Vitamin D Deficiency

Definition/Description

Vitamin D deficiency is a major public health problem in all age groups worldwide, with adverse effects on bone health and other health outcomes. Even in low-latitude countries where UV radiation is generally considered sufficient to prevent this defect, Vitamin D deficiency remains a major problem in industrialized countries where vitamin D fortification has been implemented for many years. [1]

Vitamin D regulates and regulates the physiology and function of several body systems including skeletal muscle [2]. It is an essential vitamin for calcium absorption, maintenance of serum calcium and phosphate concentrations, normal mineralization of bones and protection against hypocalcemia Tetany. It is also required for bone growth and bone remodeling by osteoblasts and osteoclasts.

Inadequate levels of vitamin D are often associated with rickets in children and osteomalacia in adults with weak and brittle bones. Blood levels less than 20 mg/mL are considered insignificant.[3]

Vitamin D, also known as calcidiol or 25(OH)D, is a fat-soluble vitamin derived from sun exposure to food and supplements. It is not found naturally in many foods but is often used as a dietary fortifier or taken as a supplement.Vitamin D is synthesized in the body when fats[3]. (7-dehydrocholesterol)[4] is activated by UVB radiation from sunlight. When ingested, the vitamin is absorbed by the intestines and transported to the liver and kidneys for further processing.

Prevalence

Vitamin D deficiency is a major public health problem worldwide in all age groups.[1]

Low levels of vitamin D are a problem even in countries with year-round sunshine. This problem is particularly high in the Middle East especially among girls and women[1].

At least the U.S. 25% to 50% of adults are vitamin D deficient.[5][6] According to a recent National Health and Nutrition Examination Survey, the overall prevalence of vitamin D deficiency is approximately 41% in the US. in the adults. As for racial deficiencies, they are often seen among African Americans followed by Hispanics.[5] Melanin absorbs UVB rays in dark-skinned people; therefore it has significantly reduced synthesis.[7]

Risk Factors

• Geriatric population[4][7]
• Infants[3]
• People with limited sun exposure[3]
• Fat malabsorption[3]
• Obesity (all ages)[8][9]: Fat-soluble vitamins are easily stored in adipose tissue –> reduce blood vitamin D[7]
• Gestational diabetes[10]
• Poor general health status[5]
• Hypertension[5]
• Insufficient daily intake of milk or other foods containing vitamin D[5][11][3]
• Depression[12]
• Burn patients[13]
• Living in polluted climates[3]

Lack may be related to geographic location and religious practices, but the evidence is inconsistent. [3] Possible causes – little sun exposure in northern countries; year-round clothing that covers major body surfaces, e.g. Arab women[4]

Characteristics/Clinical Presentation

A diagnosis of osteomalacia is usually made in adults and may include the following signs and symptoms [4][3][14]:

• General muscle weakness
• Falls
• Fractures
• Severe bone pain
• Myalgia
• Decreased functional status
• Decreased progress during rehabilitation
• Fatigue
• Depression

Children often present with rickets as their diagnosis, which may include the following signs and symptoms [4]:

• Bowing of the long bones
• Extensive wear and clubbing in areas of active bony growth primarily surrounding the metaphysis of long bones and the sternal ends of ribs.

Associated Co-morbidities

Osteoporosis [4] As we age, the hormone 7-dehydrocholesterol in the skin decreases. By age 65, only about 25% of vitamin D is retained in the body, resulting in decreased vitamin D synthesis and thus decreased calcium absorption.

Skeletal deformities [4] Children with rickets typically have curvature of the long bones, as well as wear and broadening of the digits near the epiphyseal (growth) plates. The main area includes the metaphysis of the long bones and the sternal end of the ribs, also known as the rachi rosary.

