What are the treatments for Raised AST and ALT levels?
The treatments for some common causes of raised AST or ALT levels include: People can work with their doctor to treat NAFLD with weight loss. The doctor may advise a person to make lifestyle changes to lose weight, such as: Speaking with a nutritionist or even a personal trainer can help someone stay on track with their weight loss plan.
What is the treatment for drug-induced hyperbilirubinemia?
The treatment for drug-induced hyperbilirubinemia is cessation of the medication. When bilirubin levels are elevated above 2.5 to 3 milligrams per deciliters, patients may experience yellowing of the skin, mucous membranes and the whites of the eyes, also called jaundice, explains MedicineNet.com.
What is the role of vitamin therapy in the treatment of hyperhomocysteinemia?
If effective, the simplicity, availability, and presumably favorable side effect profile of hyperhomocysteinemia treatment with combined folic acid and oral B6- and B12-vitamin supplementation (collectively referred to in this text as vitamin therapy) makes this an attractive addition to standard medical therapy for cardiovascular diseases.
What should I do if my hemoglobin is high?
If you know you have high hemoglobin, call your healthcare provider if you experience worsening symptoms. High hemoglobin count occurs when you have unusually high levels of a specific blood protein. The blood protein hemoglobin helps carry oxygen throughout your body and takes carbon dioxide to your lungs.
Is RBC 4.83 normal?
A normal range in adults is generally considered to be 4.35 to 5.65 million red blood cells per microliter (mcL) of blood for men and 3.92 to 5.13 million red blood cells per mcL of blood for women. In children, the threshold for high red blood cell count varies with age and sex.
How do you reduce high red blood cell count?
High RBC Count TreatmentExercise to improve your heart and lung function.Eat less red meat and iron-rich foods.Avoid iron supplements.Keep yourself well hydrated.Avoid diuretics, including coffee and caffeinated drinks, which can dehydrate you.Stop smoking, especially if you have COPD or pulmonary fibrosis.More items...•
What happens if RBC count is high?
A high red blood cell count can be a sign of: Dehydration. Heart disease. Polycythemia vera, a bone marrow disease that causes too many red blood cells to be made.
What causes high RBC in blood test?
Your body may increase red blood cell production to compensate for any condition that results in low oxygen levels, including: Heart disease (such as congenital heart disease in adults) Heart failure. A condition present at birth that reduces the oxygen-carrying capacity of red blood cells (hemoglobinopathy)
What cancers cause high red blood cell count?
Overview. Polycythemia vera (pol-e-sy-THEE-me-uh VEER-uh) is a type of blood cancer. It causes your bone marrow to make too many red blood cells.
What foods lower red blood cells?
No single food will cure anemia. But eating an overall healthy diet rich in dark, leafy greens, nuts and seeds, seafood, meat, beans, and vitamin C-rich fruits and vegetables can help you get the iron you need to manage anemia.
Should I worry if my hemoglobin is high?
If you have a high hemoglobin count without other abnormalities, it's unlikely to indicate a related serious condition. Conditions that can cause a high hemoglobin count include: Congenital heart disease in adults. COPD (chronic obstructive pulmonary disease) exacerbation — worsening of symptoms.
What is normal range for RBC in blood test?
Women usually have a lower RBC count than men, and the level of red blood cells tends to decrease with age. A normal RBC count would be: men – 4.7 to 6.1 million cells per microlitre (cells/mcL) women – 4.2 to 5.4 million cells/mcL.
Is RBC 6.2 high?
Mild RBC count increase (5.5 - 6 million/ µl in adult women and 6.2 - 6.75 million/ µl in adult men): RBC count is a bit high, but it is not a matter for concern.
Is RBC 6.5 high?
A high red blood cell count is generally considered to be anything above 6.1 million red blood cells for males, 5.4 million for females, and 5.5 for children. Additional tests will help your healthcare provider determine the cause of your high red blood cell count and next steps in your care.
What is a very low RBC?
Summary. A low RBC count, also known as anemia, can affect the body's ability to transport oxygen and nutrients around the cardiovascular system. It can cause fatigue, dizziness, and heart palpitations. The most common form of anemia is iron deficiency anemia.
Your CRP level of 4.83 is a High CRP level
If your CRP is in between 0 mg/L and 3 mg/L, then you need not worry as 0-3 mg/L is the normal range for CRP. But if your CRP is lesser or greater than the above values, then there may be some problem in your body.
Consult a doctor for your CRP problem
If you take a CRP blood test and the results are not in the normal range (0-3 mg/L), your physician may recommend more tests to figure out the problem. You might also get this test if your physician thinks you have some other disease.
How the CRP Test Is Done
If your doctor wants CRP test on you, you may need a CRP blood test. During the CRP blood test, a pathologist will put a needle into your veins and take out a small quantity of blood. A pathologist is a physician in the medical field who thoroughly studies the causes and effects of disease.
Your TSH 3 level of 4.83 indicates a High TSH 3 level
If your TSH 3 is in between 0.55 uIU/mL and 4.78 uIU/mL, then you need not worry as 0.55-4.78 uIU/mL is the normal range for TSH 3. But if your TSH 3 is lesser or greater than the above values, then there may be some problem in your body.
Consult a doctor for your TSH 3 problem
If you take a TSH 3 blood test and the results are not in the normal range (0.55-4.78 uIU/mL), your physician may recommend more tests to figure out the problem. You might also get this test if your physician thinks you have some other disease.
