The body uses vitamin D to promote calcium absorption in the gut. Additionally, vitamin D supports bone growth and remodeling and the neuromuscular and immune functions. Clearly, vitamin D is beneficial, regardless of how it is obtained. On the other hand, there may be instances in which too much vitamin contributes to hypercalcemia.
Full Answer
Is vitamin D really a vitamin or hormone?
Sep 02, 2016 · The ingestion of excessive amounts of vitamin D 3 (or vitamin D 2) results in hypercalcemia and hypercalciuria due to the formation of supraphysiological amounts of 25-hydroxyvitamin D [25(OH)D] that bind to the vitamin D receptor, albeit with lower affinity than the active form of the vitamin, 1,25(OH) 2 D, and the formation of 5,6-trans 25(OH)D, which binds …
Is vitamin D the same as calcium?
Jan 03, 2016 · Hyperphosphatemia-induced hypocalcemia inhibits vitamin D bioactivation in the kidney and the resulting low 1,25(OH)2 vitamin D levels may result in increased PTH secretion. Secondary hyperparathyroidism from long-term hyperphosphatemia has been well described and is usually associated with renal insufficiency.
What is hypovitaminosis D or vitamin D deficiency?
Oct 01, 2016 · The ingestion of excessive amounts of vitamin D 3 (or vitamin D 2) results in hypercalcemia and hypercalciuria due to the formation of supraphysiological amounts of 25-hydroxyvitamin D [25(OH)D] that bind to the vitamin D receptor, albeit with lower affinity than the active form of the vitamin, 1,25(OH) 2 D, and the formation of 5,6-trans 25(OH)D, which binds …
Does vitamin D increase calcium?
Absorption of calcium and phosphorous (vitamin D) Immune system responses (vitamin D) Signaling between cells (calcium) Hormonal secretion (calcium) Blood vessel flow (calcium) Without enough vitamin D or calcium, your parathyroid glands compensate by producing too much of their hormone, a condition called hyperparathyroidism.
How does vitamin D help hypocalcemia?
Why is vitamin D used to treat hypoparathyroidism?
Does vitamin D Help with hypercalcemia?
How does vitamin D regulate blood calcium levels?
How does Hypervitaminosis D cause hypercalcemia?
Hypercalcemia occurs as a result of increased calcium absorption from the intestine and increased bone mobilization.
What is the relationship between parathyroid hormone and vitamin D?
Why is neck surgery associated with hypocalcemia?
Neck explorations for reasons other than hyperparathyroidism are associated with hypocalcemia. Thyroid surgery, for example, is associated with hypocalcemia, presumably due to surgical disruption or vascular compromise of the parathyroid glands. Transient hypocalcemia is observed in 16-55% of total thyroidectomy cases (30,31). One group recently reported that of the 50% of patients who developed post-operative hypocalcemia, hypoparathyroidism persisted beyond one month in 38% (30). In another retrospective study, transient hypocalcemia was observed in 35% of patients undergoing total thyroidectomy, 3% had chronic hypocalcemia 6 months post-operatively, and 1.4% had permanent hypoparathyroidism 2 years post-operatively (31). The type of surgery performed is associated with the risk of developing hypocalcemia. For example, risk of hypocalcemia is higher after completion thyroidectomy or total thyroidectomy with node dissection (30). Transient hypocalcemia was observed more frequently after thyroidectomy for Graves’ disease than for nontoxic multinodular goiter, although incidence of permanent hypoparathyroidism was not different between groups (32).
What is hypocalcemia in medical terms?
