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is a gene which has a much higher positive prevalence in certain auto-immune/autoinflammatory diseases such as Spondyloarthritis, Uveitis/Iritis, Crohns Disease, Ulcerative Colitis and Psoriasis. Positive HLA-B27 affects people in multiple ways, when it comes to Spondyloarthritis in related to musculoskeletal (MSK). Approximately 90% (male) and 85% (female) positivity in AxSpA Approximately 40-50% positivity in Psoriatic Arthritis (PsA).

The prevalence of HLA-B27 positivity in the general population is around 8-12% although its frequency is lower in African American, South American and Middle Eastern populations than in others.HLA-B27 is the most important genetic factor for development risk of Axial spondyloarthritis (AxSpA) but there are other implicated genetic markers, all of which do vary for different populations.

Under-representation of the groups with lower HLA-B27 positivity in research and epidemiology is an issue and inclusion of these groups could provide information on other subsets. Don’t over rely on HLA-B27 in clinical practice, the interplay of the complicating factors of axial vs peripheral, population variations and HLA-B27 negative Spondyloarthritis means that interpretation is best left to Rheumatologists.

A Key Driver in Obesity-Related HFpEF

The link between obesity & HFpEF is critical. 

Epicardial adipose tissue (EAT) 

is not just storage— it’s an active organ promoting myocardial dysfunction.

EAT drives: 

➡️Fibrosis 

➡️Inflammation 

➡️Oxidative stress 

➡️Diastolic dysfunction

Understanding EAT’s  is crucial for developing new personalized therapies. 

Heart failure with preserved ejection fraction (HFpEF) 

is a growing global health problem characterized by high morbidity and mortality, with limited effective therapies available. 

Obesity significantly influences haemodynamic and structural changes in the myocardium and vasculature, primarily through the accumulation and action of visceral adipose tissue. 

Particularly, epicardial adipose tissue (EAT) contributes to HFpEF through inflammationand lipotoxic infiltration of the myocardium. 

However, the precise signalling pathways leading to diastolic stiffness in HFpEF require further elucidation. 

This review explores the dynamic role of EAT in health and disease. 

Drawing upon insights from studies in other conditions, we discuss potential 

EAT-mediated inflammatory pathways in HFpEF and 

how they may contribute to functional and structural myocardial and endothelial derangements, including 

•intramyocardial lipid infiltration, •fibrosis, 

•endothelial dysfunction, •cardiomyocyte stiffening, and 

•left ventricular hypertrophy. 

Lastly, we propose potential targets for novel therapeutic avenues.

EAT as a therapeutic target in HFpEF

The phenotypic diversity of HFpEF and the interplay with different comorbiditieswarrant a tailored treatment approach. 

In the context of the obesity-related HFpEF phenotype, targeting the pathological transformation and underlying inflammatory pathways mediated by EAT may present new therapeutic avenues. 

We therefore present therapeutic options that pose a clinical benefit that arise from changes to EAT or EAT-mediated pathways.

1) Sodium-glucose cotransporter-2 inhibitors(SGLT2i), like dapagliflozin and empagliflozin, are the first type of pharmacological drugs to reduce the risk of heart failure–related hospitalization in HFpEF trials.

Given the low expression of SGLT2 in cardiomyocytes, it is likely that SGLT2i mediate their positive effects in HFpEF by off-target mechanisms in the myocardium.

At least in part, these effects might be mediated by EAT. 

Upon SGLT2i administration, EAT volume decreases and glucose uptake by EAT is enhanced, suggesting that these types of drugs might improve EAT’s secretome and may improve metabolic regulation associated with insulin resistance in obesity.

Furthermore, SGLT2i-treated patients show a reduction of ECM and cardiomyocyte volume, along with a decrease in inflammatory biomarkers, such as FABP4, IL-1, IL-6, and TGF-β, indicating a role in improving myocardial inflammation and fibrosis.

