Sandbox:Nimmi Nath: Difference between revisions

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It has been shown that [[lactobacilli]] are particularly useful in promoting gastric ulcer healing in rats, when administered as an individual probiotic strain, such as Lactobacillus rhamnosus GG, Lactobacillus gasseri OLL2716, or Lactobacillus acidophilus or as a probiotic mixture, VSL#3. Lactobacillus rhamnosus GG increases the cellular proliferation to apoptosis ratio and therefore promotes regeneration of epithelial cells, particularly at the ulcer margins. In clinical studies, a probiotic mixture was demonstrated to be better than a single strain for improving the characteristics of indigenous microflora.
==Overview==
<references />
 
Familial hypocalciuric hypercalcemia may be caused by genetic and rarely autoimmune factors. FHH type 1(the most common type of FHH) is caused by mutations in the CASR gene, which codes for the calcium-sensing receptor, CaSR protein. FHH type 2 is caused by mutations of the GNA11 gene,which codes for the alpha subunit of a G protein called G11, which ultimately works with CaSR protein to regulate the calcium levels in the blood. FHH type 3 is caused by mutations in the AP2S1 gene, (adaptor-related protein complex 2, sigma 1 subunit).
 
==Causes==
Each subtype of FHH is caused by mutations in the following genes:
* FHH Type 1 - CaSR gene (Chromosome 3q21.1) <ref name="HannanBabinsky2016">{{cite journal|last1=Hannan|first1=Fadil M|last2=Babinsky|first2=Valerie N|last3=Thakker|first3=Rajesh V|title=Disorders of the calcium-sensing receptor and partner proteins: insights into the molecular basis of calcium homeostasis|journal=Journal of Molecular Endocrinology|volume=57|issue=3|year=2016|pages=R127–R142|issn=0952-5041|doi=10.1530/JME-16-0124}}</ref>
 
* FHH Type 2 - GNA11 gene (Chromosome 19p13.3) <ref name="HannanBabinsky2016">{{cite journal|last1=Hannan|first1=Fadil M|last2=Babinsky|first2=Valerie N|last3=Thakker|first3=Rajesh V|title=Disorders of the calcium-sensing receptor and partner proteins: insights into the molecular basis of calcium homeostasis|journal=Journal of Molecular Endocrinology|volume=57|issue=3|year=2016|pages=R127–R142|issn=0952-5041|doi=10.1530/JME-16-0124}}</ref>
 
* FHH Type 3 - AP2S1 gene ( Chromosome 19p13.3)<ref name="HannanBabinsky2016">{{cite journal|last1=Hannan|first1=Fadil M|last2=Babinsky|first2=Valerie N|last3=Thakker|first3=Rajesh V|title=Disorders of the calcium-sensing receptor and partner proteins: insights into the molecular basis of calcium homeostasis|journal=Journal of Molecular Endocrinology|volume=57|issue=3|year=2016|pages=R127–R142|issn=0952-5041|doi=10.1530/JME-16-0124}}</ref>
 
Rarely, Autoimmune Hypocalciuric Hypocalcemia should be suspected in patients with similar presentation but negative mutational analyses of CASR, GNA11, and AP2S1 for familial hypocalciuric hypercalcemia.<ref name="MiñambresCorcoy2020">{{cite journal|last1=Miñambres|first1=Inka|last2=Corcoy|first2=Rosa|last3=Weetman|first3=Anthony P|last4=Kemp|first4=E Helen|title=Autoimmune Hypercalcemia Due to Autoantibodies Against the Calcium-sensing Receptor|journal=The Journal of Clinical Endocrinology & Metabolism|volume=105|issue=7|year=2020|pages=2229–2236|issn=0021-972X|doi=10.1210/clinem/dgaa219}}</ref>
 
==References==
{{ Reflist|2}}

Latest revision as of 16:42, 8 June 2021

Overview

Familial hypocalciuric hypercalcemia may be caused by genetic and rarely autoimmune factors. FHH type 1(the most common type of FHH) is caused by mutations in the CASR gene, which codes for the calcium-sensing receptor, CaSR protein. FHH type 2 is caused by mutations of the GNA11 gene,which codes for the alpha subunit of a G protein called G11, which ultimately works with CaSR protein to regulate the calcium levels in the blood. FHH type 3 is caused by mutations in the AP2S1 gene, (adaptor-related protein complex 2, sigma 1 subunit).

Causes

Each subtype of FHH is caused by mutations in the following genes:

  • FHH Type 1 - CaSR gene (Chromosome 3q21.1) [1]
  • FHH Type 2 - GNA11 gene (Chromosome 19p13.3) [1]
  • FHH Type 3 - AP2S1 gene ( Chromosome 19p13.3)[1]

Rarely, Autoimmune Hypocalciuric Hypocalcemia should be suspected in patients with similar presentation but negative mutational analyses of CASR, GNA11, and AP2S1 for familial hypocalciuric hypercalcemia.[2]

References

  1. ↑ 1.0 1.1 1.2 Hannan, Fadil M; Babinsky, Valerie N; Thakker, Rajesh V (2016). "Disorders of the calcium-sensing receptor and partner proteins: insights into the molecular basis of calcium homeostasis". Journal of Molecular Endocrinology. 57 (3): R127–R142. doi:10.1530/JME-16-0124. ISSN 0952-5041.
  2. ↑ Miñambres, Inka; Corcoy, Rosa; Weetman, Anthony P; Kemp, E Helen (2020). "Autoimmune Hypercalcemia Due to Autoantibodies Against the Calcium-sensing Receptor". The Journal of Clinical Endocrinology & Metabolism. 105 (7): 2229–2236. doi:10.1210/clinem/dgaa219. ISSN 0021-972X.
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