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{{Vitamin D deficiency}}


 
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==Introduction to the Pathophysiology Page==
* The page name should be '''"(Disease name) pathophysiology"''', with only the first letter of the title capitalized.
* '''Goal:''' to explain the biological mechanisms underlying the disease state. To provide a description of the pathophysiology at a cellular and molecular level, the pathophysiology at a gross and functional level, and the causative factor in the disease process. The page can also include a description of the genetic abnormalities, embryological and developmental abnormalities, pathogenesis, and pathology images.
* As with all microchapter pages linking to the main page, at the top of the edit box put <nowiki>{{CMG}}</nowiki>, your name template, and the microchapter navigation template you created at the beginning.
* Remember to follow the same format and capitalization of letters  as outlined in the template below.
* You should include the name of the disease in the first sentence of every subsection.
 
 
==Overview==
==Overview==
* The overview section should include the disease name in the first sentence.
* The goal is to summarize the pathophysiology page in several sentences. This section can be the same as the pathophysiology segment on the overview page.
* To see an example of an overview section on a symptoms page, click [[Pericarditis pathophysiology#Overview|here]].
===Template===
*The overview is highly dependent on the individual disease pathophysiology. There is no specific template preference for the first sentence.
'''Template Sentences:'''
:Template Sentence 1: [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
:Template Sentence 2: Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
:Template Sentence 3: On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
:Template Sentence 4: On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
:Template Sentence 5: [Disease name] is transmitted in [mode of genetic transmission] pattern.
:Template Sentence 6: [Disease/malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
:Template Sentence 7: Development of [disease name] is the result from multiple genetic mutations.
:Template Sentence 8: Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
:Template Sentence 9: The progression to [disease name] usually involves the [molecular pathway].
:Template Sentence 10: The pathophysiology of [disease name] depends on the histological subtype.
'''Examples:'''
:Example 1: Spores of ''C. difficile'' are transmitted via the fecal-oral route to the human host.
:Example 2: Following ingestion, the acid-resistant spores of C. difficile are able to survive the human gastric acidity.
:Example 3: Following ingestion, ''Shigella spp.'' uses the M cells of the GI tract to invade the epithelial cells of the large intestine.
:Example 4: Following transcytosis and macrophage apoptosis, ''Shigella'' avoids extracellular exposure and spreads intercellularly using actin polymerization processes (rocket propulsion).
:Example 5: On gross pathology, hyperemia with development of ulcers and edema are characteristic findings of shigellosis.
:Example 6: On microscopic histopathological analysis, infiltration of PMN and inflammatory pseudomembrane formation are characteristic findings of shigellosis.
:Example 7: Duchenne muscular dystrophy is transmitted in an X-linked recessive pattern.
:Example 8: Malignant melanoma arises from the epidermal melanocytes, which are neural crest cells normally involved in the synthesis of melanin (a brown pigment with photoprotective properties).
:Example 9:  Development of melanoma is the result of multiple genetic mutations.
:Example 10: Genes involved in the pathogenesis of melanoma include ''p53'', ''RB'', ''ARF'', and ''BRAF''.
:Example 11: The progression to melanoma usually involves the serine-threonine kinases of the MAPK/ERK pathway (mitogen-activated protein kinase) following mutation of either the ''N-RAS'' or ''BRAF'' oncogene.
:Example 12: The pathophysiology of gallbladder cancer depends on the histological subtype.
==Pathogenesis==
Pathogenesis is the mechanism by which a certain factor causes disease (''pathos'' = disease, ''genesis'' = development). The term can also be used to describe the development of the disease, whether it is acute, chronic, or recurrent. It can also be used to describe whether the disease causes inflammation, malignancy, necrosis etc.
