Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient of MELAS is reported. A 28-year-old woman was admitted to Shimada Municipal Hospital because of nausea, vomiting, and right homonymous hemianopsia. She had past history of dizziness and convulsion. A brain magnetic resonance imaging showed an ischemic lesion in the left occipital lobe, which disappeared in the follow-up study. Laboratory examination indicated elevated lactate and pyruvate levels in both blood and cerebrospinal fluid. The muscle biopsy demonstrated ragged-red fibers and strongly SDH-reactive blood vessels. PCR-RFLP analysis of DNA extracted from her muscle and blood as well as her mother's blood revealed a T to C mutation at nucleophile position of 3271 in mitochondrial DNA. She was diagnosed as having MELAS and discharged. One year after the first admission, she re-visited our hospital because of three days' duration of fatigability and generalized muscle pain after alcohol intake. She had severe lactic acidosis, rhabdomyolysis and acute renal failure. Despite a continuous hemodialysis and other intensive efforts, the patient died 20 hours later. Alcohol intake has been reported to induce rhabdomyolysis in myopathy with mitochondrial DNA deletions. The course of this patient suggests that alcohol intake can be an aggravating factor also in MELAS.
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PMID:[A patient of MELAS with 3271 mutation with fatal outcome after alcohol intake]. 1108 93

The first girl of an unrelated couple was noted to have failure to thrive since age 3 months, generalized hypotonia and weakness, hepatomegaly, hypoglycemia, and lactic acidosis at 4 months. She was found to have severe mitochondrial DNA (mtDNA) depletion and respiratory chain complex IV deficiency in both skeletal muscle and liver but without other common mtDNA mutations. Her younger brother developed vomiting at age 3 weeks and was diagnosed as having pyloric stenosis. His skeletal muscle and liver also showed severe mtDNA depletion. He developed generalized weakness and hypotonia, hepatomegaly, and lactic acidosis at age 3 months. Both siblings died of hepatic failure and hemorrhagic complication before 6 months of age. The brother also had chemical pancreatitis, which had not been reported before in mtDNA depletion in children. Severe mtDNA depletion may present with nonspecific symptoms such as vomiting, failure to thrive, and developmental delay; multiorgan involvement such as hepatomegaly, pancreatitis, and myopathy occurs later. Mitochondrial DNA depletion should be considered in the differential diagnosis in children with developmental delay or failure to thrive of unknown etiology.
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PMID:Mitochondrial DNA depletion in children. 1119 1

We report three cases of hepatic steatosis associated with lactic acidosis occurring in HIV positive patients and due to a toxicity of antiviral nucleoside analogues. The clinico-pathological presentation was similar associating digestive signs (vomiting and abdominal pain), polypnea, lactic acidosis, a lethal clinical course, and an hepatomegaly with a diffuse macrovacuolar steatosis. The ultrastructural study performed in two cases showed mitochondrial alterations in hepatocytes. The toxicity of antiviral nucleoside analogues is due to a mitochondrial DNA polymerase inhibition. The incidence of this disease is actually low but probably underestimated. The diagnosis should be rapidly performed and the treatment immediatly interrupted.
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PMID:[A rare etiology of hepatic steatosis associated with lactic acidosis: the toxicity of antiviral nucleoside analogues]. 1137 88

