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An unusual presentation of tumor lysis syndrome in a patient with advanced gastric adenocarcinoma: case report and literature review.

Vodopivec DM, Rubio JE, Fornoni A, Lenz O - Case Rep Med (2012)

Bottom Line: We also provide information regarding the total cases of TLS in solid tumors reported from 1977 to present day.Then, we looked for new reported cases from 2004 to present day.All reports (case reports, brief reports, letters to editor, correspondence, reviews, journals, and short communications) identified through these searches were reviewed and included.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology and Hypertension, Jackson Memorial Hospital, 1611 North West 12th Avenue, Miami, FL 33101, USA.

ABSTRACT
Tumor lysis syndrome (TLS) is characterized by hyperuricemia, hyperkalemia, hyperphosphatemia, and secondary hypocalcemia in patients with a malignancy. When these laboratory abnormalities develop rapidly, clinical complications such as cardiac arrhythmias, acute renal failure, seizures, or death may occur. TLS is caused by rapid release of intracellular contents by dying tumor cells, a condition that is expected to be common in hematologic malignancies. However, TLS rarely occurs with solid tumors, and here we present the second chemotherapy-induced TLS in a patient with advanced gastric adenocarcinoma to be reported in the literature. We also provide information regarding the total cases of TLS in solid tumors reported from 1977 to present day. Our methodology involved identifying key articles from existing reviews of the literature and then using search terms from these citations in MEDLINE to find additional publications. We relied on a literature review published in 2003 by Baeksgaard et al., where they gathered all total 45 cases reported from 1977 to 2003. Then, we looked for new reported cases from 2004 to present day. All reports (case reports, brief reports, letters to editor, correspondence, reviews, journals, and short communications) identified through these searches were reviewed and included.

No MeSH data available.


Related in: MedlinePlus

Mechanism of action of hypouricemic agents. Hyperuricemia is a consequence of the catabolism of purine nucleic acids to hypoxanthine and xanthine and then to uric acid via the enzyme xanthine oxidase. Allopurinol is a competitive inhibitor of the enzyme xanthine oxydase. Rasburicase (exogenous urate oxidase) leads uric acid to a more soluble compound, allantoin.
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fig4: Mechanism of action of hypouricemic agents. Hyperuricemia is a consequence of the catabolism of purine nucleic acids to hypoxanthine and xanthine and then to uric acid via the enzyme xanthine oxidase. Allopurinol is a competitive inhibitor of the enzyme xanthine oxydase. Rasburicase (exogenous urate oxidase) leads uric acid to a more soluble compound, allantoin.

Mentions: Allopurinol is a competitive inhibitor of xanthine oxidase (Figure 4), and it has been successfully prescribed for the treatment of hyperuricemia. Allopurinol is metabolized to oxypurinol, which in turn inhibits xanthine oxidase; therefore, it blocks the metabolic process of xanthine and hypoxanthine to uric acid, leading to an increase in the levels of these two metabolites [1, 3–6]. As a result, patients with massive TLS who have been prescribed allopurinol may develop xanthine precipitation leading to acute renal failure [1, 2, 4, 5, 7, 65]. This can be avoided by replacing allopurinol with urate oxidase, which catabolizes uric acid to the more soluble compound allantoin [1–6] (Figure 4). Urate oxidase is an enzyme that can be found in many mammals except humans [1, 3, 4, 6]. The two available commercial forms of urate oxidase are a nonrecombinant form (uricozyme) and a recombinant form (rasburicase), which is the preferred one. Rasburicase has been shown to be more effective than allopurinol, since it has higher uricolytic effect [1, 3–7], it does not increase xanthine levels [1, 2, 4, 5, 7], and it reduces high uric acid levels prior treatment initiation [1–7].


An unusual presentation of tumor lysis syndrome in a patient with advanced gastric adenocarcinoma: case report and literature review.

Vodopivec DM, Rubio JE, Fornoni A, Lenz O - Case Rep Med (2012)

Mechanism of action of hypouricemic agents. Hyperuricemia is a consequence of the catabolism of purine nucleic acids to hypoxanthine and xanthine and then to uric acid via the enzyme xanthine oxidase. Allopurinol is a competitive inhibitor of the enzyme xanthine oxydase. Rasburicase (exogenous urate oxidase) leads uric acid to a more soluble compound, allantoin.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3368228&req=5

fig4: Mechanism of action of hypouricemic agents. Hyperuricemia is a consequence of the catabolism of purine nucleic acids to hypoxanthine and xanthine and then to uric acid via the enzyme xanthine oxidase. Allopurinol is a competitive inhibitor of the enzyme xanthine oxydase. Rasburicase (exogenous urate oxidase) leads uric acid to a more soluble compound, allantoin.
Mentions: Allopurinol is a competitive inhibitor of xanthine oxidase (Figure 4), and it has been successfully prescribed for the treatment of hyperuricemia. Allopurinol is metabolized to oxypurinol, which in turn inhibits xanthine oxidase; therefore, it blocks the metabolic process of xanthine and hypoxanthine to uric acid, leading to an increase in the levels of these two metabolites [1, 3–6]. As a result, patients with massive TLS who have been prescribed allopurinol may develop xanthine precipitation leading to acute renal failure [1, 2, 4, 5, 7, 65]. This can be avoided by replacing allopurinol with urate oxidase, which catabolizes uric acid to the more soluble compound allantoin [1–6] (Figure 4). Urate oxidase is an enzyme that can be found in many mammals except humans [1, 3, 4, 6]. The two available commercial forms of urate oxidase are a nonrecombinant form (uricozyme) and a recombinant form (rasburicase), which is the preferred one. Rasburicase has been shown to be more effective than allopurinol, since it has higher uricolytic effect [1, 3–7], it does not increase xanthine levels [1, 2, 4, 5, 7], and it reduces high uric acid levels prior treatment initiation [1–7].

Bottom Line: We also provide information regarding the total cases of TLS in solid tumors reported from 1977 to present day.Then, we looked for new reported cases from 2004 to present day.All reports (case reports, brief reports, letters to editor, correspondence, reviews, journals, and short communications) identified through these searches were reviewed and included.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology and Hypertension, Jackson Memorial Hospital, 1611 North West 12th Avenue, Miami, FL 33101, USA.

ABSTRACT
Tumor lysis syndrome (TLS) is characterized by hyperuricemia, hyperkalemia, hyperphosphatemia, and secondary hypocalcemia in patients with a malignancy. When these laboratory abnormalities develop rapidly, clinical complications such as cardiac arrhythmias, acute renal failure, seizures, or death may occur. TLS is caused by rapid release of intracellular contents by dying tumor cells, a condition that is expected to be common in hematologic malignancies. However, TLS rarely occurs with solid tumors, and here we present the second chemotherapy-induced TLS in a patient with advanced gastric adenocarcinoma to be reported in the literature. We also provide information regarding the total cases of TLS in solid tumors reported from 1977 to present day. Our methodology involved identifying key articles from existing reviews of the literature and then using search terms from these citations in MEDLINE to find additional publications. We relied on a literature review published in 2003 by Baeksgaard et al., where they gathered all total 45 cases reported from 1977 to 2003. Then, we looked for new reported cases from 2004 to present day. All reports (case reports, brief reports, letters to editor, correspondence, reviews, journals, and short communications) identified through these searches were reviewed and included.

No MeSH data available.


Related in: MedlinePlus