Additionally, SGLT2i show a mild, sustained diuretic effect that can improve volume overload and congestion seen in HFpEF, while reducing the need for diuretics use.

2)Glucagon-like peptide 1 agonists (GLP-1a), such as semaglutide and liraglutide, are a class of anti-diabetic drugs known for their glucose-lowering effects and insulin sensitization, which show a rapid and significant reduction of EAT thickness independent of body weight loss.

Clinical trials in patients with HFpEF show symptom reduction and exercise capacity improvement after GLP-1a administration, across the entire obesity spectrum.

It is suggested that part of the effect of GLP-1a might be mediated by EAT, given that this fat depot expresses specific GLP-1 receptors.

While GLP-1a primarily enhances insulin sensitivity, in EAT, it induces adipocyte browning through activation of the AMPK pathway and reduces local adipogenesis by improving FFA oxidation.

However, a reduction in EAT is likely accompanied by simultaneous reductions in other fat depots. GLP-1a reduces both VAT and SAT in equal proportions, and these reductions correspond with overall weight loss.

However, due to the presence of specific GLP-1 receptors on EAT, these agonists may directly remodel EAT into a more cardioprotective fat depot, and therefore have a direct effect mediated by EAT, independent of overall weight loss.

3)Bariatric surgery causes drastic and often lasting weight loss, triggering favourable metabolic changes in obese patients.

Significant weight loss is typically accompanied by a reduction of abdominal and visceral fat depots, including EAT.

Although robust and longitudinal data in patients with HFpEF is lacking, significant weight loss may improve haemodynamics, exercise capacity, and symptoms.

This effect could be mediated, at least in part, by reducing EAT-mediated pericardial constraint, which may alleviate pressure on the LV and improve its (diastolic) function.

4)Statins, particularly atorvastatin, show improved cholesterol profiles and reduction in EAT.

Known for their lipid-lowering and anti-inflammatory effects, statins could influence EAT expansion and hamper the secretion of proinflammatory molecules, contributing to improvements in cardiovascular health. 

While statins are not recommended in the guidelines for HFpEF treatment, they are often prescribed for patients with HFpEF to address cardiovascular comorbidities, such as hypertension, CAD, and dyslipidaemia.

Furthermore, some suggest that early initiation of statin use is associated with improved outcomes in HFpEF, although this is a topic of current debate.

is a growing global health problem characterized by high morbidity and mortality, with limited effective therapies available. 

Obesity significantly influences haemodynamic and structural changes in the myocardium and vasculature, primarily through the accumulation and action of visceral adipose tissue. 

Particularly, epicardial adipose tissue (EAT) contributes to HFpEF through inflammation and lipotoxic infiltration of the myocardium. 

However, the precise signalling pathways leading to diastolic stiffness in HFpEF require further elucidation. 

This review explores the dynamic role of EAT in health and disease. 

Drawing upon insights from studies in other conditions, we discuss potential 

EAT-mediated inflammatory pathways in HFpEF and 

how they may contribute to functional and structural myocardial and endothelial derangements, including 

intramyocardial lipid infiltration, fibrosis, 

endothelial dysfunction, cardiomyocyte stiffening, and left ventricular hypertrophy. 

Novel therapeutic avenues are available.

is an infectious disease caused by a gram-negative bacterium called Burkholderia pseudomallei. Most people exposed to B. pseudomallei experience no symptoms, but complications can range from fever and skin changes to pneumonia, abscesses, and septic shock, which can be fatal. 

Approximately 10% of people with melioidosis develop symptoms that last longer than two months, termed “chronic melioidosis”. 

Melioidosis is a serious and often underdiagnosed infectious disease caused by the environmental bacterium Burkholderia pseudomallei. 

It’s sometimes called “Whitmore’s disease” and is endemic to tropical and subtropical regions, especially Southeast Asia, northern Australia, and increasingly parts of India. 

Melioidosis—caused by Burkholderia pseudomallei—has seen a surge of research interest recently, especially due to its expanding global footprint and potential as a biothreat. 

