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Página 1 a partir de 24 resultados
Phase I trial of alpha-difluoromethyl ornithine (DFMO) and methylglyoxal bis (guanylhydrazone) (MGBG) in patients with advanced prostatic cancer.
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Both alpha-difluoromethyl ornithine (DFMO) and methylglyoxal bis (guanylhydrazone) (MGBG) inhibit sequential enzymatic reactions in the pathway of polyamine biosynthesis. Since polyamines may be important factors in proliferation of cancer cells and DFMO combined with MGBG has shown synergistic
Female heterozygotes for the hypomorphic R40H mutation can have ornithine transcarbamylase deficiency and present in early adolescence: a case report and review of the literature.
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BACKGROUND
Ornithine transcarbamylase deficiency is the most common hereditary urea cycle defect. It is inherited in an X-linked manner and classically presents in neonates with encephalopathy and hyperammonemia in males. Females and males with hypomorphic mutations present later, sometimes in
[Aspartate-ornithine granules in the treatment of nonalcoholic steatohepatitis: a multiple-dose parallel controlled clinical trial].
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OBJECTIVE
To investigate the therapeutic efficacy and safety of aspartate-ornithine granules in patients with nonalcoholic steatohepatitis (NASH).
METHODS
Seventy-two patients with NASH were included in this multiple-dose parallel controlled clinical trial and received a 12-week course of
Safety, Tolerability and Pharmacokinetics of L-Ornithine Phenylacetate in Patients with Acute Liver Injury/Failure and Hyperammonemia.
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Cerebral edema remains a significant cause of morbidity and mortality in patients with acute liver failure (ALF) and has been linked to elevated blood ammonia levels. l-ornithine phenylacetate (OPA) may decrease ammonia by promoting its renal excretion as phenylacetylglutamine (PAGN), decreasing the
Hyperammoniemic coma in an adolescent girl: an unusual case of ornithine transcarbamylase deficiency.
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Ornithine transcarbamylase deficiency (OTCD) is caused by an alteration of urea synthesis, linked with partial modification of the X-chromosome, whose clinical manifestations are: lethargy, nausea, vomiting and cerebral edema. While in newborn males OTCD presents with hyperammoniemia leading to
Posterior fossa syndrome in a patient with an ornithine transcarbamylase deficiency.
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The posterior fossa syndrome (PFS) is a well-known clinical entity and mainly occurs in children. Ornithine transcarbamylase deficiency (OTC) is the most common urea cycle disorder, which occurs in an estimated 1 per 50.000 live births in Japan. Symptoms are mostly due to hyperammonemia and include
[Abrupt onset and rapid deterioration in the course of congenital ornithine transcarbamylase deficiency: a case report].
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We report a 17-year-old female case of ornithine transcarbamylase (OTC) deficiency who died of brain edema due to hyperammonemic attack. The patient had a brother with OTC deficiency who had died of hyperammonemia at 17 years of age. She firstly had a symptom of headache, nausea, vomiting and
[Ornithine transcarbamylase deficiency in adolescence and adulthood: first manifestation with life-threatening decompensation].
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BACKGROUND
Ornithine transcarbamylase (OTC) deficiency is the most frequent innate disorder of the urea cycle and is X-chromosome linked. The disease normally manifests itself shortly after birth and is fatal when untreated. Due to the different expression and X-chromosomal inheritance the
Ornithine transcarbamylase deficiency that developed at the age of 19 years with acute brain edema.
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A 19-year-old man had nausea, diarrhea, and general malaise the day before requesting emergency transport to his former primary physician. The patient became restless and had tonic seizures after admission. The patient was transferred to our hospital as there had been no improvement in his level of
Case 252: Acute Hyperammonemic Encephalopathy Resulting from Late-Onset Ornithine Transcarbamylase Deficiency.
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History A 19-year-old woman with no pertinent medical history was brought to the emergency department after being found unconscious on her bathroom floor by her roommate. In the preceding weeks, she had reported intractable nausea and vomiting, for which she had been taking ondansetron. No other
Phase I evaluation of intravenous difluoromethylornithine--a polyamine inhibitor.
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Difluoromethylornithine (DFMO), a non-competitive inhibitor of ornithine decarboxylase (ODC), the rate limiting enzyme of the polyamine synthetic pathway was evaluated in a Phase I trial. Intravenous DFMO was given to twenty patients with refractory leukemia by continuous infusion in doses from 5.5
Psychiatric Symptoms as the First or Solitary Manifestation of Somatic Illnesses: Hyperammonaemia Type II
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Aim: We describe the difficulties encountered in making a diagnosis where a somatic condition manifests itself alongside psychiatric symptoms associated with possible psychiatric comorbidities.
Methods:
A Phase II study of the polyamine analog N1,N11-diethylnorspermine (DENSpm) daily for five days every 21 days in patients with previously treated metastatic breast cancer.
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OBJECTIVE
Polyamines are ubiquitous intracellular polycationic molecules essential for cell growth and differentiation. Polyamine analogs down-regulate ornithine decarboxylase, induce spermidine/spermine N1-acetyltransferase, deplete natural polyamine pools, inhibit growth, and induce programmed
Effect of lysine infusion on urea cycle in lysinuric protein intolerance.
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Poor intestinal absorption and excessive renal loss of dibasic amino acids result in low plasma concentrations in patients with lysinuric protein intolerance (LPI). Arginine and ornithine deficiency impair the function of the urea cycle and cause hyperammonemia after protein intake, while chronic
[Cystinuria therapy by ascorbic acid (author's transl)].
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At the beginning of the four chapters on phenomena, analysis, pathophysiology and therapy of cystinuria the essentials of the published literature are summarized. The frequency of cystinuria is in the order of 1:10,000. Besides the cystine lithiasis occurring in nine tenths of all cystinuria
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