==== Template Sentences ====
IF the pathogenesis of the disease is unclear:
*The exact pathogenesis of [disease name] is not fully understood.
*It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
IF the disease is infectious…
*…and the route of transmission is known:
**[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
**Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
IF the disease has a known genetic component:
*[Disease name] is transmitted in [mode of genetic transmission] pattern.
*Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
IF certain pathology findings are characteristic of the disease:
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
*On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Other relevant information may include the action of the pathogen on a molecular level, the body’s response, whether or not mutations play a role in the disease development, whether the pathophysiology of the disease is different among subgroups of the disease, etc. Additional template sentences are listed below. Due to the highly variable nature of pathophysiology among various diseases, this list is not comprehensive.
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
*The development of [disease name] is the result of multiple genetic mutations.
*The progression to [disease name] usually involves the [molecular pathway].
*The pathophysiology of [disease/malignancy] depends on the histological subtype.
* For an example of a pathogenesis section within a pathophysiology page, click [[Pericarditis pathophysiology#Pathogenesis|here]]
==Genetics==
*Some diseases are genetic, and have particular inheritance patterns, and express different phenotypes.
*The effect that genetics may have on the pathophysiology of a disease can be described in this section.
==== Template sentences ====
*[Disease name] is transmitted in [mode of genetic transmission] pattern.
*Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
==Associated Conditions==
*Conditions associated with the disease can be detailed in this section.
==== Template sentences ====
*The most important conditions/diseases associated with [disease name] include:
**Condition 1: A brief explanation of the condition and its association with the disease
**Condition 2: A brief explanation of the condition and its association with the disease
For an example of an associated conditions sub-section of pathophysiology, click [[Clubbing pathophysiology#Associated Conditions|here]].
==Gross Pathology==
* Gross pathology refers to macroscopic or larger scale manifestations of disease in organs, tissues and body cavities. The term is commonly used by pathologist to refer to diagnostically useful findings made during the gross examination portion of surgical specimen processing or an autopsy.
====== Template Sentences ======
* Template Sentences 1: On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
* Template Sentence 2: The most important characteristics of [disease name] on gross pathology are:
** Organ 1: List of characteristics + image
** Organ 2: List of characteristics + image
** Organ 3: List of characteristics + image
* This section is a good place to include pictures. Search for copyleft images on The Pathology Wiki [http://pathinfo.wikia.coom/wiki/Pathology_Resident_Wiki] and Ask Dr. Wiki [http://askdrwiki.com/mediawiki/index.php?title=Category:Pathology].
* For an example of this section, click [[Pericarditis pathophysiology#Gross Pathology Images|here]].
==Microscopic Pathology==
* Microscopic pathology is the disease process as it occurs at the microscopic level.
* Template Sentence 1: On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
* Template Sentence 2: The most important histopathological characteristics of [disease name] are summarized in the table below:
{| class="wikitable"
!Organs
!Light microscope
!Electron microscope
!Images
|-
|Organ 1
|Characteristic 1a
|Characterstic 1b
|Image 1
|-
|Organ 2
|Characteristic 2a
|Characterstic 2b
|Image 2
|-
|Organ 3
|Characterstic 3a
|Characterstic 3b
|Image 3
|}
* This section is a good place to include pictures. Search for copyleft images on The Pathology Wiki [http://pathinfo.wikia.coom/wiki/Pathology_Resident_Wiki] and Ask Dr. Wiki [http://askdrwiki.com/mediawiki/index.php?title=Category:Pathology].
* For an example of this section, click [[Pericarditis pathophysiology#Microscopic Pathology Images|here]].