Recent advances: 

Emerging infections with Melioidosis—caused by Burkholderia pseudomallei—has seen a surge of research interest recently, especially due to its expanding global footprint and potential as a biothreat. —a highly pathogenic, Gram-negative β-proteobacterium. 

B. pseudomallei is a saprophyte found in soil, groundwater, stagnant streams, rice paddies, and ponds. 

Although melioidosis is mainly endemic in Southeast Asia and northern Australia, it is also increasingly reported in regions outside the Asia-Pacific region including India, Mauritius, the Americas, and Africa. 

Melioidosis can present as an acute, subacute, or chronic process. 

Disease manifestations

include subclinical infections, localized abscesses, severe pneumonia, and fulminant sepsis. 

Case fatality rates ranged from 19 to 36% in endemic areas. Although the epidemiology and routes of transmission are not yet fully understood, it is believed that melioidosis is acquired through contact with contaminated soil and water by percutaneous inoculation, inhalation of aerosols, and ingestion.

The incubation period of melioidosis varies widely from two days to 62 years. Human cases are often spatially and temporally clustered, following heavy rains and winds with resultant human exposure to soil and water B. pseudomallei also causes melioidosis in a wide range of animals in endemic areas. In Hong Kong, melioidosis is an endemic disease not only in humans but also in captive marine mammals and birds, including bottlenose dolphins, 

California sea lions, pilot whales, and zebra 

Transmission & Risk Factors. 

B. pseudomallei thrives in soil and surface water. Infection typically occurs through:• Inhalation of contaminated dust or water droplets• Ingestion of contaminated water or food• Direct contact with contaminated soil or water via skin abrasions or woundsHigh-risk groups include:• People with diabetes, chronic kidney or lung disease, cancer, or alcohol use disorder• Farmers, construction workers, and others exposed to muddy soil or floodwaters 

Clinical Manifestations

Melioidosis is known for its wide spectrum of presentations:• Localized infection: Skin ulcers, abscesses• Pulmonary infection: Cough, chest pain, high fever—often mistaken for TB-Tuberculosis & Chest Diseases

Localized Skin Infections. Swelling, redness, and ulceration around a woundAbscess formationPulmonary (Lung) InfectionCough, often with mucus or phlegm. Chest pain. Fever. Difficulty breathing

Septicemia (Blood Infection)

High fever and chills. 

Abdominal discomfort. 

Confusion or dizziness.

Muscle or joint pain 

Disseminated Infection 

Abscesses in multiple organs (liver, spleen, lungs). 

Weight loss and fatigueMuscle aches and joint pain. 

Disseminated infection: Sepsis, organ abscesses (liver, spleen, prostate), joint and bone involvement, neurological symptoms. 

Symptoms may appear within 1–3 weeks, but latent infections can emerge months or even years later.

Predisposing factors:

Diabetes mellitus is one of the most important risk factors in developing melioidosis. 

The disease should be considered in anyone who has spent time in endemic areas who develops a fever, pneumonia, or abscesses in their liver, spleen, prostate, or parotid gland. Latent infections as pseudomallei can remain latent in the human body for up to 29 years until it is reactivated during human immunosuppression or stress response. However, the site of bacteria during latent infection and the mechanism by which they avoid immune recognition for years are both unclear.
Amongst mechanisms suggested are: residing in the nucleus of the cell to prevent being digested, entering a stage of slower growth, antibiotic resistance, and genetic adaption to the host environment. 

Granulomas (containing neutrophils, macrophages, lymphocytes, and multinucleated giant cells) formed at the infection site in melioidosis have been associated with latent infection in humans.

Diagnosis & Treatment

Diagnosis: Blood or abscess fluid cultures are the gold standard.

Misdiagnosis is common.