Electrolyte imbalance [4] often associated with hypomagnesemia

Hyperparathyroidism Parathyroid hormone (PTH) is a key hormone that regulates the renal synthesis of calcifediol, or 25(OH)D, thereby maintaining calcium ions in the blood. Low levels of vitamin D (calcifediol) and calcium ions in the blood can stimulate PTH. Through this mechanism, active vitamin D The metabolite [125(OH)2D], also known as calcitriol, promotes calcium supply in the blood. As the cascade progresses, hyperstimulation of the parathyroid glands leads to secondary hyperparathyroidism. [7] [11]

Cancer Vitamin D may play a role in preventing colon, prostate and breast cancers. Vitamin D receptors normally play a role in cell proliferation and their response to various stimuli, as they are found in colon, prostate, and breast tissue. so lack of possibility Indicates a possible increased risk of cancer. [7] Research in this area is often conflicting. [3]

Myofascial Trigger Points/Myalgia[4]

Other potential comorbidities [3] Diabetes (type I and II) Insulin intolerance Hypertension Multiple sclerosis (MS) and Alzheimer’s disease Cognitive decline [14]

Medications

Drugs that block vitamin D absorption [7] Drug effects Anticonvulsants: (phenytoin, carbamazepine, phenobarbital) induce hepatic p450 enzymes to accelerate the catabolism of vitamin D29 Thiazide diuretics can accelerate metabolism by hepatic p450 enzymes Vitamin D catabolism Corticosteroid metabolism by hepatic p450 enzymes accelerates vitamin D metabolism Nicotine metabolism by liver p450 enzymes accelerates vitamin D catabolism Cholesterol-lowering drugs: (cholestyramine colestipol ezetimibe) by blocking absorb Lipids in the gut These drugs also block the absorption of vitamin D and other fat-soluble vitamins Xenical Alli, which blocks the absorption of fat in the gut, also blocks the absorption of vitamin D and other fat-soluble vitamins

Diagnostic Tests/Lab Tests

The risk marker used to measure deficiency levels is the plasma metabolite of vitamin D 25-hydroxyvitamin D (25(OH)D)[6][11]

Various methods that can be used to measure 25(OH)D concentrations include [11]:

• Competitive Protein Binding Assay (CPBA)
• Radioimmunoassay (RIA)
• Enzyme-linked Immunoassay (EIA, ELISA)
• Random Access Automated Detection Using Chemiluminescent Assay (RAAA)
• High Performance Liquid Chromatography (HPLC)
• Liquid Chromatography-Mass Spectrometry (LC-MS)
• 24-hour Urine Calcium Excretion[6]

X-rays of patients with vitamin D deficiency typically show: decalcification of the spine, pelvis, and lower extremities; transverse fracture-like lines in the affected bones; demineralization of the bone matrix [4]

Etiology/Causes

Adults

Leading causes include: Insufficient sun exposure[4] Insufficient supplementation during pregnancy/lactation and obesity[7]

Children and Adolescents

The main causes include: insufficient sun exposure [4] insufficient vitamin supplementation and breastfeeding without vitamin D supplementation. [7]

Other Causes

• Low intake of vitamin D in diet [4]
• Poor renal function: decreased conversion of 25(OH)D to the active metabolite in the kidney [11]
• Intestinal malabsorption problems are often associated with aging [4]; irritable bowel syndrome (IBS) [7]
• Long-term use of anticonvulsants (see relevant section in link) can accelerate the breakdown of the active form of vitamin D [4]
• Autoimmune diseases: Helper T cells (Th) are a key component of antigen-specific immunity misguided. Th cells (1 and 2) have vitamin D receptors that help suppress autoimmune disease –> vitamin D cannot bind to misguided Th cells and does not help suppress Disease (periodic) [7]