==Pathophysiology==
===Synthesis and Metabolism===
*The main sources of vitamin D are sunlight exposure, diet, and dietary supplements.<ref name="pmid18329892">{{cite journal| author=Holick MF| title=Vitamin D status: measurement, interpretation, and clinical application. | journal=Ann Epidemiol | year= 2009 | volume= 19 | issue= 2 | pages= 73-8 | pmid=18329892 | doi=10.1016/j.annepidem.2007.12.001 | pmc=2665033 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18329892  }} </ref>
*The vitamin D synthesized in the skin is ergocalciferol or vitamin D3. The vitamin D which comes from plant sources is called D2 or cholecalciferol.
*Both cholecalciferol and ergocalciferol are inactive forms of vitamin D and sequentially activated in the liver and kidney to the active form of vitamin D, which exerts the biologic effects.
*Vitamin D refers to both cholecalciferol and ergocalciferol or vitamin D2 and vitamin D3.
'''Synthesis in the skin'''
*The synthesis of ergocalciferol (vitamin D3) occurs in the deeper layers of epidermis namely stratum spinosum and stratum basalis by the help of a chemical reaction involving UVB radiations (wavelength, 290 - 315 nm ) from sunlight.<ref name="pmid16886050">{{cite journal| author=Holick MF| title=Resurrection of vitamin D deficiency and rickets. | journal=J Clin Invest | year= 2006 | volume= 116 | issue= 8 | pages= 2062-72 | pmid=16886050 | doi=10.1172/JCI29449 | pmc=1523417 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16886050  }} </ref>
*The UVB (wavelength, 290 - 315 nm ) radiations convert 7- dehydrocholesterol to pre-vitamin D3, which isomerizes to D3.
*The formation of vitamin D3 in the skin depends on sunlight exposure, the intensity of UVB and level of melanin pigment in the skin.
*The UVB intensity varies with season and latitude.
*The clothing and sun-screen also limit the exposure.
*Vitamin D synthesized in the skin and ingested from food is transported in the blood to the liver, while it is bound to vitamin D binding protein.
'''25 - Hydroxylation in the liver'''
* In the liver, vitamin D undergoes hydroxylation into 25 - hydroxyvitamin D3 with the help of one or more cytochrome P450 vitamin D hydroxylases.<ref name="pmid18329892">{{cite journal| author=Holick MF| title=Vitamin D status: measurement, interpretation, and clinical application. | journal=Ann Epidemiol | year= 2009 | volume= 19 | issue= 2 | pages= 73-8 | pmid=18329892 | doi=10.1016/j.annepidem.2007.12.001 | pmc=2665033 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18329892  }} </ref>
* The common P 450 hydroxylases involved are CYP2R1, CYP2D11, and CYP2D25.
* The homozygous mutation of CYP2R1 gene was found in a patient with low circulating levels of 25 - hydroxyvitamin D3 with symptoms of vitamin D3 deficiency which suggests that CYP2R1 is the main enzyme involved in vitamin D hydroxylation in the liver.
* 25 - hydroxyvitamin D3 or calcifediol is the major circulating form of vitamin D and its serum level is used to assess the individual's vitamin D status.
* After hydroxylation, 25 - hydroxyvitamin D3 is released into plasma where it is bound to the vitamin D binding protein and carried to the kidneys for activation.
'''1 Alpha hydroxylation in kidneys'''
* In the proximal renal tubule of the kidney, 25 - hydroxylated vitamin D undergoes further hydroxylation into 1,25-dihydroxy vitamin D3 (1,25(OH)2D3) or calcitriol.<ref name="pmid15585789">{{cite journal |vauthors=DeLuca HF |title=Overview of general physiologic features and functions of vitamin D |journal=Am. J. Clin. Nutr. |volume=80 |issue=6 Suppl |pages=1689S–96S |year=2004 |pmid=15585789 |doi= |url=}}</ref>
* The hydroxylation in the kidney is carried by  25-hydroxyvitamin D3 1-alpha-hydroxylase, which is the product of the CYP27B1 human gene.
* This hydroxylation is under the influence of parathyroid hormone (PTH).
* 1,25-dihydroxy vitamin D3 (1,25(OH)2D3) or calcitriol is the active form of vitamin D and responsible for most of the biologic actions of vitamin D.