Culture Microscopy. By microscopy, 

B. pseudomallei is seen as gram-negative and rod-shaped, with bipolar staining similar in appearance to a safety pin. 

Bacteria can sometimes be seen directly in clinical samples from infected people; however, identification by light microscopy is neither specific nor sensitive. Immunofluorescence microscopy is highly specific for detecting bacteria directly from clinical specimens, but has less than 50% sensitivity. Imaging 

Various imaging modalities can also help with the diagnosis of melioidosis. 

In acute melioidosis with the spreading of the bacteria through the bloodstream, the chest X-ray shows multifocal nodular lesions. 

It may also show merging nodules or cavitations. 

For those with acute melioidosis without the spread to the bloodstream, chest X-ray most commonly shows upper lobe consolidation or cavitations. In chronic melioidosis, the slow progression of upper lobe consolidation of the lungs resembles tuberculosis. 

For abscesses located in other parts of the body apart from the lungs, especially in the liver and spleen, CT scan has higher sensitivity when compared with an ultrasound scan. In liver and splenic abscesses, an ultrasound scan shows “target-like” lesions while a CT scan shows “honeycomb sign” (abscess with loculations separated by thin septa) in liver abscesses. 

For melioidosis involving the brain, MRI has higher sensitivity than a CT scan in diagnosing the lesion. MRI shows ring-enhancing lesions for brain melioidosis

Prevention

Bacterial culture has 60% sensitivity in diagnosing melioidosis.

B. pseudomallei is never part of human flora. Therefore, any growth of the bacteria is diagnostic of melioidosis.
Other samples such as throat, rectal swabs, pus from abscesses, and sputum can also be used for culture. However, culture from CSF is difficult because in one case series, only 29% of the neuromelioidosis cases are culture-positive. When bacteria do not grow from people strongly suspected of having melioidosis, repeated cultures should be taken as subsequent cultures can become positive B. pseudomallei can be grown on any blood agar, MacConkey agar, and agar containing antibiotics such as Ashdown’s medium (containing gentamicin)nand Ashdown’s broth (containing colistin for better isolation of B. pseudomallei from other types of bacteria. Agar plates for melioidosis should be incubated at 37 °C (98.6 °F) in air and inspected daily for four days. On the agar plates, B. pseudomallei forms creamy, non-haemolytic, colonies after 2 days of incubation. After 4 days of incubation, colonies appear dry and wrinkled. Colonies ofB. pseudomallei that are grown on Franci’s medium (a modification of Ashdown medium with gentamicin concentration increased to 8 mg/L and neutral red indicator replaced with 0.2% bromocresol purple) are yellowed to symptom overlap with TB and other infections.

Treatment:

Intensive phase: IV antibiotics (e.g., ceftazidime or meropenem) for 2–8 weeks

Eradication phase: Oral antibiotics (e.g., trimethoprim-sulfamethoxazole) for 3–6 months to prevent relapseDelayed diagnosis and treatment can lead to mortality rates as high as 90% in severe cases. doves. 

Treatment of melioidosis can be difficult, as B. pseudomallei is often resistant to multiple antibiotics, and a prolonged course of antibiotics is required to prevent disease relapse. Due to the severity of melioidosis and aerosol transmissibility of the infectious agent, B. pseudomallei has been classified as a category B bioterrorism and Tier 1 select agent by the Center for Disease Control, USA.

Prevention – Efforts to prevent melioidosis include: wearing protective gear while handling contaminated water or soil, practicing hand hygiene, drinking boiled water, and avoiding direct contact with soil, water, or heavy rain.

There is little evidence to support the use of melioidosis prophylaxis in humans. 

The antibiotic co-trimoxazole is used as a preventative only for individuals at high risk of getting the disease after being exposed to the bacteria in laboratory settings.

Public Health Implications. Melioidosis is increasingly recognized as a neglected tropical disease. 

Its burden is underestimated, especially in resource-limited settings. 

Climate change, extreme weather events, and expanding endemic zones (including parts of India) are raising global concern.

Vaccine Development Breakthroughs.

