Episodic acidity

Many lakes also suffer from a phenomenon called episodic acidity. Episodic acidity means that most of the time the lake has a pH within acceptable levels. But occasionally, the pH of the lake becomes much lower when heavy rainstorms or snow melts bring in large amounts of runoff. Episodic acidity sometimes results in large fish kills. The Northeastern part of the United States and Canada are especially hard hit due to the poor buffering capacity of the soil in those areas. 

It has been estimated that 1.4-7.4 times as many streams in the eastern United States undergo episodic acidification than are chronically acidic (108). Similarly, the number of episodically acidic Adirondack lakes is estimated to be 3 times higher than the number of chronically acidic lakes (108). Wigington et al. (109) reported that acidic episodes occur in a wide range of geographic locations in the northeastern, southeastern, and western United States, as well as in Scandinavia, Europe, and Canada. 

Mortalities of fish due to short term acid episodes ( acid flushes ) associated with meltwater or spate conditions have probably been occurring naturally in upland streams prior to the advent of acidic deposition. However reports of fish kills (Prigg, 1983 Milner Hemsworth, 1984) and other effects of acidity on fish are now more common (Hardman Morrison, 1982 Stoner et al, 1984). Laboratory tests quickly established that acid waters with low calcium and high levels of aluminium adversely affected fish survival, particularly at early stages in the life cycle. Salmonids are particularly fected with salmon being more sensitive than trout. Many acid waters where salmonid fish are now sparse or absent have met these toxicological... 

Marmorek, D.R. Thornton, K.W. Baker, J.P. Bernard, D.P. Jones, M.L. Reuber,B. Acidic Episodes in Surface Waters The State of ence. Final Rept., US/EPA, Corvallis, OR, 1987. 

Lesch-Nyhan syndrome, an overproduction hyperuricemia characterized by frequent episodes of uric acid hthiasis and a bizarre syndrome of self-mutilation, reflects a defect in hypoxanthme-guanine phosphoribo-syl transferase, an enzyme of purine salvage (Figure 34—4). The accompanying rise in intracellular PRPP results in purine overproduction. Mutations that decrease or abohsh hypoxanthine-guanine phosphoribosyltrans-ferase activity include deletions, frameshift mutations, base substitutions, and aberrant mRNA splicing. 

Allopurinol is well absorbed with a short half-life of 2 to 3 hours. The half-life of oxypurinol approaches 24 hours, allowing allopurinol to be dosed once daily. Oxypurinol is cleared primarily renally and can accumulate in patients with reduced kidney function. Allopurinol should not be started during an acute gout attack because sudden shifts in serum uric acid levels may precipitate or exacerbate gouty arthritis. Rapid shifts in serum uric acid can change the concentration of monosodium urate crystals in synovial fluid, causing more crystals to precipitate. Thus some clinicians advocate a prophylactic dose of colchicine (0.6 mg/day) during initiation of antihyperuricemic therapy. Acute episodes should be treated appropriately before maintenance treatment is started. 

Fukuoka was found to be homozygous for the 1615 G to A (539 Asp to Asn) mutation. This mutation occurred at relatively conserved amino acid residues and caused an alteration in hydrophobicity. Recently, we examined the structure-function relationship of these variants using the recombinant protein (F14). Although all of the four variants were found to be heat labile, the residual GPI activity seems to reflect clinical severity, such as the degree of anemia and episodes of hemolytic crisis. GPI Matsumoto, associated with severe anemia and hemolytic crisis, was extremely unstable, and GPI Iwate, which is associated with compensated hemolytic anemia, showed moderate heat instability. Affinity for substrate, fructose-6-phosphate, was slightly decreased in GPI Narita and GPI Fukuoka, which were associated with moderate anemia and hemolytic crisis. 

A study of 55 adolescents who had been treated for lead intoxication in early childhood (11-17 years earlier) revealed no evidence of chronic nephropathy, as evidenced by endogenous creatinine clearance, BUN, serum uric acid, and routine urinalysis (Chisolm et al. 1976). PbB levels during the acute poisoning episode ranged from 100 to 650 pg/dL all patients received immediate chelation therapy. At the time of the study, their PbB levels had decreased to less than 40 pg/dL. 

Effective treatment of maple syrup urine disease involves the restriction of dietary branched-chain amino acids. Long-term treatment entails the dietary restriction of the BCAAs. This is accomplished by administration of a special formula from which these amino acids are removed. The outlook for intellectual development is favorable in youngsters in whom diagnosis is made early and who do not suffer recurrent, severe episodes of metabolic decompensation [17]. 

Prophylactic treatment can be withheld if the first episode of acute gouty arthritis was mild and responded promptly to treatment, the patient s serum urate concentration was only minimally elevated, and the 24-hour urinary uric acid excretion was not excessive (less than 1,000 mg/24 hours on a regular diet). 

If the patient had a severe attack of gouty arthritis, a complicated course of uric acid lithiasis, a substantially elevated serum uric acid (greater than 10 mg/dL), or a 24-hour urinary excretion of uric acid of more than 1,000 mg, then prophylactic treatment should be instituted immediately after resolution of the acute episode. 

In episodic HE, lactulose is initiated at 45 mL every hour (or 300 mL lactulose syrup with 700 mL water given as a retention enema) until catharsis begins. The dose is then decreased to 15 to 30 mL orally every 8 to 12 hours and titrated to produce two to three soft, acidic stools per day. 

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