysteine level, also called hyperhomocysteinemia, can contribute to arterial damage and blood clots in your blood vessels. High homocysteine levels usually indicate a deficiency in vitamin B-12 or folate. A normal level of homocysteine in the blood is less than 15 micromoles per liter (mcmol/L) of blood.

What is the difference between Homocysteinemia and homocystinuria?

Homocysteine is an intermediary amino acid formed by the conversion of methionine to cysteine (figure 1). Homocystinuria is a rare autosomal recessive disorder characterized by severe elevations in plasma and urine homocysteine concentrations.

What diagnosis will covers homocysteine?

Homocysteine levels will be covered by Medicare to confirm Vitamin B12 or folate deficiency. known vascular disease or risk thereof (based upon abnormal lipid metabolism, high blood pressure (BP) or diabetes mellitus (DM)) for the purpose of risk stratification.

What is homocystinuria?

Homocystinuria (HCU) is a rare but potentially serious inherited condition. It means the body can't process the amino acid methionine. This causes a harmful build-up of substances in the blood and urine.

What is the cause of high homocysteine levels?

Some people have elevated homocysteine levels (Table 1) caused by a deficiency of B vitamins and folate in their diets. High homocysteine levels are also seen in people with kidney disease, low levels of thyroid hormones, psoriasis, and with certain medications (such as antiepileptic drugs and methotrexate).

Does B12 lower homocysteine levels?

The most important nutrients that help lower homocysteine levels are folate, the vitamins B12, B6 and B2, zinc and trimethylglycine (TMG).

How do you test for high homocysteine levels?

A healthcare provider such as a nurse, doctor, phlebotomist or laboratory technician takes a blood sample for the test. Then, staff in a laboratory measure the level of homocysteine in the blood.

What is the most common non genetic cause of elevated homocysteine?

CausesVitamin deficiency. Deficiencies of vitamins B6, B9 and B12 can lead to high homocysteine levels. ... Alcohol. Chronic consumption of alcohol may also result in increased plasma levels of homocysteine.Tobacco. Smokeless tobacco is implicated as risk factor for hyperhomocysteinemia. ... Genetic.

What are the types of homocystinuria?

Classical Homocystinuria is divided into two types; Vitamin B6 responsive and Vitamin B6 non-responsive. This will be discussed more later. The second route of Homocysteine metabolism is the Remethylation Pathway that depends on Folate, a B vitamin. This pathway converts Homocysteine back to Methionine.

What is the treatment for homocysteine?

Folic acid and vitamin B12 deficiencies should be corrected by supplementation. Increases in folate intake by dietary changes or fortification can also lower plasma homocysteine in vitamin-replete subjects with normal plasma homocysteine levels.

Does exercise lower homocysteine?

Although exercise increases homocysteine short-term, in the long term, it is associated with lower homocysteine levels. A systematic review of 34 studies found that regular exercise may be able to decrease homocysteine levels [91].

How can I lower my homocysteine levels naturally?

Folic acid and vitamins B-6 and B-12 have been shown to have the greatest effect at breaking down harmful homocysteine from within the body. Foods rich in folic acid, vitamins B6 and B12 include: Green leafy vegetables such as spinach, savoy cabbage, curly kale, Brussels sprouts, broccoli and asparagus.

What medications cause high homocysteine levels?

Drugs such as methotrexate, 6-azauridine, nicotinic acid, and bile acid sequestrants cause elevations in homocysteine levels.

Hyperhomocysteinemia Symptoms

The homocysteine is good for overall human health and this amino acid plays a key part to develop the tissues, muscles, bones and the bone mass. If there is any disturbance or deficiency, then the human body may suffer from critical problems.

Hyperhomocysteinemia Causes

The medical research has discovered several important and basic hyperhomocysteinemia causes through the experiments. It has been evaluated that homocysteine may elevate up to down due to disturbance or deficiency in the Vitamin B6, B9 and B12. These vitamins are more compulsory and valuable for the bone growth, muscle and tissue development.

Hyperhomocysteinemia Treatment

There are plenty of casual and routine treatments of this health disorder, but if you go through official hyperhomocysteinemia treatment, then you will have something special. The Vitamin B6, B9 & B12 supplements are the best to treat this medical condition.

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ICD-10-CM Codes that Support Medical Necessity

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What is the name of the amino acid that is formed from the conversion of methionine into cysteine?

Excess levels in the blood are purported to increase the risk of stroke, certain types of heart disease or peripheral artery disease (PAD). Homocysteine (Hcy), a sulphur-containing amino acid, is formed from the conversion of methionine into cysteine. It is usually rapidly metabolized via 1 of 2 pathways:

How is homocysteine formed?

Homocysteine (Hcy), a sulphur-containing amino acid, is formed from the conversion of methionine into cysteine. It is usually rapidly metabolized via 1 of 2 pathways:

Which pathway converts HCY to cysteine?

a vitamin B6-dependent trans-sulphuration pathway that converts Hcy to cysteine.

What vitamins are used to treat cerebral infarction?