'''Parathyroid hormone (PTH), Vitamin D and mineral homeostasis'''
The effect of [[parathyroid hormone]] on [[mineral]] [[metabolism]] is as follows:<ref name="pmid14184232">{{cite journal |vauthors=HARRISON MT |title=INTERRELATIONSHIPS OF VITAMIN D AND PARATHYROID HORMONE IN CALCIUM HOMEOSTASIS |journal=Postgrad Med J |volume=40 |issue= |pages=497–505 |year=1964 |pmid=14184232 |pmc=2482768 |doi= |url=}}</ref><ref>{{cite book | last = Nussey | first = Stephen | title = Endocrinology : an integrated approach | publisher = Bios NCBI | location = Oxford, UK Bethesda, Md | year = 2001 | isbn = 1-85996-252-1 }}</ref>
*Effect of [[parathyroid hormone]] on [[calcium]] [[metabolism]]:
**Direct effect:
***Increased [[resorption]] of [[Bone (disambiguation)|bones]].
***Decreases [[excretion]] from [[kidney]].
**Indirect effect:
***Increases conversion of inactive [[25-hydroxy vitamin D]] to the active [[1,25-dihydroxy vitamin D]] which increases absorption of [[calcium]] from [[gut]]. Decreased phosphate concentration also increases this conversion process. [[Vitamin D]] shows synergism with [[parathyroid hormone]] action on [[bone]].
***Decreased serum [[inorganic phosphate]] concentration prevents [[Precipitation (chemistry)|precipitation]] of [[calcium phosphate]] in [[Bone (disambiguation)|bones]].
***Both these direct and indirect mechanism results in an increased serum [[calcium]] concentration.
*Effect of [[parathyroid hormone]] on [[inorganic phosphate]] [[metabolism]]:
**Increases [[excretion]] of [[Phosphate|inorganic phosphate]] from [[kidney]] resulting in decreased serum concentration of [[phosphate]].
*Effect of [[parathyroid hormone]] on [[magnesium]] concentration:
**Decreases [[excretion]] of [[magnesium]] resulting in increased serum [[magnesium]] concentretion.
Effect of [[Mineral|minerals]] and [[vitamin D]] on [[parathyroid hormone]]:
*Decrease in serum [[calcium]] concentration stimulates [[parathyroid hormone]].
*[[Calcium]] provides [[negative feedback]] on [[parathyroid hormone]].
*[[Magnesium]] provides [[negative feedback]] on [[parathyroid hormone]].
*[[Vitamin D]] decreases the concentration of [[parathyroid hormone]].
<br><br><br>
<div style="text-align: center;">'''The Sequence of Events in Parathyroid, Vitamin D, and Mineral Homeostasis''' </div>
<br>
{{familytree/start |}}
{{familytree | | | | | | | | | | | | A01 |A01='''Parathyroid hormone'''}}
{{familytree | | | | | | | |,|-|-|-|-|^|-|-|-|-|-|-|-|-|-|-|-|-|-|-|.|}}
{{familytree | | | | | | | B01 | | | | | | | | | | | | | | | | | | B02 | | |B01=[[Kidney]]|B02=[[Bone]]}}
{{familytree | |,|-|-|-|-|-|+|-|-|-|-|v|-|-|-|-|-|-|.| | | | | | | |!| }}
{{familytree | C01 | | | | C02 | | | C03 | | | | | C04 | | | | | | C05 |C01=Decreased [[excretion]] of [[magnesium]]|C02=Increasead conversion of inactive [[25-hydroyx vitamin D]] to the active [[1,25-dihydroy xvitamin D]]|C03=Increase [[excretion]] of inorganic [[phosphate]]|C04=Decrease [[excretion]] of [[calcium]]|C05=Increased [[resorption]] of [[bone]]}}
{{familytree | |!| | | | | |!| | | | |!| | | | | | |!| | | | | | | |!| |}}
{{familytree | D01 | | | | D02 | | | D03 | | | | | |`|-|-|-|-|.| | |!|D01=Increased serum concentration of [[magnesium]]|D02=Increased absorption of [[calcium]] from [[gut]]|D03=Decreased [[serum]] concentration of inorganic [[phosphate]]}}
{{familytree | | | | | | | |!| | | | |!| | | | | | | | | | | |!| | |!|}}
{{familytree | | | | | | | |!| | | | |`|-|-| E01 |-|-|-|-|.| |!| | |!| E01=Prevents precipitation of [[calcium phosphate]] in [[bones]]}}
{{familytree | | | | | | | |!| | | | | | | | | | | | | | |!| |!| | |!| | | | | |}}
{{familytree | | | | | | | |`|-|-|-|-|-|-|-|-|-|-|-|-|-|-| F01 |-|-|'| | |F01=Increased serum concentration of [[calcium]]}}
{{familytree/end}}
<br><br>
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Latest revision as of 19:18, 9 October 2017