Hypocalcemia is an electrolyte derangement commonly encountered on surgical and medical services. This derangement can result from a vast spectrum of disorders. The condition may be transient, reversing with addressing the underlying cause expeditiously, or chronic and even lifelong, when due to a genetic disorder or the result of irreversible damage to the parathyroid glands after surgery or secondary to autoimmune destruction. Adult and pediatric endocrinologists must carefully assess patients with hypocalcemia, factoring into that assessment clinical presentation and symptomatology, concomitant laboratory abnormalities, past medical and family histories, recent medications, and even genetic sequencing analysis on the patient or affected family members. Critical initial laboratory testing involves measuring serum phosphate, magnesium, intact parathyroid hormone (PTH), 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D levels. Further evaluation is directed by the clinical and laboratory profiles that emerge. Significant fundamental insights into the molecular pathogenesis of several disorders that cause hypocalcemia have been made. These insights involve the molecular etiologies for PTH resistance (i.e., the different subtypes of pseudohypoparathyroidism); the role of the AIRE (autoimmune regulator) protein in autoimmune hypoparathyroidism and in mediating central tolerance to self-antigens; and the molecular bases for different genetic forms of magnesium wasting (that in turn causes hypocalcemia) and hypoparathyroidism. Genetic etiologies for hypoparathyroidism involve mutations in the calcium-sensing receptor, the G protein subunit alpha 11 that couples the receptor to downstream signaling molecules in parathyroid cells, transcription factors essential for parathyroid gland development, and the PTH molecule itself. Treatment of hypocalcemia depends on severity and chronicity. A calcium infusion is indicated for severe acute and or symptomatic hypocalcemia, while the standard mainstays of oral therapy are calcium supplements and activated vitamin D metabolites. Finally, and importantly, despite the rarity of chronic hypoparathyroidism, there have been several clinical trials supporting the use of recombinant human PTH (1-84) in the management of patients not well controlled on standard treatment. These trials have led to the approval of PTH (1-84) by the US Food and Drug Administration for adults with this disorder not well regulated on the usual therapy. Future research is being directed toward designing ideal treatment regimens with PTH (1-84) as well as developing a better understanding of the risks for post-surgical hypoparathyroidism, the most common etiology of hypoparathyroidism in adult patients. For complete coverage of this and all related ares of Endocrinology, please see our FREE web-book www.endotext.org.
What are the effects of hypocalcemia on the autonomic ganglia?
Changes in smooth muscle function with low serum levels of calcium may cause irritability of the autonomic ganglia and can result in dysphagia, abdominal pain, biliary colic, wheezing, and dyspnea. Subscapular cataracts occur in chronic, longstanding hypocalcemia (12) and with treatment, especially when the calcium x phosphate product is chronically elevated. Paravertebral ligamentous ossification has been noted in 50% of cases with hypoparathyroidism, and antalgic gait may be noted. In some cases of chronic hypoparathyroidism, psychoses, organic brain syndrome, and subnormal intelligence have been noted. Treatment of the hypocalcemia may improve mental functioning and personality, but amelioration of psychiatric symptoms is inconsistent. Delayed development, subnormal IQ, and poor cognitive function could also be a component of a syndrome that includes hypoparathyroidism as one of its features (7,8). This is critically important to consider in young patients being evaluated for the condition. In the elderly population, disorientation or confusion may be manifestations of hypocalcemia.
What are the symptoms of hypocalcemia?
The hallmark of acute hypocalcemia is neuromuscular irritability. Patients often complain of numbness and tingling in their fingertips, toes, and the perioral region. Paresthesias of the extremities may occur, along with fatigue and anxiety. Muscle cramps can be very painful and progress to carpal spasm or tetany. In extreme cases of hypocalcemia, bronchospasm and laryngospasm with stridor may occur . Muscle symptoms can be so severe as to present with a polymyositis-like picture with elevated muscle isoenzymes. These symptoms are corrected by calcium replacement. Clinically, neuromuscular irritability can be demonstrated by eliciting Chvostek's or Trousseau's signs. Chvostek's sign is elicited by tapping the skin over the facial nerve anterior to the external auditory meatus. Ipsilateral contraction of the facial muscles occurs in individuals with hypocalcemia. Chvostek's sign is also present in 10% of normal individuals. Trousseau's sign is elicited by inflation of a blood pressure cuff to 20 mm Hg above the patient's systolic blood pressure for 3-5 minutes. Carpal spasm presents as flexion of the wrist and of the metacarpal phalangeal joints, extension of the interphalangeal joints, and abduction of the thumb. It can be very painful.
Can hypocalcemia cause seizures?