In a double-blind, randomized controlled trial, Toole and associates (2004) examined if high doses of folic acid, vitamin B6, and vitamin B12, given to lower total Hcy levels would reduce the risk of recurrent stroke over a 2-year period compared with low doses of these vitamins. A total of 3,680 adults with non-disabling cerebral infarction were included in this study. Subjects received best medical and surgical care plus a daily multi-vitamin containing the United States Food and Drug Administration's reference daily intakes of other vitamins; patients were randomly assigned to receive once-daily doses of the high-dose formulation (n = 1,827), containing 25 mg of vitamin B6 , 0.4 mg of vitamin B12, and 2.5 mg of folic acid; or the low-dose formulation (n = 1,853), containing 200 microg of vitamin B6, 6 microg of vitamin B12 and 20 microg of folic acid. Main outcome measures were recurrent cerebral infarction (primary outcome); coronary heart disease (CHD) events and death (secondary outcomes). Mean reduction of total Hcy was 2 micromol/L greater in the high-dose group than in the low-dose group, but there was no treatment effect on any end point. The unadjusted risk ratio for any stroke, CHD event, or death was 1.0 (95 % confidence interval [CI]: 0.8 to 1.1), with chances of an event within 2 years of 18.0 % in the high-dose group and 18.6 % in the low-dose group. The risk of ischemic stroke within 2 years was 9.2 % for the high-dose and 8.8 % for the low-dose groups (risk ratio, 1.0; 95 % CI: 0.8 to 1.3) (p = 0.80 by log-rank test of the primary hypothesis of difference in ischemic stroke between treatment groups). There was a persistent and graded association between baseline total Hcy level and outcomes. A 3-micromol/L lower total Hcy level was associated with a 10 % lower risk of stroke (p = 0.05), a 26 % lower risk of CHD events (p < 0.001), and a 16 % lower risk of death (p = 0.001) in the low-dose group and a non-significantly lower risk in the high-dose group by 2 % for stroke, 7 % for CHD events, and 7 % for death. The authors concluded that in this trial, moderate reduction of total Hcy after non-disabling cerebral infarction had no effect on vascular outcomes during the 2 years of follow-up. However, the consistent findings of an association of total Hcy with vascular risk suggested that further exploration of the hypothesis is warranted and longer trials in different populations with elevated total Hcy may be necessary.

Does MS cause elevated pH?

Ramsaransing and associates (2006) stated that there is evidence that Hcy contributes to various neurodegenerative disorders, and elevated pHcy levels have been observed in patients with MS. These investigators examined if and why pHcy levels are increased in MS, and whether they play a role in the disease course. They compared pHcy in 88 patients with MS and 57 healthy controls. In the MS group, 28 had a benign course, 37 were secondary progressive, and 23 primary progressive. To explore the underlying mechanisms, these investigators measured serum levels of vitamins B6 and B12, folate, interleukin (IL)-12, tumor necrosis factor (TNF)-alpha, leukocyte nitric oxide production, and plasma diene conjugate levels (measure of oxidative stress). Mean pHcy was higher in patients (13.8 micromol/L) than in controls (10.1 micromol/L; p < 0.0001). However, there were no significant differences in Hcy levels between the three clinical subgroups of MS. Serum concentrations of vitamin B6, vitamin B12, and folate were not different between patients with MS and controls. In the MS group, there were no correlations between pHcy and the serum levels of IL-12 or TNF-alpha, leukocyte nitric oxide production, or plasma diene conjugate levels. The authors concluded that elevated pHcy occurs in both benign and progressive disease courses of MS, and seems unrelated to immune activation, oxidative stress, or a deficiency in vitamin B6, vitamin B12, or folate.

Does B12 affect MS?

Vrethem and colleagues (2003) examined if multiple sclerosis (MS) is associated with vitamin B12 deficiency. These researchers measured serum vitamin B12, plasma folate, serum methylmalonic acid (MMA), pHcy as well as cerebrospinal fluid (CSF) MMA and Hcy in 72 patients with MS and 23 controls. The mean pHcy level was significantly increased in MS patients (11.6 micromol/L) compared with controls (7.4 micromol/L) (p = 0.002). Seven patients showed low serum vitamin B12 levels but only 1 of them had concomitant high pHcy. None of them showed high serum MMA. Plasma or blood folate levels did not differ between MS patients and controls. These researchers found no significant differences in mean values or frequency of pathological tests of serum B12, serum MMA, mean corpuscular volume (MCV), hemoglobin concentration, CSF Hcy or CSF MMA between patients and healthy subjects. There were no correlations between CSF and serum/plasma levels of MMA or Hcy. Serum vitamin B12, serum MMA, pHcy, CSF Hcy or CSF MMA were not correlated to disability status, activity of disease, duration of disease or age. The authors concluded that the relevance of the increased mean value of pHcy thus seems uncertain and does not indicate functional vitamin B12 deficiency. However, they can not exclude the possibility of a genetically induced dysfunction of the Hcy metabolism relevant for the development of neuro-inflammation/degeneration. These findings indicated that, regardless of a significant increase in pHcy in MS patients, the disease is not generally associated with vitamin B12 deficiency since they did not find any other factors indicating vitamin B12 deficiency. Analysis of CSF MMA and CSF Hcy, which probably reflects the brain vitamin B12 status better than serum, are not warranted in MS. The authors concluded that B12 deficiency, in general, is not associated with MS.

Is HCY a causal risk factor for stroke?

Hankey (2006) noted that there is insufficient evidence to confirm that Hcy is a modifiable causal risk factor for stroke, or to recommend routine screening for, or treatment of, raised plasma total Hcy levels with folic acid and other vitamins, to prevent ischemic stroke.