Systemic Involvement

1. Musculoskeletal system: Severe vitamin D deficiency may be associated with nonspecific musculoskeletal pain causing skeletal muscle and/or joint pain. [15][16] Vitamin D affects muscle function and structure, and vitamin D deficiency can lead to muscle weakness. Several studies have shown that vitamin D Supplements can improve certain aspects of performance and prevent injury in athletes. However, according to the results of a recent systematic review, vitamin D does not appear to improve post-exercise recovery [17]. Not inhibited when vitamin D deficiency is present Autoimmune diseases via Th1 cells. Common autoimmune diseases may include: RA and MS. [7] There are also vitamin D receptors on skeletal muscle. When a deficiency is present, the risk of falls increases. [7]
2. Endocrine system: secondary hyperparathyroidism [11][7]
3. Cardiovascular system: Studies have shown that low vitamin D may be a risk factor for certain arterial diseases, such as peripheral arterial disease, congestive heart failure, and aortic aneurysm. [18][19] It may also help reduce protection and increase lung function There are fewer smokers. [20] Vitamin D may affect myocardial contractility, vascular tone, and cardiac tissue maturation due to vitamin D receptors on the myocardium. Therefore, vitamin D may play a role in the pathogenesis of CV problems. [7]
4. Gastrointestinal tract: Since vitamin D receptors are found in colon tissue, vitamin D receptors play a role in cell proliferation and their response to stimuli. Therefore, vitamin D deficiency may play a role in colon cancer. Also as mentioned earlier, the lack of Autoimmune diseases such as irritable bowel syndrome (IBS) when vitamin D deficiency is present. [7]
5. Psychosocial systems: Low vitamin D levels linked to depression. [12]
6. Outer skin: In the literature, children with burns are at risk of further or contracting vitamin D deficiency and its associated side effects due to insufficient sun exposure. No studies have been conducted in adults. [13]

Medical Management

Diagnosis:

Despite the prevalence of vitamin D deficiency, screening for vitamin D deficiency is not universally supported due to cost. [19]

• Some clinicians may perform bone decalcification testing via medical imaging and proceed with serum testing after the results are obtained. (See Diagnostic Tests) .
• Low serum vitamin D levels are classified as insufficient and severe deficiency[21]: Insufficient 25(OH)D 21-29 ng/mL Deficient 25(OH)D <20 ng/mL

Due to the lack of foods with adequate levels of vitamin D, treatment relies mostly on adequate diet and sun exposure as follows:[21]

Supplementation Recommendations

• Different doses vary depending on the cause of the severity of the deficiency and physician preference for higher doses[14]
• Doses of vitamin D supplementation range from 800 to 1000 IU/d
• Or less than 2000 IU/d to avoid toxicity for 1- and 1-year-olds
• Recommended Dietary Allowances (RDA’s) for Vitamin D[3].

AgeMaleFemalePregnancy0-months 12*400 IU(10 mcg)400 IU(10 mcg)1-13 years600 IU(15 mcg)600 IU(15 mcg)14-18 years600 IU(15 mcg)600 IU(15 mcg)600 IU( 15 mcg)19-50 years600 IU(15 mcg)600 IU(15 mcg)600 IU(15 mcg)51-71 yes600 IU(15 mcg)600 IU(15 mcg)> years 70800 IU(20 mcg)800 IU( 20 mcg) is available.

Physical Therapy Management

Physical therapists can take a team approach to implement medical supervision through patient education on: Vitamin D-rich foods; The importance of following medical recommendations for vitamin D intake; The importance of proper sun exposure with risks of overexposure. One study suggests that to implement a fall a treatment program consisting of a Family Medicine (FM) physician and an Internal Medicine (IM) physician and a multidisciplinary team of physical therapist and Home Health (HH) nurse provides care for elderly patients who experience falls the constant. But it needs to be reviewed and updating the plan based on outcomes and follow-up assessments is essential to improve patient care[22][22].

There is no direct exercise intervention for vitamin D deficiency. The patient will be referred to physical therapy to treat problems that may be the cause of vitamin D deficiency such as decreased muscle strength decreased physical activity or prevention of falls. (See Clinical Presentation). In these cases, the options may include:

Fall prevention training e.g. Otago program and fall gym class

General muscle-strengthening exercises

In older adults, the response to resistance training is impaired and muscle mass is reduced compared with younger adults. There is evidence that both exercise training and vitamin D supplementation can support musculoskeletal health in older adults and it stands to reason that in combination their effects may be additive.[23] Vitamin D deficiency is associated with poor muscle strength and function in community-dwelling older people[24].

