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Bone Disorders01:29

Bone Disorders

Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
Roles of Electrolytes: Calcium and Phosphate01:27

Roles of Electrolytes: Calcium and Phosphate

Calcium and phosphate are essential electrolytes in the human body, with calcium being the most abundant mineral. Around 99% of the body's calcium is stored in the skeleton and teeth, forming a crystal lattice of mineral salts in combination with phosphates. Calcium plays crucial roles in various bodily functions such as blood clotting, neurotransmitter release, muscle tone maintenance, and nervous and muscle tissue excitability.
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Introduction to Electrolytes01:33

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In humans, electrolytes play a vital role in various physiological processes. Balancing electrolyte levels is essential for normal body functions; their imbalance can be life-threatening. The major electrolytes include sodium, potassium, chloride, calcium, phosphate, and bicarbonate. They are primarily involved in physiological processes, such as nerve signal transmission, membrane trafficking, muscle contraction, buffering body fluids, and balancing water levels in the body.
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Chronic Kidney Disease II: Clinical Manifestations01:24

Chronic Kidney Disease II: Clinical Manifestations

Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...
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What is the Skeletal System?

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Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
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Published on: July 3, 2020

Hypophosphatemic rickets.

Varsha S Jagtap1, Vijaya Sarathi, Anurag R Lila

  • 1Department of Endocrinology, Seth G. S. Medical College, Parel, Mumbai, India.

Indian Journal of Endocrinology and Metabolism
|April 4, 2012
PubMed
Summary
This summary is machine-generated.

Hypophosphatemic rickets involves bone mineralization defects due to kidney phosphorus handling issues. This review covers clinical, biochemical, genetic features, and management of these disorders, including X-linked hypophosphatemic rickets.

Keywords:
125(OH)2D3X-linked hypophosphatemic ricketsautosomal dominant hypophosphatemic ricketsfibroblast growth factor 23hypophosphatemiatumor-induced osteomalacia

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Area of Science:

  • Endocrinology
  • Genetics
  • Nephrology

Background:

  • Hypophosphatemic rickets are bone mineralization disorders stemming from impaired renal phosphorus regulation.
  • Common forms include X-linked hypophosphatemic rickets, autosomal dominant hypophosphatemic rickets, and tumor-induced osteomalacia.
  • Elevated phosphatonins, notably fibroblast growth factor 23 (FGF23), are a unifying feature across diverse etiologies.

Purpose of the Study:

  • To review the clinical, biochemical, and genetic characteristics of hypophosphatemic disorders.
  • To discuss current management strategies for conditions causing defective bone mineralization.
  • To highlight the role of the osteo-renal axis and phosphatonins in phosphorus homeostasis.

Main Methods:

  • Literature review of inherited and acquired hypophosphatemic disorders.
  • Analysis of genetic studies on phosphorus homeostasis.
  • Synthesis of clinical, biochemical, and genetic data.

Main Results:

  • Defective renal phosphorus handling underlies hypophosphatemic rickets.
  • Increased phosphatonin levels, particularly FGF23, are implicated.
  • The complex osteo-renal axis mechanisms are still being elucidated.

Conclusions:

  • Hypophosphatemic disorders result from disruptions in phosphorus regulation.
  • Understanding the osteo-renal axis is crucial for diagnosing and managing these conditions.
  • Ongoing research continues to identify new disorders and refine therapeutic approaches.