Researchers are actively pursuing vaccines to combat melioidosis, 

with several promising candidates emerging: Over the years, numerous different strategies have been explored to develop melioidosis vaccines. Based on the choice of protective antigens, many of the resulting candidates would also be predicted to provide some level of protection against Burkholderia mallei, the etiologic agent of glanders. Using these approaches, several promising melioidosis and glanders candidates have been identified with pre-clinical animal studies providing valuable insights into the immunogenic and protective capacities of these potential vaccines. Collectively, this review summarizes recent advancements in melioidosis vaccine research and highlights critical findings that will help guide a path toward the development of a safe, effective and affordable vaccine to combat disease caused by B. pseudomallei.- Subunit vaccinesusing protective antigens from B. pseudomallei have shown strong immunogenicity in preclinical modelsYet there are no vaccines available for humans 

Hand and Skin Hygiene. 

Wash hands thoroughly with soap and clean water after handling soil or water in affected areas, particularly before eating or drinking.

Getting enough vitamin D helps the growth and development of bones and teeth. It may also provide improved resistance to certain diseases.

Vitamin D is a fat-soluble vitamin in a family of compounds that includes vitamins D1, D2, and D3.

Your body produces vitamin D naturally when it’s directly exposed to sunlight. You can also get vitamin D from certain foods and supplements to ensure adequate levels of the vitamin in your blood.

Vitamin D has several important functions. Perhaps the most vital are regulating the absorption of calcium and phosphorus and healthy immune system function. 

Getting enough vitamin D is important for the typical growth and development of bones and teeth and for improving resistance to certain diseases.

Here is more information about the benefits of vitamin D, its downsides, how much you need, and foods with vitamin D.

1. Vitamin D may fight disease

In addition to its primary benefits, research suggests that vitamin D may also play a role in:

Reducing the risk of multiple sclerosis (MS): A 2017 review
 of population-based studies found that low levels of vitamin D are linked with an increased risk of MS.

Decreasing the chance of heart disease: Low vitamin D levels have been linked to increased risk of heart diseases such as hypertension, heart failure, and stroke. However, it’s unclear
 whether vitamin D deficiency contributes to heart disease or indicates poor health when you have a chronic condition.

Reducing the likelihood of severe illnesses: Although studies
 are mixed, vitamin D may make severe flu and COVID-19 infections less likely. A recent review found that low vitamin D levels contribute to acute respiratory distress syndrome. 

Supporting immune health: People who do not have adequate vitamin D levels might be at increased risk of infections and autoimmune diseases, such as rheumatoid arthritis, type 1 diabetes, and inflammatory bowel disease.

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2. May regulate mood and reduce depression

Research has shown that vitamin D might play an important role in regulating mood and decreasing the risk of depression. A review of 7,534 people found that those experiencing negative emotions who received vitamin D supplements noticed an improvement in symptoms. Vitamin D supplementation may help people with depression who also have a vitamin D deficiency.

Another study identified low vitamin D levels as a risk factor for more severe fibromyalgiasymptoms, anxiety, and depression.

3. May support weight loss

People with higher body weights have a greater chance of low vitamin D levels, and some studies suggest there may be a link between vitamin D and obesity, though more research is needed to verify this.

In an older study, people taking daily calcium and vitamin D supplements lost more weight than subjects taking a placebo supplement. The researchers suggest that the extra calcium and vitamin D may have had an appetite-suppressing effect.

Current research doesn’t support the idea that vitamin D causes weight loss, but there appears to be a relationship between vitamin D and weight. 

Vitamin D deficiency 

Several factors can affect your ability to get adequate vitamin D from sunlight alone.

You may be less likely to absorb enough vitamin D from the sun if you:

live in an area with high pollution

use sunscreen

spend most of your time indoors

live in a big city where buildings block sunlight

have darker skin (The higher the levels of melanin, the less vitamin D your skin can absorb.

These factors can increase your risk of vitamin D deficiency, so it’s important to get some of your vitamin D from sources other than sunlight.