Grand mal, petit mal, or focal seizures have been described. Increased intracranial pressure and papilledema may be present. If the patient has pre-existing subclinical epilepsy, hypocalcemia may lower the excitation threshold for seizures (11). Electroencephalographic changes may be acute and nonspecific or present with distinct changes in the electroencephalogram (EEG). EEG changes may be present with or without symptoms of hypocalcemia. The relationship between calcification of basal ganglia (9,10-12), cerebral cortex, or cerebellum with pre-existing epileptic or convulsive disorders is not well understood.
Can hypocalcemia cause cardiac manifestations?
Acute hypocalcemia may have cardiac manifestations. Prolongation of the QT-interval due to lengthening of the ST-segment on electrocardiogram is fairly common in hypocalcemic patients. T-waves are abnormal in approximately 50% of patients (1). A pattern of acute anteroseptal injury on EKG without infarction has been associated with hypocalcemia and other electrolyte abnormalities (2). Hypomagnesemia in concert with hypocalcemia may magnify the EKG abnormalities. Rarely, congestive heart failure may occur (1,3,4). Reversible cardiomyopathy due to hypocalcemia has been reported (5). In patients with mild, asymptomatic hypocalcemia, calcium replacement can result in improved cardiac output, and exercise tolerance (6).
Why are there so few cases of vitamin D deficiency in children in the United States?
The fortification of milk, cereals, breads, and other foods with vitamin D and the use of supplements are why there are so few cases of vitamin D deficiency in children in the United States. Vitamin D deficiency has been recognized in the United States in children who have restricted diets or specialized diets (18). In countries that do not fortify foods, childhood vitamin D deficiency is more common. Vitamin D deficiency is recognized as a worldwide problem in older adults as well (15,16). Exclusively breastfed infants are at high risk for vitamin D deficiency, as there is little vitamin D in human milk.
How to treat hypercalcemia with vitamin D?
Treatment of hypercalcemia associated with hypervitaminosis D includes withholding the vitamin D preparation. In individuals with no previous renal dysfunction, the administration of isotonic fluids with or without a loop diuretic such as furosemide and the administration of glucocorticoids are usually effective in reducing serum calcium concentrations. In patients with chronic renal failure receiving 1α-hydroxylated vitamin D analogs, withholding the drug may be sufficient. If sufficient renal function is still present, administration of isotonic fluids and a loop diuretic will be of value. Glucocorticoids, which act by inhibiting intestinal calcium absorption through the inhibition of enterocyte basolateral membrane calcium extrusion and inhibition of intestinal cell RNA polymerase activity ( 323 – 325 ), will also help in this circumstance. Patients on hemodialysis will need to have the offending drug withheld and, if hypercalcemia persists, may require dialysis against a low calcium hemodialysis bath (2 mEq/L calcium).
What is hypercalcemia associated with?
Hypercalcemia associated with excessive ingestion of vitamin D and active vitamin D metabolites/analogs
What are the symptoms of vitamin D toxicity?
The clinical symptoms of vitamin D toxicity are the result of hypercalcemia and hypercalciuria and are similar to those of hypercalcemia due to any other cause. Symptoms include neuropsychiatric manifestations such as lethargy, confusion, irritability, depression, hallucinations, and in extreme cases, stupor, and coma; gastrointestinal symptoms such as anorexia, nausea, vomiting, and constipation; cardiovascular manifestations such as ectopy; and renal symptoms such as polyuria and renal colic from the passage of renal stones.
What mutations in CYP24A1 are reduced degradation of 1,25 (OH) 2 D 3?
Mutations of the CYP24A1 gene: reduced degradation of 1,25 (OH) 2 D 3: infantile and adult hypercalcemia
Why does hypercalcemia occur in primary hyperparathyroidism?
It occurs as a result of an increase in intestinal and renal phosphate absorption. In contrast, patients with primary hyperparathyroidism have hypercalcemia and hypophosphatemia on account of PTH-mediated losses of phosphate in the urine. Hypercalciuria is frequently present.
How to measure vitamin D levels?
