RESUMO
A 22-month-old female with high-risk neuroblastoma completed 5 cycles of chemotherapy then underwent high-dose chemotherapy with autologous stem cell rescue (ASCR). Parenteral nutrition was administered from day +2 following ASCR, as she was unable to tolerate nasogastric feeds because of grade IV mucositis and vomiting. On day +12, she developed worsening metabolic acidosis with above reportable levels of lactic acid. Given the patient's well clinical appearance and paucity of evidence of end-organ dysfunction on physical examination and on laboratory studies, there was high suspicion that the patient's lactic acidosis did not result from tissue hypoxia and was, in fact, a type B lactic acidosis. Thiamin was empirically administered, with rapid improvement in lactic acidosis. Thiamin deficiency was later confirmed by laboratory studies drawn prior to thiamin administration.
Assuntos
Acidose Láctica , Transplante de Células-Tronco Hematopoéticas , Deficiência de Tiamina , Acidose Láctica/etiologia , Acidose Láctica/terapia , Feminino , Transplante de Células-Tronco Hematopoéticas/efeitos adversos , Humanos , Lactente , Tiamina , Deficiência de Tiamina/etiologia , Transplante AutólogoRESUMO
Dihydrolipoamide dehydrogenase (DLD, E3) is a flavoprotein common to pyruvate, α-ketoglutarate and branched-chain α-keto acid dehydrogenases. We found two novel DLD mutations (p.I40Lfs*4; p.G461E) in a 19 year-old patient with lactic acidosis and a complex amino- and organic aciduria consistent with DLD deficiency, manifesting progressive exertional fatigue. Muscle biopsy showed mitochondrial proliferation and lack of DLD cross-reacting material. Riboflavin supplementation determined the complete resolution of exercise intolerance with the partial restoration of the DLD protein and disappearance of mitochondrial proliferation in the muscle. Morphological and functional studies support the riboflavin chaperon-like role in stabilizing DLD protein with rescue of its expression in the muscle.
Assuntos
Acidose Láctica/complicações , Acidose Láctica/terapia , Doença da Urina de Xarope de Bordo/complicações , Doença da Urina de Xarope de Bordo/terapia , Miopatias Mitocondriais/patologia , Miopatias Mitocondriais/terapia , Riboflavina/administração & dosagem , Complexo Vitamínico B/administração & dosagem , Biópsia , Expressão Gênica/efeitos dos fármacos , Humanos , Masculino , Músculos/patologia , Fenótipo , Estabilidade Proteica/efeitos dos fármacos , Adulto JovemRESUMO
Salmeterol, a long-acting ß2-adrenergic receptor agonist used for the treatment of asthma and chronic obstructive pulmonary disease, has an adverse effects profile that is similar to that of salbutamol and other ß2-agonists. We report a sympathomimetic syndrome with metabolic acidosis and hyperlactatemia after intentional inhalation of salmeterol in a suicide attempt. A 16-year-old female patient was admitted to the emergency department approximately 2 hours after having inhaled 60 puffs of a combination of salmeterol xinafoate 25 µg and fluticasone propionate 50 µg. She presented in an anxious state with complaints of palpitations and chest pain. The electrocardiogram demonstrated sinus tachycardia and ST-segment depression in the inferior and anterolateral leads. Laboratory findings showed hypokalemia, hypophosphatemia, and lactic acidosis. Cardiac troponin I and creatine kinase MB remained within the normal range. Treatment was supportive and included intravenous fluids and cautious potassium supplementation. The next day, electrocardiographic and laboratory findings returned to normal. We hypothesize that stimulation of ß2-adrenergic receptors by inhalation of salmeterol caused this patient's lactic acidosis. This observation is consistent with the hypothesis that the hyperlactatemia observed during asthma attacks is due in part to the administration of high doses of ß2-agonists. Salmeterol overdose by inhalation appears to be sufficient to cause lactic acidosis.
Assuntos
Acidose Láctica/induzido quimicamente , Albuterol/análogos & derivados , Androstadienos/efeitos adversos , Asma/tratamento farmacológico , Overdose de Drogas/complicações , Intenção , Ácido Láctico/sangue , Acidose Láctica/sangue , Acidose Láctica/terapia , Administração por Inalação , Adolescente , Agonistas de Receptores Adrenérgicos beta 2/administração & dosagem , Agonistas de Receptores Adrenérgicos beta 2/efeitos adversos , Albuterol/administração & dosagem , Albuterol/efeitos adversos , Androstadienos/administração & dosagem , Broncodilatadores/administração & dosagem , Broncodilatadores/efeitos adversos , Esquema de Medicação , Overdose de Drogas/sangue , Overdose de Drogas/diagnóstico , Quimioterapia Combinada , Feminino , Hidratação , Fluticasona , Humanos , Potássio/uso terapêutico , Xinafoato de SalmeterolRESUMO
D-lactic acidosis, a complication of short bowel syndrome, presents with a variety of neurological symptoms and metabolic acidosis. Treatment is hydration, replacement of nutritional deficiency replacement, and selective antibiotics. Prevention entails complex carbohydrate diet and vitamin and mineral supplements.
