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🍋 Top remedies to control Uric Acid level👨‍⚕🔝

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Analysis of Uric Acid 💉 is the final product of Purine's metabolism and varies from hour to hour.
Affected by long fasting and food.
@Biochem_Lab

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Uric Acid Measurement:
=================
♦️Measurement of plasma uric acid is used in the investigation of gout and it is also used in diagnosis and monitoring of pregnancy induced hypertension (preeclamptic toxemia).
Primary gout occurs due to overproduction of uric acid and secondary gout occurs due to retention of uric acid.

♦️Analytical methodology:
1️⃣Phosphotungstate Method (Caraway method):
This method requires a protein-free filtrate for serum or plasma.
cUric acid + phosphotungstic acid + Na2CO2 (in alkaline pH) → allantoin + CO + tungsten blue.
Glucose, ascorbic acid, glutathione, hemoglobin, and drugs such as acetaminophen and caffeine commonly interfere.
@Biochem_Lab

2️⃣Methods using uricase:
The simplest of these methods measures the differential absorption of uric acid and allantoin at 293 nm.
The difference in absorbance before and after incubation with uricase is proportional to the uric acid concentration. Proteins can cause high background absorbance, reducing sensitivity; hemoglobin and xanthine can cause negative interference.
👉Uric acid+H2O+O2→allantoin+CO2+H2O2
@Biochem_Lab

3️⃣Coupled enzyme(uricase&Peroxidase) methods:
It measure the hydrogen peroxide produced as uric acid is converted to allantoin. Peroxidase or catalase is used to catalyze a chemical indicator reaction.
Bilirubin and ascorbic acid, which destroy peroxide, if present in sufficient quantity,
can interfere. Commercial reagent preparations often include potassium ferricyanide and ascorbate oxidase to minimize these interferences.
👉Uric acid +O2+2H2O→Alantoin+CO2+H2O2
👉2H2O2+4–Aminoantipyrine+DCFS→Quinoneimine+4 H2O
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♦️Reference Ranges:
===============
🔻Uricase Method:
Male 3.5–7.2 mg/dL Female 2.6–6.0 mg/dL

🔻Phosphotungstate Method:
M: 4.2–8.0 mg/dL F: 3.5–7.3 mg/dL

🔻Values are lower in children.

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💠Calcium Studies

●Serum Ca2+
✧Causes of ↑
>10.2 mg/dL

↑ Vit. D or Ca2+ intake. ↑ PTH. ↑ Bone breakdown. Hereditary disorders: e.g., Familial hypocalciuria. Metabolic: e.g., ↑↑ Thyroid, acromegaly, Addison's. Drugs: e.g., Thiazides, Li+

✧Causes of ↓
<8.5 mg/dL

Vit. D/Ca2+ ↓ intake / ↓ absorption. ↓ PTH or ↑ calcitonin Ca2+ sequestration: e.g., Saponification. ↓ Albumin e.g., Liver disease. ↓ Mg2+ or ↑ phosphorus (binds Ca2+) Osteoblastic malignancy. Drugs: e.g., Aminoglycosides .

◎●━ @Biochem_Lab ━●◎•

●Ionized Ca2+

✧Causes of ↑
⇨>5.3 mg/dL
Measures physiologically

✧Causes of ↓
⇨<4.4 mg/dL
↓ with ↑ blood pH / ↑ protein

◎●━ @Biochem_Lab ━●◎•
⇹⇹⇹⇹⇹⇹⇹⇹

⇨pH 7.4
active nonbound Ca2+, ↑ with ↓ blood pH or ↓ protein or ↓ albumin

⇨pH 7.4
↑ albumin: e.g., Multiple myeloma, dehydration

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●Urine Ca2+ (UCa)
✧Causes of ↑
→>300 mg/24hr
↑ serum Ca2+, also specific renal disease: e.g., Idiopathic hypercalciuria, RTA

✧Causes of ↓
→<100 mg/24hr
↓ serum Ca2+, also specific renal disease and drugs: 
e.g., thiazides

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●Parathyroid hormone (PTH)
✧Causes of ↑
>55 pg/mL
Primary / secondary ↑ Pparathyroid ↓ Vit. D

✧Causes of ↓
<10 pg/mL
↓ Pparathyroid, ↑ thyroid, ↓ Mg, ↑ nonparathyroid Ca2+

◎●━ @Biochem_Lab ━●◎•

●Vitamin D3 25-hydroxy [25(OH)D3]

✧Causes of ↑
>50 ng/mL

↑ Ca2+ ↑ Vit. D intake ↑ Sunlight exposure

✧Causes of ↓
<10 ng/mL

↓ Sunlight exposure, ↓ Vit D intake / absorption . Pregnancy.
Drugs: phenobarbital, phenytoin.

•◎●━ @Biochem_Lab ━●◎•

●Vitamin D3 1,25-hydroxy [1,25(OH)2D3]

✧Causes of ↑
>76 ng/mL
↑ Ca2+ ↑ Vit. D intake ↑ Sunlight exposure

✧Causes of ↓
<20 ng/mL
↓ Sunlight exposure,
↓ Vit D intake /absorption . 
Pregnancy. 
Drugs: phenobarbital, phenytoin.

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