How the TSH 3 Test Is Done
If your doctor wants TSH 3 test on you, you may need a TSH 3 blood test. During the TSH 3 blood test, a pathologist will put a needle into your veins and take out a small quantity of blood. A pathologist is a physician in the medical field who thoroughly studies the causes and effects of disease.
What are the three vitamins that are required for homocysteine metabolism?
Normal homocysteine metabolism is dependent upon adequate stores of three dietary vitamins: folic acid, vitamin B12(cobalamin), and vitamin B6(pyridoxal phosphate). Folic acid, or pteroylmonoglutamic acid, is a substrate for cellular production of tetrahydrofolate (THF), a precursor to 5-methyl-THF that is required for normal methionine synthase enzyme activity. By increasing S-adenosylmethionine (SAM) levels, folates transfer 1-carbon moieties to various organic compounds (37), thus contributing to the synthesis of key macromolecules (e.g., purines) integral to basic cellular processes, such as cell growth and proliferation (38).
How does homocysteine convert to cystathionine?
Homocysteine metabolism occurs via three pathways; i) remethylation of homocysteine to form methionine by methionine synthase in a vitamin B12and folate-dependent reaction, ii) the transsulfuration pathway, by which, after the addition of a serine group, homocysteine is converted to cystathionine by cystathionine β-synthase (CBS), and, in certain tissues such as liver and kidney, by iii) remethylation of homocysteine to methionine via betaine:homocysteine methyltransferase (BHMT) (Figure 1) (28).
What mutations cause elevated homocysteine levels?
Several genetically inherited enzyme mutations responsible for elevated homocysteine levels have been described, perhaps the most common of which encodes a cytosine to thymine mutation at nucleotide 677 (C677T) of N5,N10-methylenetetrahydrofolate reductase (MTHFR). MTHFR facilitates conversion of homocysteine to methionine by methionine synthase; impaired MTHFR activity can increase homocysteine levels by ∼25%, and may occur in up to 40% of some U.S. subpopulations (29). Despite a prevailing consensus that the homozygous T/T genotype is an independent risk factor for hyperhomocysteinemia (30, 31), evidence from observational studies has been unable to link definitively this mutation to an increased risk for CAD.
What are the different types of homocysteine?
A variety of unstable homocysteine species exist in human plasma, presented here in descending relative concentration: protein (albumin)-bound, free circulating disulfide, and sulfhydryl forms (22). Current laboratory methods detect the presence of all three forms and report this as total homocysteine concentration, but reference intervals published for clinical practice may be misleading since they are generally not corrected for factors known to influence circulating homocysteine levels (e.g., ethnicity, gender, etc.). According to the American Heart Association (AHA) advisory statement, normal homocysteine concentrations range from 5-15 μmol/L, although 12 μmol/L is regarded as elevated by others (22, 23). Intermediatelyelevated homocysteine levels are between 31-100 μmol/L, while severelyelevated levels are >100 μmol/L, and are essentially pathognomonic for the presence of an inborn error of homocysteine metabolism causing homocystinuria.
What are the risks of homocysteine?
Numerous epidemiological reports have established an increased risk for CAD, MI, stroke, venous thromboembolism, and peripheral vascular disease in patients with elevated levels of homocysteine. An early meta-analysis that included 27 retrospective and prospective studies showed an incremental increase in risk of CAD per 5 μmol/L increase in tHcy concentration (men, OR=1.6, CI 95% 1.4-1.7; women OR=1.8, CI 95% 1.3-1.9) (1). From this result, the authors extrapolated that 10% of the populations' CAD risk was attributable to hyperhomocysteinemia, and that up to 50,000 deaths from CAD could be prevented annually by homocysteine level reduction. These conclusions were supported by findings from the Homocysteine Studies' Collaboration meta-analysis (2) that showed a risk reduction for ischemic heart disease by 11% and for stroke by 19% per 3 μmol/L reduction in homocysteine concentration.
Does folic acid reduce homocysteine?
The unique biochemical profile of homocysteine is characterized by chemical reactivity supporting a wide range of molecular effects, and a tendency to promote oxidant stress-induced cellular toxicity. Numerous epidemiological reports have established hyperhomocysteinemia as an independent risk factor for cardiovascular disease, cerebrovascular disease, dementia-type disorders, and osteoporosis-associated fractures. Although combined folic acid and B-vitamin therapy substantially reduces homocysteine levels, results from randomized placebo-controlled clinical trials testing the effect of vitamin therapy on outcome in these diseases are mixed, but have generally fallen short of expectations. These results have led some to abandon homocysteine monitoring in the management of patients with cardiovascular or cognitive disorders. These trials, however, have generally included patients with only mildly elevated homocysteine levels, and have not addressed several clinical scenarios in which homocysteine level reduction may be effective, including the primary prevention of atherothrombotic disease in individuals at low- or intermediate-risk, or those with severe hyperhomocysteinemia.
Is homocysteine lowering therapy effective?
In the past decade, multiple randomized clinical trials have tested the efficacy of homocysteine-lowering therapy on various outcome measures including the secondary prevention of cardiovascular (1, 14-18) and cerebrovascular disease (19), progression of cognitive decline (20), and prevention of osteoporosis-related bone fractures (21). Within these outcome measures, conclusions from different trials are mixed, but have, in general, reported negative results. Rather than discounting altogether the potential therapeutic benefit of homocysteine reduction therapy, however, results from these studies may be useful for the enhanced targeting of those in whom hyperhomocysteinemia is a modifiable risk factor for disease. This review provides a comprehensive assessment of current principles in homocysteine pathobiology and summarizes recently published clinical data evaluating the efficacy of treatment for hyperhomocysteinemia.