Although vitamin D (vitamin D 3 and vitamin D 2) can be measured in serum and plasma and quantitated by various methods such as ultraviolet spectroscopy and competitive protein binding, its measurement is technically difficult, and few reports have appeared on its use in the measurement of vitamin D in patients with hypervitaminosis D ( 264, 265 ). Measurements of serum 25 (OH)D, which can be performed by a variety of methods—including competitive protein binding assay ( 266 – 268 ), RIA ( 269 – 272 ), HPLC/ultraviolet spectroscopy ( 273, 274 ), automated, antibody-, and microparticle-based, chemiluminescent immunoassay ( 275 ), and liquid chromatography mass spectrometry ( 272, 276 – 279 )—are widely used in the assessment of vitamin D status. Various epimers contribute to the total 25 (OH)D measurement and appear to be most prominent in infants and very young patients in whom C-3 epimers of 25 (OH)D can account for a significant proportion of 25 (OH)D measured by liquid chromatography-tandem mass spectrometry unless measures are taken to separate metabolites by chromatography ( 279 ). In hypervitaminosis D [25 (OH)D 3 >64–439 ng/mL], the mean relative contribution of 3-epi-25 (OH)D 3 was <4%, and concentrations ranged from 2–28.6 ng/mL ( 280 ). Serum levels of the C-3 epimer correlate with serum 25 (OH)D 3 concentrations. In subjects with 25 (OH)D 3 concentrations indicative of hypervitaminosis D, the presence and concentrations of the C-3 epimer were unrelated to age, serum markers of renal and liver function, acute-phase reactants, and the presence of hypercalcemia. Subjects with significant PTH suppression (<14 pg/mL) showed higher concentrations of 3-epi-25 (OH)D 3.
What is the cause of hypercalcemia?
Hypercalcemia occurs as a result of increased calcium absorption from the intestine and increased bone mobilization . The 25 (OH)D 3 or 25 (OH)D 2 which are present in increased amounts bind to the vitamin D receptor in sufficient amounts to induce processes that enhance intestinal calcium absorption and enhance bone mobilization ( 81, 82, 83, 308, 309, 311 ). In in vitro radioligand binding assays with the vitamin D receptor, the B50 (B50 value is defined as the concentration of material necessary to cause 50% displacement of the radiolabel from the protein) of 1α,25 (OH) 2 D 3 is approximately 1.62 × 10 −10m, whereas, the B50 of 25 (OH)D for the vitamin D receptor is approximately 1.38 × 10 −7m. These concentrations of 25 (OH)D may be present in vitamin D target tissues in hypervitaminosis D. A second possible mechanism is the endogenous production of 5,6- trans- 25 (OH)D 3, which has a 1α hydroxyl group and which binds to the vitamin D receptor with increased affinity ( 312) ( Figure 3 ). We have shown that 5,6- trans -25 (OH)D 3 is present in the serum of rats administered large doses of vitamin D 3 ( 312 ). Because of the presence of a 1α hydroxyl group, binding of 5,6- trans -25 (OH)D 3 to the vitamin D receptor is increased—6.9 × 10 −8m for 5,6- trans -25 (OH)D 3, 1.95 × 10 −7m for 25 (OH)D 3, and 2.2 × 10 −10m for 1α,25 (OH)D 3 ( 312 ). It should be noted, however, that although we have isolated 5,6- trans- 25 (OH)D 3 from the serum of rats dosed with vitamin D 3, it is not known whether this metabolite is present in the serum of humans with hypervitaminosis D.
What are the problems with vitamin D and calcium?
Other problems from calcium and vitamin D deficiencies include: Skeletal deformities ( rickets) in children ages 6-24 months. Muscle weakness in children and the elderly (vitamin D only) Given the crucial role of both nutrients in bone health, The Endocrine Society and the Institute of Medicine recommend certain consumption levels based on age ...
What happens if you don't get enough calcium?
Blood vessel flow (calcium) Without enough vitamin D or calcium, your parathyroid glands compensate by producing too much of their hormone, a condition called hyperparathyroidism. That can lead to bone weakening ( osteoporosis) and increased fracture risk.
Is too much vitamin D bad for kidneys?
Taking too much of either nutrient appears to be harmful, with: Kidney stones associated with too much calcium from supplements. Very high levels of vitamin D (above 10,000 IUs per day) potentially causing kidney and tissue damage.
Why is hypervitaminosis D so rare?