Dietary Management 

Adequate Sources of Intake:

• D2 (ergocalciferol) is available in herbal sources and oral medications
• D3 (cholecalciferol) is primarily derived from skin exposure to ultraviolet B (UVB) radiation in sunlight consuming food sources such as fatty fish and variable fortified foods (milk juice margarines yogurts cereals). and soy) and in oral supplements

Most foods contain between 50 and 200 IU per serving varying with geographic location and th fortification process [6].

Food Sources of Vitamin D[3]FoodIUs per Serving*Percentage DV**1 tablespoon of cod liver oil13603403 ounces of cooked swordfish5661423 ounces of cooked salmon (sockeye)447112Canned tuna fish in a steamer in 3 ounces15439Fortified orange juice vitamin D fortified cup 1115-12429-31Yogurt fortified with vitamin D DV 20% 6 ounces8020Fortified margarine 1 tablespoon6015Canned oiled sardines 2 sardines4612Cooked liver beef 3 ounces42111 egg large (vitamin D found in yolk)

IUs= International Units

DV= U.S. Daily Values. Food and Drug Administration

Proper sun exposure[3]:

• Cloud cover can reduce absorption by up to 50% .
• The sun through the windows is not ideal-Glass hinders the synthesis process
• Sunscreen may inhibit synthesis if it exceeds the entire body
• Get 5-30 minutes twice a week between 10AM – 3PM without sunscreen
• Best exposure points: face, arms, legs and back
• Sunbeds emit 2-6% UVB (not a medically recommended source)
• Limit sun exposure without sunscreen to reduce risk of deadly cancer

Differential Diagnosis

Fibromyalgia [15]

• Myofascial Trigger Points[4]
• Rheumatic diseases [15]
• Polymyositis[4]
• Muscular Dystrophy[4]

Case Report

Case Report[25] 

Authors:Clement Z Ashford M and Sivakumaran

Abstract:

• Vitamin D deficiency is very common in multiple myeloma and represents a surrogate for the clinical multiple myeloma disease state. Patients may complain of generalized chronic musculoskeletal pain and dull aches with fatigue or decreased muscle strength.
• This case confirms that vitamin D deficiency is common in patients with multiple myeloma and can lead to generalized musculoskeletal pain and increase the risk of stroke but is often undiagnosed . . . . In patients with nonspecific musculoskeletal pain who do not receive medical sun exposure physicians should be highly suspicious of vitamin D deficiency.

Patient Characteristics:

• 63 year old man with multiple myeloma
• Current reactivation of herpes zoster

Subjective: Chief complaints include:

• Generalized weakness
• Nonspecific musculoskeletal pain
• Reported multiple falls

Examination:

• Pale presentation with depressive effects
• Resting tremor generalized bone tenderness impairment in movement and weight bearing
• Muscle weakness
• Waddling gait
• Bone biopsy revealed osteoporosis with very low Vitamin D levels less than 20 nmol/L

Past Medical History:

• She was previously diagnosed with solitary plasmacytoma in 2001 and then progressed to smoldering myeloma in
• 2007 her indolent version of myeloma evolved into more aggressive myeloma without musculoskeletal chest pain anorexia weight loss and tumor-lysis requiring hospitalization and plasmapheresis.
• June 2010 the patient was admitted after repeated falls and zoster recurrence including ocular zoster with right first and third trigeminal branches.

Intervention: Physical Therapy

Co-intervention: vitamin D supplementation 3000 nmol/L per day Results: after 4 months

• Significantly less musculoskeletal pain throughout his body
• Blood showed normal vitamin D level of 109 nmol/L
• Alkaline phosphatase decreased to 182 U/L
• currently undergoing palliative rehabilitation