Assuntos
Acidose Láctica/complicações , Acidose Láctica/terapia , Confusão/etiologia , Antibacterianos/uso terapêutico , Feminino , Hidratação , Humanos , Pessoa de Meia-Idade , Síndrome do Intestino Curto/complicaçõesRESUMO
We encountered a case of total parenteral nutrition-associated lactic acidosis that did not respond to sodium bicarbonate or other conventional emergency treatments. He was characterized by minimal food intake before surgery, delayed gastric emptying after pylorus-preserving pancreatoduodenectomy due to pancreas head cancer and long-term total parenteral nutrition without food intake and vitamin supplements after surgery. After thiamine administration, the patient very quickly recovered with dramatic reestablishment of the acid-base balance. We emphasize the need to supplement total parenteral nutrition with thiamine-containing vitamins for the patients whose food intake does not meet nutritional requirements and to intravenously replenish using high-dose thiamine simultaneously with the manifestation of signs and symptoms of severe lactic acidosis with unknown cause. In conclusion, thiamine deficiency should be included in the differential diagnosis of lactic acidosis for the patients who received total parenteral nutrition without food intake and vitamin supplements.
Assuntos
Acidose Láctica/etiologia , Nutrição Parenteral Total/efeitos adversos , Deficiência de Tiamina/etiologia , Acidose Láctica/terapia , Esvaziamento Gástrico , Humanos , Infusões Intravenosas , Masculino , Diálise Renal , Tiamina/administração & dosagem , Deficiência de Tiamina/diagnóstico , Deficiência de Tiamina/terapiaRESUMO
We report the case of a leukemic child treated with chemotherapy and parenteral nutrition for three weeks, who developed a severe lactic acidosis. Clinical features included both digestive and neurological disorders associated with a moderate cardiovascular collapse. After elimination of a toxic, a neoplastic or a septic cause, a thiamin (or vitamin B1) deficiency was suspected because of the lack of vitamin supply to parenteral nutrition. Intravenous administration of thiamin rapidly controlled lactic and clinical features. The diagnosis was confirmed by a low plasmatic concentration of thiamin. Thiamin deficiency must be suspected in case of severe lactic acidosis during parenteral nutrition and systematically prevented by supply of vitamins.
Assuntos
Acidose Láctica/etiologia , Nutrição Parenteral/efeitos adversos , Leucemia-Linfoma Linfoblástico de Células Precursoras/terapia , Deficiência de Tiamina/etiologia , Tiamina/uso terapêutico , Acidose Láctica/terapia , Criança , Humanos , Masculino , Leucemia-Linfoma Linfoblástico de Células Precursoras/tratamento farmacológico , Tiamina/administração & dosagem , Deficiência de Tiamina/sangue , Deficiência de Tiamina/tratamento farmacológicoRESUMO
OBJECTIVE: To emphasize the continued incidence of phenformin-associated lactic acidosis. CASE REPORT: We report a case of phenformin-associated lactic acidosis in a Chinese man who received phenformin while in China. Diagnosis was made; the patient was treated appropriately and survived. COMMENTS: Phenformin-associated lactic acidosis may still occur in the U.S.
Assuntos
Acidose Láctica/induzido quimicamente , Diabetes Mellitus Tipo 2/tratamento farmacológico , Hipoglicemiantes/efeitos adversos , Fenformin/efeitos adversos , Acidose Láctica/terapia , Idoso , Glicemia/análise , China/etnologia , Hidratação , Humanos , Masculino , Panax , Plantas Medicinais , Respiração Artificial , Estados UnidosRESUMO
A 7-year-old boy with deficient activity of methylmalonyl coenzyme A mutase (mut-methylmalonic acidemia) was seen in severe metabolic crisis. After hemodialysis and clearance of toxic metabolites, severe lactic acidosis persisted with multiorgan failure. Glutathione deficiency was noted and high-dose ascorbate therapy (120 mg/kg) commenced. Glutathione deficiency may contribute to the lactic acidosis observed during decompensation in patients with methylmalonic acidemia.