Diagnosis. Treatment. Prevention. Hypervitaminosis D is a rare but potentially serious condition. It occurs when you take in too much vitamin D. It’s usually the result of taking high-dose vitamin D supplements. Too much vitamin D can cause abnormally high levels of calcium in the blood.
How to get vitamin D levels back to normal?
Your doctor may also recommend that you lower the amount of calcium in your diet. Careful monitoring is necessary until your vitamin D levels are back to normal. To ingest vitamin D naturally, you can eat foods that are rich in it, including: cod liver oil. fatty fish, such as salmon and tuna. beef liver.
What tests are done for hypervitaminosis D?
If your doctor suspects that you may have hypervitaminosis D, they may order tests, including: blood tests to check vitamin D levels, calcium, and phosphorus (to determine if kidney damage is present) urine tests to check for excessive amounts of calcium in the urine.
What happens if you take too much vitamin D?
Too much vitamin D can cause abnormally high levels of calcium in the blood. This can affect bones, tissues, and other organs. It can lead to high blood pressure, bone loss, and kidney damage if not treated.
What are the symptoms of high calcium levels?
This can lead to a condition called hypercalcemia (too much calcium in your blood). Symptoms include: fatigue. loss of appetite. weight loss. excessive thirst. excessive urination.
Is vitamin D poisonous?
Daily use of high-dose vitamin D supplements for several months is toxic. You are more likely to develop hypervitaminosis D if you take vitamin D supplements and have other existing health problems, such as: kidney disease. liver disease. tuberculosis. hyperparathyroidism. sarcoidosis.
Can you get vitamin D from tanning?
You probably aren’t getting too much vitamin D from the foods you eat or from exposure to the sun. However, there have been cases reported due to tanning bed use. . And there has been an increase in overall hypervitaminosis D cases in the past few years.
What is the treatment for hypocalcemia?
Treatment focuses on oral calcium and vitamin D supplements, as well as magnesium if deficiency is present . Treatment can be further intensified with thiazide diuretics, phosphate binders, and a low-salt and low-phosphorus diet when treating hypo calcemia secondary to hypoparathyroidism. Acute and life-threatening calcium deficit requires treatment with intravenous calcium. The current treatment recommendations are largely based on expert clinical opinion and published case reports, as adequately controlled clinical trial data are not currently available. Complications of current therapies for hypoparathyroidism include hypercalciuria, nephrocalcinosis, renal impairment, and soft tissue calcification. Current therapy is limited by serum calcium fluctuations. Although these complications are well recognized, the effects of therapy on overall well-being, mood, cognition, and quality of life, as well as the risk of complications, have not been adequately studied.
What is the role of family physicians in the management of hypocalcemia?
Family physicians play a crucial role in educating patients about the long-term management and complications of hypocalcemia. Currently, management is suboptimal and marked by fluctuations in serum calcium and a lack of approved parathyroid hormone replacement therapy for hypoparathyroidism.
What causes hypoparathyroidism?
Uncommon causes of hypoparathyroidism include heavy metal infiltration of the parathyroid glands with iron, as seen in hemochromatosis, or thalassemia. Copper deposition as seen in Wilson disease is also an uncommon cause, as is metastatic infiltration of the parathyroid glands. Magnesium deficiency or excess can impair PTH secretion and also result in hypoparathyroidism.10
What are the causes of DiGeorge syndrome?
Abnormalities in the embryonic development of the parathyroid glands can result in DiGeorge syndrome, which can be associated with cardiac defects, abnormal facies, thymic hypoplasia, cleft palate, and hypocalcemia. Other genetic abnormalities can also cause hypoparathyroidism or pseudoparahyperthyroidism.
What is the range of calcium levels in the body?
Hypocalcemia is a common biochemical abnormality that can range in severity from being asymptomatic in mild cases to presenting as an acute life-threatening crisis.1Serum calcium levels are regulated within a narrow range (2.1 to 2.6 mmol/L) by 3 main calcium-regulating hormones—parathyroid hormone (PTH), vitamin D, and calcitonin—through their specific effects on the bowel, kidneys, and skeleton.1,2Approximately half of the total serum calcium is bound to protein, and the remaining free ionized calcium is physiologically active.2Serum calcium levels must be corrected for the albumin level before confirming the diagnosis of hypercalcemia or hypocalcemia.1
Why is vitamin D insufficient?