A substantial body of evidence provides support (but not definitive proof of efficacy) for the use of antiretroviral agents as postexposure prophylaxis for occupational exposures to HIV in the healthcare workplace. Despite the lack of definitive evidence of the efficacy of these agents in this setting, over the past decade this intervention has become the standard of care for healthcare workers who sustain occupational exposures to HIV. Administration of these agents--even for a relatively short 28-day postexposure course--is often fraught with difficulty. All of the agents currently used for postexposure prophylaxis regimens have substantial adverse effects, and significant adverse effects occur in more than two-thirds of individuals electing prophylaxis. This manuscript reiterates current US Federal Government guidelines for the administration of postexposure prophylaxis, specifically noting that zidovudine plus lamivudine (with or without a protease inhibitor) remains the recommended regimen. The paper summarises the significant toxicities associated with nucleoside reverse transcriptase inhibitors (primarily nausea, vomiting, diarrhoea and bone marrow suppression), non-nucleoside reverse transcriptase inhibitors (rash, fever, gastrointestinal symptoms and hepatitis, including hepatic decompensation necessitating liver transplantation) and protease inhibitors (nausea, vomiting, diarrhoea, abdominal pain, hyperglycaemia, hyperlipidaemia, headache and anorexia). As a class, the antiretroviral agents have an extraordinary number of drug interactions. The non-nucleoside reverse transcriptase inhibitors and the protease inhibitors are metabolised through the cytochrome P450 pathway, and the effects of concomitant administration of protease inhibitors with other agents in the same class are discussed, as well as the effects of concomitant administration of protease inhibitors with non-nucleoside agents. The potential for numerous and medically risky drug interactions emphasises the importance of planning antiretroviral prophylaxis in consultation with practitioners or clinical pharmacists who are skilled in the use of these agents and knowledgeable about the potential for significant drug interactions that could either reduce the benefit of prophylaxis or increase the potential for toxicity. Another common problem encountered by individuals managing postexposure prophylaxis programmes relates to the administration of chemoprophylaxis to a pregnant healthcare worker who has sustained an occupational exposure to HIV. We address what is known about the potential for toxicity and emphasise the recently published warning concerning the deaths of pregnant women and their offspring from lactic acidosis while receiving regimens containing stavudine and didanosine.
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PMID:Tolerability of postexposure antiretroviral prophylaxis for occupational exposures to HIV. 1148 Apr 91

We retrospectively investigated the clinical and histopathologic features of hospitalized patients infected with human immunodeficiency virus who had symptomatic lactic acidosis syndrome at a university teaching hospital during 1995-2000. Twelve patients were identified, 11 during 1998-2000; of these, 5 died with rapid progression to otherwise unexplained multiple-organ failure. All had extensive prior exposure to nucleoside analog reverse-transcriptase inhibitors (NRTIs). At presentation, the most commonly identified NRTI component of antiretroviral regimens was stavudine plus didanosine. Eleven patients presented with abdominal pain, nausea, and/or emesis. Eight patients had prior acute weight loss (mean [+/-SD], 12+/-5.3 kg). Median venous plasma lactate levels were > or =2-fold greater than the upper limit of normal (2.1 mmol/L). Serum transaminase levels were near normal limits at presentation. Histopathologic studies confirmed hepatic macrovesicular and microvesicular steatosis in 6 patients. Concurrent chemical pancreatitis was identified in 6 patients. The increasing number of cases identified during the study period suggests that physicians better recognize symptomatic lactic acidosis and/or that cumulative NRTI exposure may increase the risk for this syndrome.
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PMID:Symptomatic lactic acidosis in hospitalized antiretroviral-treated patients with human immunodeficiency virus infection: a report of 12 cases. 1169 4

Type B lactic acidosis is a rare and often fatal complication seen in patients receiving the nucleotide analogues zidovudine, stavudine, didanosine, and lamivudine. We describe a case of a 51-year-old human immunodeficiency virus (HIV)-positive woman receiving three nucleotide analogues. She presented with nausea, vomiting, abdominal pain, and hepatic steatosis. Signs of mitochondrial toxicity were demonstrated by diffuse myopathy and pancreatitis. Serum riboflavin levels documented a deficiency that was treated with 50 mg of riboflavin daily. Immediately after treatment, serum blood urea nitrogen level, lactic acid levels, and arterial blood pH all returned to normal values. Her signs of mitochondrial toxicity also improved after treatment with riboflavin. Successful reversal of the patient's type B lactic acidosis after riboflavin therapy suggested that riboflavin deficiency plays a direct role in the development of nucleotide analogue-induced lactic acidosis. It is impossible to predict which patients are predisposed to the development of this syndrome. For this reason, it may be important to screen and treat riboflavin deficiency in patients on nucleoside analogues.
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PMID:Emerging role of riboflavin in the treatment of nucleoside analogue-induced type B lactic acidosis. 1178 75