What are the signs you need vitamin D?

The symptoms of a vitamin D deficiency in adults may include:

tiredness, aches, and pains

severe bone or muscle pain or weakness

stress fractures, especially in your legs, pelvis, and hips

A healthcare professional can diagnose a vitamin D deficiency by performing a simple blood test. 

If you have a deficiency, your doctor may order X-rays to check the strength of your bones.

Is it good to take vitamin D every day?

If you receive a diagnosis of vitamin D deficiency, a healthcare professional will likely recommend that you take vitamin D supplements. If you have a severe deficiency, they may instead recommend high dose vitamin D tablets or liquids. 

You should also make sure to get vitamin D through sunlight and the foods you eat.

Risks of getting too much vitamin D

If you take excessive amounts of vitamin D supplements, you may get too much of it. However, this is unlikely to happen through diet or sun exposure because your body regulates the amount of vitamin D produced through sun exposure.

Vitamin D toxicity can lead to an increase in your blood calcium levels. This can result in a variety of health issues, such as:

frequent urination

apathy

vomiting

abdominal pain

dehydration

confusion

increased thirst

What food is highest in vitamin D?

Some foods contain vitamin D naturally, and others are fortified with it. You can find vitamin D 

in the following foods:

salmon

sardines

herring

canned tuna

cod liver oil

beef liver

egg yolk

regular mushrooms and those treated with ultraviolet light

milk (fortified)

certain cereals and oatmeals (fortified)

yogurt (fortified)

orange juice (fortified)

It can be hard to get enough vitamin D each day through sun exposure and food alone, so taking vitamin D supplements could help.

How much do you need?

There has been some debate over the amount of vitamin D required for optimal functioning. Recent studies indicate that we need more vitamin D than previously thought.

Some of the main controversies surrounding vitamin D

 are:

standardization of methods for measuring vitamin D levels

the difference between free and total vitamin D testing

defining low vitamin D status (insufficiency versus deficiency)

screening versus treatment

vitamin D threshold for the general population relative to a particular condition (such as pregnancy or nursing) and health issues (such as kidney failure or osteoporosis)

Blood serum levels considered adequate range from 50–100 nanomoles per liter (nmol/L). Depending on your blood level, you may need more vitamin D.

The Recommended Dietary Allowances for vitamin D are as follows: 

infants (0–12 months): 10 micrograms (mcg) or 400 international units (IU)Trusted Source

children and teens: 15 mcg (600 IU)

adults ages 18–70: 15 mcg (600 IU)

adults over age 70: 20 mcg (800 IU)

pregnant people or those who are breastfeeding to chestfeeding: 15 mcg (600 IU)

Frequently asked questions

What does vitamin D help with the most?

Vitamin D mainly helps the body absorb and retain calcium and phosphorus, which are crucial for maintaining strong bones. This means it’s really important for bone health.

How can I raise my vitamin D level quickly?

To increase your vitamin D levels, you can spend more time in the sun, take a supplement, and include certain foods in your diet. If you spend more time outdoors, make sure to use sunscreen.

Just one thing

Try this today: Add fish to your diet a couple of times per week to help boost your vitamin D intake. Try salmon in a mustard sauce, grilled sardines, or canned tuna on a salad to create different meal options.

The bottom line

Vitamin D has many potential benefits. It may reduce the risk of certain diseases, help improve mood reduce depression symptoms, and help with weight management. 

It’s hard to get enough vitamin D through your diet alone, so you may want to ask a healthcare professional for a blood test and consider taking a vitamin D supplement. 

25-Hydroxy Vitamin D Test

Doctors use the 25-hydroxy vitamin D test to monitor your vitamin D levels. Low levels can mean you need to spend more time outdoors or adjust your diet. But it can also occur with certain medical conditions.

Vitamin D helps your body absorb calcium and maintain strong bones throughout your entire life. Your body produces vitamin D when the sun’s UV rays contact your skin. Other good sources of the vitamin include fish, eggs, and fortified dairy products. It’s also available as a dietary supplement.