Vitamin D inadequacy is also caused by reduced skin synthesis (owing to limited sun exposure, skin pigmentation, or skin thinning with age). Decreased absorption, increased catabolism, impaired hepatic or renal hydroxylation to form 1,25-dihydroxyvitamin D, or acquired and genetic disorders of vitamin D metabolism and responsiveness also lead to low vitamin D levels.1,2,4,7Vitamin D requirements increase during and after pregnancy, and low maternal vitamin D levels are associated with hypocalcemia in breastfed infants.9
What is the effect of vitamin D on bone?
The presence of 1,25-dihydroxyvitamin D enhances intestinal absorption of calcium and phosphorus, and promotes bone remodeling.4,6Vitamin D inadequacy (25-hydroxyvitamin D [25(OH)D] level < 75 nmol/L) remains common in children and adults.1,2,4,7,8Inadequate vitamin D levels lead to a reduction in gastrointestinal calcium absorption of up to 50%, resulting in only 10% to 15% of dietary intestinal calcium being absorbed.4
What is vitamin D hypercalcemia?
Vitamin D Hypercalcemia: Here’s What You Need to Know. Hypercalcemia is a medical condition that causes calcium in the blood to surpass a normal level. Too much calcium can result in bone weakness, kidney stones, and heart and brain disruptions. Hyperparathyroidism (HPT) is one of the leading causes of hypercalcemia.
What is the role of vitamin D in the body?
Additionally, vitamin D supports bone growth and remodeling and the neuromuscular and immune functions.
Why do parathyroids produce excess calcium?
They produce parathyroid hormone (PTH) to help manage calcium in the body. But, if one or more of the parathyroid glands malfunctions, they may produce an excess amount of calcium. In this instance, HPT and hypercalcemia can occur. In addition to HPT, other reasons why people experience hypercalcemia include:
How much vitamin D is safe?
It also points out that 1,000 to 2,000 IU of vitamin D is safe and helps ensure the blood maintains an adequate amount of vitamin D to support various body functions. Conversely, too much vitamin D may actually cause hypercalcemia and therefore symptoms include: ● Depression. ● Fatigue.
What is the best test for hypercalcemia?
Blood tests are commonly used to diagnose hypercalcemia. These tests enable a doctor to see if a patient’s blood calcium level is higher than normal. They can also show if a patient’s PTH level is above-average, which indicates the patient may be dealing with HPT.
Can metastasis cause hypercalcemia?
Additionally, people who experience metastasis (spread of cancer) are increasingly susceptible to hypercalcemia. ● Diseases: Tuberculosis, sarcoidosis, and other diseases have been shown to increase vitamin D in the blood and may lead to hypercalcemia.
Can vitamin D be taken in the body?
Ultimately, vitamin D supplementation can do harm in the body, if not monitored or done properly. . If people are considering vitamin D supplements, they should first consult with a doctor. This allows people to determine if vitamin D supplements can safely and effectively be incorporated into an everyday diet.
What is the most important investigation for hypocalcaemia?
If the cause of hypocalcaemia is not clinically obvious the most important investigation is to measure serum parathyroid hormone. A standard biochemical profile, a parathyroid hormone measurement, and the clinical history will usually provide the likely cause of hypocalcaemia. Figure 55shows an algorithm for investigating hypocalcaemia.
What are the symptoms of hypocalcaemia?
Thus, classic symptoms of hypocalcaemia are neuromuscular excitability in the form of muscle twitching, spasms, tingling, and numbness. Carpopedal spasm is characteristic but in severe cases can progress to tetany, seizures, and cardiac dysrhythmias. In patients without overt signs, underlying neuromuscular excitability can become evident with provocation—tapping the parotid gland over the facial nerve can induce facial muscle spasm (Chvostek’s sign; fig 3)3).. However, 10% of normal people have a positive Chvostek’s sign. Conversely, a small study of patients with hypoparathyroidism and biochemically confirmed hypocalcaemia found that 29% were negative for Chvostek’s sign, which makes this test a poor discriminator.10
What is the best medication for parathyroid deficiency?