Vitamin D deficiency Microchapters

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Overview

Historical Perspective

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Pathophysiology

Causes

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Husnain Shaukat, M.D [2]

Overview

Pathophysiology

Synthesis and Metabolism

  • The main sources of vitamin D are sunlight exposure, diet, and dietary supplements.[1]
  • The vitamin D synthesized in the skin is ergocalciferol or vitamin D3. The vitamin D which comes from plant sources is called D2 or cholecalciferol.
  • Both cholecalciferol and ergocalciferol are inactive forms of vitamin D and sequentially activated in the liver and kidney to the active form of vitamin D, which exerts the biologic effects.
  • Vitamin D refers to both cholecalciferol and ergocalciferol or vitamin D2 and vitamin D3.

Synthesis in the skin

  • The synthesis of ergocalciferol (vitamin D3) occurs in the deeper layers of epidermis namely stratum spinosum and stratum basalis by the help of a chemical reaction involving UVB radiations (wavelength, 290 - 315 nm ) from sunlight.[2]
  • The UVB (wavelength, 290 - 315 nm ) radiations convert 7- dehydrocholesterol to pre-vitamin D3, which isomerizes to D3.
  • The formation of vitamin D3 in the skin depends on sunlight exposure, the intensity of UVB and level of melanin pigment in the skin.
  • The UVB intensity varies with season and latitude.
  • The clothing and sun-screen also limit the exposure.
  • Vitamin D synthesized in the skin and ingested from food is transported in the blood to the liver, while it is bound to vitamin D binding protein.

25 - Hydroxylation in the liver

  • In the liver, vitamin D undergoes hydroxylation into 25 - hydroxyvitamin D3 with the help of one or more cytochrome P450 vitamin D hydroxylases.[1]
  • The common P 450 hydroxylases involved are CYP2R1, CYP2D11, and CYP2D25.
  • The homozygous mutation of CYP2R1 gene was found in a patient with low circulating levels of 25 - hydroxyvitamin D3 with symptoms of vitamin D3 deficiency which suggests that CYP2R1 is the main enzyme involved in vitamin D hydroxylation in the liver.
  • 25 - hydroxyvitamin D3 or calcifediol is the major circulating form of vitamin D and its serum level is used to assess the individual's vitamin D status.
  • After hydroxylation, 25 - hydroxyvitamin D3 is released into plasma where it is bound to the vitamin D binding protein and carried to the kidneys for activation.

1 Alpha hydroxylation in kidneys

  • In the proximal renal tubule of the kidney, 25 - hydroxylated vitamin D undergoes further hydroxylation into 1,25-dihydroxy vitamin D3 (1,25(OH)2D3) or calcitriol.[3]
  • The hydroxylation in the kidney is carried by 25-hydroxyvitamin D3 1-alpha-hydroxylase, which is the product of the CYP27B1 human gene.
  • This hydroxylation is under the influence of parathyroid hormone (PTH).
  • 1,25-dihydroxy vitamin D3 (1,25(OH)2D3) or calcitriol is the active form of vitamin D and responsible for most of the biologic actions of vitamin D.

Parathyroid hormone (PTH), Vitamin D and mineral homeostasis The effect of parathyroid hormone on mineral metabolism is as follows:[4][5]

Effect of minerals and vitamin D on parathyroid hormone:




The Sequence of Events in Parathyroid, Vitamin D, and Mineral Homeostasis


 
 
 
 
 
 
 
 
 
 
 
Parathyroid hormone
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Kidney
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Bone
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Decreased excretion of magnesium
 
 
 
Increasead conversion of inactive 25-hydroyx vitamin D to the active 1,25-dihydroy xvitamin D
 
 
Increase excretion of inorganic phosphate
 
 
 
 
Decrease excretion of calcium
 
 
 
 
 
Increased resorption of bone
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Increased serum concentration of magnesium
 
 
 
Increased absorption of calcium from gut
 
 
Decreased serum concentration of inorganic phosphate
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Prevents precipitation of calcium phosphate in bones
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Increased serum concentration of calcium
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 



References

  1. ↑ 1.0 1.1 Holick MF (2009). "Vitamin D status: measurement, interpretation, and clinical application". Ann Epidemiol. 19 (2): 73–8. doi:10.1016/j.annepidem.2007.12.001. PMC 2665033. PMID 18329892.
  2. ↑ Holick MF (2006). "Resurrection of vitamin D deficiency and rickets". J Clin Invest. 116 (8): 2062–72. doi:10.1172/JCI29449. PMC 1523417. PMID 16886050.
  3. ↑ DeLuca HF (2004). "Overview of general physiologic features and functions of vitamin D". Am. J. Clin. Nutr. 80 (6 Suppl): 1689S–96S. PMID 15585789.
  4. ↑ HARRISON MT (1964). "INTERRELATIONSHIPS OF VITAMIN D AND PARATHYROID HORMONE IN CALCIUM HOMEOSTASIS". Postgrad Med J. 40: 497–505. PMC 2482768. PMID 14184232.
  5. ↑ Nussey, Stephen (2001). Endocrinology : an integrated approach. Oxford, UK Bethesda, Md: Bios NCBI. ISBN 1-85996-252-1.

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