Vitamin D must go through several processes in your body before your body can use it. The first transformation occurs in the liver. Here, your body converts vitamin D to a chemical known as 25-hydroxyvitamin D, also called calcidiol.

The 25-hydroxy vitamin D test is the best way to monitor vitamin D levels. The amount of 25-hydroxyvitamin D in your blood is a good indication of how much vitamin D your body has. The test can determine if your vitamin D levels are too high or too low.

The test is also known as the 25-OH vitamin D test and the calcidiol 25-hydroxycholecalcifoerol test. It can be an important indicator of osteoporosis (bone weakness) and rickets (bone malformation).

Why is a 25-hydroxy vitamin D test done?

Your doctor may request a 25-hydroxy vitamin D test for several different reasons. It can help them figure out whether too much or too little vitamin D is causing bone weakness or other abnormalities. It can also monitor people who are at risk for having a vitamin D deficiency.

Those who are at high risk of having low levels of vitamin D include:

people who don’t get much exposure to the sun

older adults

people with obesity

babies who are breastfed only (formula is usually fortified with vitamin D)

people who have had gastric bypass surgery

people who have a disease that affects the intestines and makes it difficult for the body to absorb nutrients, such as Crohn’s disease

Your doctor may also want you to do a 25-hydroxy vitamin D test if they’ve already diagnosed you with a vitamin D deficiency and want to see if treatment is working.

How is the 25-hydroxy vitamin D test performed?

Your doctor will tell you not to eat anything for four to eight hours before the test.

The 25-hydroxy vitamin D test requires a common blood test. Your healthcare provider will draw blood from a vein in your arm using a needle. A quick finger prick will more than likely provide enough for a blood sample in children and infants.

Evaluating the results of a 25-hydroxy vitamin D test

Results will depend on your age, sex, and the testing methods used. Results can also slightly vary from lab to lab.

According to the Office of Dietary Supplements (ODS), levels of vitamin D are measured by the 25-hydroxy level in nanomoles/liter (nmol/L) or nanograms/milliliter (ng/mL). The results can indicate the following:

deficiency: less than 30 nmol/L (12 ng/mL)

potential deficiency: between 30 nmol/L (12 ng/mL) and 50 nmol/L (20 ng/mL)

normal levels: between 50 nmol/L (20 ng/mL) and 125 nmol/L (50 ng/mL)

high levels: higher than 125 nmol/L (50 ng/mL)

If your vitamin D levels are low and you’re having symptoms of bone pain, a doctor may recommend a special scan to check bone density. 

Doctors use this painless scan to evaluate a person’s bone health.

Low blood levels of 25-hydroxy vitamin D usually mean one (or more) of the following:

you aren’t eating a balanced, complete diet

your intestines aren’t absorbing the vitamin properly

you’re not spending enough time outside to absorb adequate vitamin D levels through sun exposure

Some evidence links vitamin D deficiency to a higher risk of certain cancers, immune diseases, and cardiovascular disease.

High vitamin D blood levels generally result from taking too many vitamin pills and other nutritional supplements. High doses of vitamin D can result in a condition called hypervitaminosis D. Hypervitaminosis is a rare but serious condition that could put you at risk for liver or kidney problems.

High levels are rarely due to consuming too much of the vitamin through foods or sun exposure.

Your doctor will help explain the results of your test and determine if you have a vitamin D deficiency.

Risks of a 25-hydroxy vitamin D test

As with any routine blood test, risks of the 25-hydroxy vitamin test are minimal and include: 

excessive bleeding

lightheadedness

a slight chance of infection where the needle pierces your skin

Outlook

Vitamin D is vital to the body. Deficiencies at any age can cause problems.

Your doctor may recommend supplements or other treatment options if you’re very deficient. Eating foods that contain vitamin D in addition to adding supplements to your regimen can help keep your vitamin D levels stable.