Patients with parathyroid hormone deficiency need calcitriol or alfacalcidol rather than conventional doses of colecalciferol or ergocalciferol
What hormones interact with calcium?
Fig 1Regulation of serum calcium. Parathyroid hormone and vitamin D normally interact to protect against hypocalcaemia. Problems at any level can lead to low serum calcium, but the most common problems are vitamin D deficiency and hypoparathyroidism
What hormones are responsible for calcium absorption?
The concentration of calcium in the serum (normal range 2.10-2.60 mmol/l)is regulated by the action of parathyroid hormone and vitamin D on the kidneys, bones, and gastrointestinal tract (fig 1)1).. Parathyroid hormone stimulates calcium resorption in the kidney and calcium release from bone. It also stimulates renal production of 1,25-dihydroxyvitamin D (calcitriol) from 25-hydroxyvitamin D. 1,25-Dihydroxyvitamin D is the most active form of vitamin D, and it acts on the gastrointestinal tract to increase calcium absorption. Vitamin D is obtained mainly through synthesis in the skin, with a small contribution from the diet. Skin synthesis requires exposure to ultraviolet light and is reduced by skin pigmentation.
What is hypoparathyroidism a result of?
Hypoparathyroidism as a result of autoimmune disease
Why do bisphosphonates cause hypocalcaemia?
Severe hypocalcaemia has been reported in patients with pre-existing vitamin D deficiency who receive intravenous bisphosphonates because these compounds block bone resorption.9Table 11outlines common and less common causes of hypocalcaemia.
What vitamin deficiency is an ignored cause of hypocalcemia in actue illness?
10. Noto H, Heller H. Vitamin D deficiency as an ignored cause of hypocalcemia in actue illness: report of 2 cases and review of the literature. The Open Endocrinology Journal. 2009;3:1–4. [Google Scholar]
Why is vitamin D important for elderly?
Vitamin D deficiency is particularly important within the elderly population due to its direct relationship with increased morbidity and frailty [1]. Vitamin D deficiency is common in the elderly [2, 3]. The prevalence of vitamin D deficiency ranges from 5–25% in independent, community dwelling elderly, to 48–80% in institutionalized elderly [4–6]. Vitamin D deficiency is an established risk factor for osteoporosis, falls, and fractures within the elderly. Additionally, vitamin D deficiency is associated with breast, prostate and colon cancer, type 2 diabetes, and cardiovascular disorders such as hypertension [7], conditions which commonly afflict the elderly.
Does vitamin D affect blood pressure?
The active form of vitamin D, indirectly and directly regulates hundreds of genes, including blunting renin production in the kidney [13]. Several epidemiological studies have shown a relationship between elevated systolic blood pressure and vitamin D deficiency [13]. It is worthwhile to note that a cohort of Framingham patients with vitamin D deficiency and HTN has exhibited a higher CV risk of fatal or nonfatal MI, ischemia, stroke, or heart failure [13].
Can vitamin D deficiency cause numbness?
In general, hypocalcemia has a spectrum of clinical manifestations. In mild or chronic hypocalcemia, symptoms may be few, such as numbness or muscle cramps, or they may be absent . In severe or acute hypocalcemia, symptoms may be life threatening. Presentations may include severe neuromuscular irritability, tetany, papilledema, arrhythmias, seizures, or death [8, 9].
Does vitamin D help with bone health?
Higher 25-hydroxy vitamin D status correlates with better bone and muscle health . A meta-analysis in 2004 showed that vitamin D reduced the risk of falling by 22% in older adults [1]. Similar findings were observed in subsequent epidemiological studies [1]. Calcium adequacy is also critical for fracture prevention. Low calcium levels lead to weak bone susceptible to fracture. Considering that one out of every three older adults falls each year, hypovitaminosis D can result in significant morbidity and mortality among the elderly [12].
Does secondary hyperparathyroidism cause CV?
Additionally, secondary hyperparathyroidism has also been associated with a doubling of CV disease and mortality [13]. It is reasonable then to hypothesize that our asymptomatic patient with vitamin D deficiency, secondary hyperparathyroidism, and HTN may have been at very high risk for CV complications. However, given her asymptomatic presentation, her very high risk status could have remained unknown.