Assuntos
Erros Inatos do Metabolismo dos Aminoácidos/complicações , Ácido Ascórbico/administração & dosagem , Glutationa/deficiência , Ácido Metilmalônico/sangue , Acidose Láctica/etiologia , Acidose Láctica/terapia , Doença Aguda , Erros Inatos do Metabolismo dos Aminoácidos/terapia , Criança , Humanos , Masculino , Diálise RenalRESUMO
The effect of 6 weeks dietary lipid manipulation on the acute physiologic response to 7-hour continuous endotoxin infusion in guinea pigs was examined. One diet was enriched with N-3 fatty acids, whereas the other contained N-6 fatty acids, primarily linoleic acid. Animals fed N-6 fatty acids developed significant lactic acidemia, microvascular muscle hypoperfusion, and pulmonary infiltrates in response to endotoxin infusion. N-3 fatty acid-fed animals demonstrated improved lactate levels, microvascular muscle perfusion, and lung morphology compared to N-6 fatty acid-fed animals after endotoxin infusion. There was no significant change in cardiac output, PaO2, or mean arterial blood pressure at the end of the endotoxin infusion in either group. Pretreatment with indomethacin, or BM 13505, a specific thromboxane A2 receptor blocker, ameliorated the development of metabolic acidosis in N-6 fatty acid-fed animals, demonstrating a role for prostanoids in the sequelae of endotoxemia. The ability of dietary pretreatment with N-3 fatty acids to influence favorably the physiologic response to endotoxin represents a novel nutrient-metabolic interaction with potential therapeutic implications.
Assuntos
Acidose Láctica/sangue , Hemodinâmica/efeitos dos fármacos , Choque Séptico/fisiopatologia , Acidose Láctica/etiologia , Acidose Láctica/terapia , Animais , Gorduras na Dieta/administração & dosagem , Gorduras na Dieta/farmacologia , Ácidos Graxos Ômega-3/administração & dosagem , Ácidos Graxos Insaturados/administração & dosagem , Óleos de Peixe/administração & dosagem , Cobaias , Indometacina/farmacologia , Pulmão/patologia , Masculino , Músculos/irrigação sanguínea , Fenilacetatos/administração & dosagem , Fluxo Sanguíneo Regional/efeitos dos fármacos , Óleo de Cártamo/administração & dosagem , Choque Séptico/complicações , Choque Séptico/patologia , Pele/irrigação sanguínea , Sulfonamidas/administração & dosagem , Tromboxanos/antagonistas & inibidoresRESUMO
The authors report a case of severe lactic acidosis in a 3-year-old boy, after 20 days of total parenteral nutrition without vitamin supplementation. This child with acute lymphoblastic leukemia underwent a period of severe refractory lactic acidosis (pH between 6.81 and 7.00 and a serum lactate level up to 38 mmol/liter) leading to cardiac arrest. After the initial resuscitation and the subsequent treatment of shock and vitamin K deficiency, acute peritoneal dialysis was instituted to correct the severe lactic acidosis. Initial low plasma thiamine levels confirmed the diagnosis of thiamine deficiency. An associated transient pancreatic dysfunction was also noted. The patient's overall course with thiamine replacement therapy led to a complete recovery within 5 days and no sequelae were noted after 12 months.
Assuntos
Acidose Láctica/etiologia , Nutrição Parenteral Total/efeitos adversos , Leucemia-Linfoma Linfoblástico de Células Precursoras/terapia , Deficiência de Tiamina/complicações , Acidose Láctica/terapia , Doença Aguda , Pré-Escolar , Humanos , Concentração de Íons de Hidrogênio , Lactatos/sangue , Masculino , Diálise Peritoneal , Tiamina/administração & dosagem , Tiamina/uso terapêutico , Deficiência de Tiamina/tratamento farmacológicoRESUMO
Twenty infants and young children admitted with severe metabolic acidosis and a positive history of 'muti' ingestion were investigated. All had accompanying gastroenteritis and significant dehydration. Biochemical data was diagnostic of high anion/gap metabolic acidosis in the majority (70 per cent). Further biochemical data indicated that lactic acidosis and pre-renal azotaemia resulting from severe hypovolaemia were likely causes of the high anion GAP metabolic acidosis. There was no evidence to suggest that the ingested muti per se was associated directly with the acidosis or acute renal failure seen in these children.
Assuntos
Acidose Láctica/induzido quimicamente , Plantas Medicinais , Acidose Láctica/sangue , Acidose Láctica/terapia , Bicarbonatos/sangue , Eletrólitos/sangue , Feminino , Hidratação , Humanos , Concentração de Íons de Hidrogênio , Lactente , Lactatos/sangue , Masculino , Salicilatos/sangue , ZimbábueRESUMO
An 18-year-old man with theophylline overdose developed an increased anion gap metabolic acidosis. Serum lactate levels were markedly elevated. A direct correlation was found between the increasing theophylline level, clinical hyperadrenergic state, and the worsening acidosis. Early hemoperfusion reversed the acidosis, the elevated serum theophylline level, and the hyperadrenergic state. This case substantiates the role of lactate accumulation in the metabolic acidosis associated with isolated theophylline toxicity.