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PBGPressure Breathing for Gravity
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References in periodicals archive ?
Monthly administration of givosiran has the potential to significantly lower induced liver ALAS1 levels in a sustained manner and thereby decrease neurotoxic heme intermediates, aminolevulinic acid (ALA) and porphobilinogen (PBG), to near normal levels.
Accumulation of porphobilinogen (PBG) leads to acute attacks.
[2] Nonstandard abbreviations: AIP, acute intermittent porphyria; ALA, aminolevulinic acid (ALA); PBG, porphobilinogen; ALAD, ALA dehydratase.
Acute intermittent porphyria (AIP) is a rare metabolic disorder that is the most common of the acute porphyries and is characterized by enzymatic defect of porphobilinogen deaminase with depot and increased excretion of porphyrins and their precursors (1).
Acute porphyria, characterized by a potent, variable, catalytic defect of enzymes involved in the heme pathway, is accompanied by overproduction of heme-precursor molecules, specifically delta-ALA and porphobilinogen [16, 17].
Further researches on the characteristics of chlorophyll metabolism indicated that the precursors of D-aminolevulinic acid (ALA), porphobilinogen (PBG), uroporphyrinogen III (Urogen III), coproporphyrinogen III (Coprogen III), protoporphyrin IX (Proto IX), Mg-protoporphyrin IX (Mg-Proto IX) and protochlorophyllide (Pchlide) in chlorophyll biosynthesis in Burley21 were lower than in Maryland609 at vigorous growing period; the activity of D-aminolevulinate dehydratase (ALAD) in Burley21 was 0.43% as compared to Maryland609, but the activity of chlorophyllase in Burley21 was 2.04 times as high as in that of Maryland609.
The urinary porphobilinogen (PBG) level was 378 [micro]mol/L (reference value <9), the faecal porphyrins were marginally elevated at 374 nmol/g dry weight (reference value <200) and the plasma emission spectrum was maximal at 619 nm.
Parameters Matrices Value Coproporphyrin I Urine/24 h 7.65 microg/24h Coproporphyrin III Urine/24 h 59.3 microg/24h Uroporphyrin Urine/24 h 12.7 microg/24h S-Aminolevulinic Acid Urine/24 h 2.1 mg/24h Porphobilinogen Urine/24 h 1.22 mg/24h N-Acetyl-beta-D-glucosaminidase Urine/24 h 5.14 IU/L [delta]-Aminolevulinic acid dehydratase Blood 75 U/mL Zinc protoporphyrin 67 microg/dL * Reference Parameters normal levels Coproporphyrin I <25 Coproporphyrin III <75 Uroporphyrin <25 S-Aminolevulinic Acid 0.25-6.4 Porphobilinogen 0.1-1.7 N-Acetyl-beta-D-glucosaminidase 0.3-12 [delta]-Aminolevulinic acid dehydratase >20 Zinc protoporphyrin <40 * Out of normal levels.
This method is based in analysis of porphobilinogen (PBG) formation after [delta]-aminolevulinic acid addition.
Keywords: Acute intermittent porphyria, Porphobilinogen deaminase, Gene mutation, Menstruation.
Acute intermittent porphyria (AIP) is an autosomal dominant inborn error of metabolism caused by deficiency of porphobilinogen (PBG) deaminase, also known as hydroxymethylbilane synthase (HMBS), the third enzyme in the heme biosynthetic pathway.