Despite the abundance of reports emerging in the literature on metabolic disorders, some disorders remain undiagnosed or misdiagnosed, not only in clinical pathology but also in forensic pathology. The authors report a patient who had recurrent episodes characterized by nausea, vomiting, and signs of dehydration necessitating admission to the hospital. At each admission, he was found to have lactic acidosis. On the first admission, glycolic acid was detected in his blood and he was diagnosed as having ethylene glycol intoxication. Only at the third admission, 2 years after the first, was the possibility of an underlying metabolic disorder considered. Laboratory investigations showed a deficiency of complex I in the mitochondrial oxidative phosphorylation. Possible medicolegal implications are discussed.
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PMID:An inherited metabolic disorder presenting as ethylene glycol intoxication in a young adult. 1195 4

Anti-retroviral therapy has still many difficulties for the continuous viral suppression, although it has markedly improved the prognosis of the patients with HIV/AIDS. It is essential that anti-retroviral therapy requires strict adherence of the patients. More than 95% of adherence to have medicine is required for the success of the therapy. Severe and frequent adverse reactions, many pill burden, food restriction and patients' poor recognition to the therapy influence adherence. Of those, adverse reaction of the drugs is the strongest factor for disturbing adherence. Digestive tract symptoms such as nausea, vomiting, abdominal pain and/or diarrhea are common and affect to reduce adherence. Recently, lactic acidosis/hepatic steatosis and lipodystrophy syndrome have been recognized as novel and important adverse reactions with anti-retroviral medicines. Physicians should be aware of the importance of adherence, and assist the patients to improve it with multiple approaches.
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PMID:[Challenges of the anti-retroviral therapy]. 1196 83

Nucleoside analog reverse transcriptase inhibitors (NRTI) have been used to treat HIV-infected patients for >10 years. Some severe adverse events have been attributed to mitochondrial dysfunction. Since 1991, cases of severe lactic acidosis have been reported in association with nucleoside therapy. Our objective was to report two cases of metabolic acidosis and hepatic steatosis in patients receiving stavudine (d4T) and to review the literature. A male and a female, 47 and 45 years of age, respectively, presented with abdominal pain, nausea, vomiting, and weakness after 9 and 6 months, respectively, of treatment with stavudine. At presentation, both patients had severe metabolic acidosis and liver failure. Ultrasonography showed hepatic steatosis (confirmed by biopsy in one case). All antiretroviral drugs were withdrawn and patients were treated with bicarbonate. Both patients developed fulminant liver dysfunction and multiple organ failure. We reviewed the literature and found 75 cases of lactic acidosis and hepatic steatosis associated with use of NRTI; 57 of these patients received d4T (76%). Of all cases reported in association with nucleoside therapy, 63% were females and mortality was 47%. General weakness, hepatic enzyme elevation, and liver steatosis are data that should alert physicians to this serious adverse event and to respond with prompt interruption of antiretroviral drugs and measurement of lactic acid in plasma. It is important to report serious adverse events in commercially released drugs to know prevalence in an exposed population. Physicians should be aware of risk and early signs of this serious adverse event.
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PMID:Metabolic acidosis and hepatic steatosis in two HIV-infected patients on stavudine (d4T) treatment. 1260 78

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome has various presentations. We report on a case of MELAS in which alternate-sided homonymous hemianopia was the main symptom of recurrent neurological defects. A 19-year-old woman suffered from blurred vision, headaches, vomiting, and fever that subsided within days. The ophthalmic examination demonstrated right homonymous hemianopia. One month later a similar episode occurred again. Computed tomography (CT) and magnetic resonance imaging (MRI) of her brain revealed an infarct in the left temporo-occipital lobes. Exercise tests showed lactic acidosis, and a muscle biopsy confirmed the diagnosis of mitochondrial myopathy. Half a month later, a third episode occurred. Visual field examination demonstrated left homonymous hemianopia and partial recovery of the right visual field. The infarct in the brain, as revealed by CT and MRI, was compatible with the visual field changes. MELAS should be ruled out in young patients who present with homonymous hemianopia accompanied by recurrent headaches or other recurrent symptoms.
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PMID:Alternate-sided homonymous hemianopia as the solitary presentation of mitochondrial encephalomyopathy, lactic acidosis, stroke-like episodes syndrome. 1279 Feb 25


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