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PubMed2004

Acute lung injury as an adverse event of gefitinib.

Gefitinib, a selective epidermal growth factor receptor tyrosine kinase inhibitor, is an effective treatment for patients with non-small cell lung cancer (NSCLC). Some investigators have recently reported several patients complicated by acute lung injury after the initiation of gefitinib administration. In this report, we investigated the efficacy and adverse events during treatment with gefitinib. The subjects of this study were all of the 110 patients with NSCLC who were treated in our hospital and its eight branch hospitals. Patients received gefitinib at a dose of 250 mg once daily. The response rate was 30%. The frequently reported adverse events were skin disorders, gastrointestinal disturbances, liver dysfunction and acute lung injury. Five of the 12 patients who were considered to have suffered acute lung injury died of progressive respiratory failure. Of the nine patients who had pulmonary fibrosis before use of gefitinib, five developed acute lung injury during the treatment. Sera from three of the 12 patients were evaluated and all three showed increases of surfactant protein (SP)-A, SP-D and KL-6. We conclude that gefitinib was clinically useful. However, several patients suffered acute lung injury which could have been caused by gefitinib. A detection system including SP-A, SP-D and KL-6 as prime candidates as markers should be established as promptly as possible. Clinicians should be aware that treatment of NSCLC with gefitinib involves the risk of acute lung injury and therefore careful consideration should be given before deciding whether or not gefitinib is indicated for treatment. Further study is necessary to elucidate the mechanism of acute lung injury by gefitinib.

Adult↗
PubMedDate not supplied

Melatonin responsive hemicrania continua.

Hemicrania continua is one of the indomethacin-responsive headache syndromes. There are very few effective alternative therapies for hemicrania continua, thus patients may require daily indomethacin for years. The risks of long-term indomethacin include gastrointestinal and renal dysfunction. Melatonin is a pineal hormone with a chemical structure very similar to indomethacin. Recently, melatonin was shown to be effective for primary stabbing headache, another indomethacin-responsive syndrome. Three cases of melatonin responsive hemicrania continua are now reported.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2002

Gut adaptation and the glucagon-like peptides.

The glucagon-like peptides GLP-1 and GLP-2 are synthesised and then released from enteroendocrine cells in the small and large intestine. GLP-1 promotes efficient nutrient assimilation while GLP-2 regulates energy absorption via effects on nutrient intake, gastric acid secretion and gastric emptying, nutrient absorption, and mucosal permeability. Preliminary human studies indicate that GLP-2 may enhance energy absorption and reduce fluid loss in subjects with short bowel syndrome suggesting that GLP-2 functions as a key regulator of mucosal integrity, permeability, and nutrient absorption. Hence GLP-2 may be therapeutically useful in diseases characterised by injury or dysfunction of the gastrointestinal epithelium.

Adaptation, Physiological↗
PubMed2003

The impact of solid-phase gastric emptying studies in the management of children with dyspepsia.

Information on the utility of solid-phase gastric emptying studies (SPGES) in the evaluation of children with symptoms of upper gastrointestinal (GI) motor dysfunction is limited. This study was conducted to evaluate the impact of SPGES in the clinical management and outcome of children with upper GI symptoms suggestive of gastroparesis. The records of 45 children who underwent SPGES (31F; 3-17 years) were reviewed. All patients had GI symptoms suggesting gastroparesis. Patients were fed with Tc-99m-sulfur colloid-labeled chicken liver. Adult normal half-life (T1/2) values (F 103 +/- 14 minutes; M 66 +/- 13.6 minutes) were used. The relationships among symptoms, treatment, and outcome were evaluated. Of the 45 patients 9 had delayed, 16 had rapid, and 20 had normal gastric emptying. Six of 9 patients with delayed gastric emptying responded to cisapride. Four of 16 patients with rapid emptying were diagnosed with the dumping syndrome. Of the children with rapid gastric emptying, 87% were females. Twenty patients with normal emptying were diagnosed with gastroesophageal reflux (8), nonulcer dyspepsia (5), irritable bowel syndrome (2), Helicobacter pylori (1), lactose intolerance (1), eosinophilic gastroenteritis (1), duodenitis (1), and constipation (1). In patients who had SPGES for possible gastroparesis, 20% had gastroparesis, 36% had rapid gastric emptying, and 44% had normal gastric emptying. The high number of females in the rapid gastric emptying group might be secondary to normal adult female T1/2 values that were used. The practice of using adult normal T1/2 values in prepubertal girls may need to be revised. Patients with delayed gastric emptying responded to cisapride.

Adolescent↗
PubMed1999

Age-related changes in antral endocrine cells in mice.

Antral endocrine cells in four age groups of mice, namely prepubertal (1 month old), young (3 months old), ageing (12 months old) and senescent (24 months old), were detected by immunocytochemistry and quantified by computerized image analysis. A statistical difference was detected between the different age groups regarding the numbers of gastrin-, somatostatin-, and serotonin-immunoreactive cells. The number of gastrin-immunoreactive cells significantly increased between 1 and 12 months, whereas they became significantly fewer between 12 and 24 months. Somatostatin-immunoreactive cell number increased significantly in 1-, 12- and 24-month-old mice, compared with young mice (3 months old). The number of serotonin-immunoreactive cells also increased significantly in 1- and 12-month-old mice as compared with young mice. There was a statistical difference between different age-groups regarding the cell secretory index (CSI) of somatostatin- and gastrin-immunoreactive cells, the CSI of both somatostatin- and serotonin-immunoreactive cells increased significantly in 1-, 12-, and 24-month-old mice, compared with young mice. There was no statistical difference between the different age-groups regarding the CSI of gastrin-immunoreactive cells, nor between males and females regarding the number and CSI of all the endocrine cell types investigated. It is suggested that the large number of somatostatin-immunoreactive cells in ageing and senescent mice might have an impact on the gastric delay seen in the elderly. It was concluded also that the changes in the antral endocrine cells could be involved in the development of dysfunction of the gastrointestinal tract inherent in ageing, or could be secondary to structural and functional changes in the alimentary tract caused by ageing.

Aging↗
PubMed2004

Hereditary motor and autonomic neuronopathy 1 maps to chromosome 20q13.2-13.3.

The spinal muscular atrophies (SMA) or hereditary motor neuronopathies result from the continuous degeneration and death of spinal cord lower motor neurons, leading to progressive muscular weakness and atrophy. We describe a large Brazilian family exhibiting an extremely rare, late-onset, dominant, proximal, and progressive SMA accompanied by very unusual manifestations, such as an abnormal sweating pattern, and gastrointestinal and sexual dysfunctions, suggesting concomitant involvement of the autonomic nervous system. We propose a new disease category for this disorder, 'hereditary motor and autonomic neuronopathy', and attribute the term, 'survival of motor and autonomic neurons 1' (SMAN1) to the respective locus that was mapped to a 14.5 cM region on chromosome 20q13.2-13.3 by genetic linkage analysis and haplotype studies using microsatellite polymorphic markers. This locus lies between markers D20S120 and D20S173 showing a maximum LOD score of 4.6 at D20S171, defining a region with 33 known genes, including several potential candidates. Identifying the SMAN1 gene should not only improve our understanding of the molecular mechanisms underlying lower motor neuron diseases but also help to clarify the relationship between motor and autonomic neurons.

Chromosome Mapping↗
PubMed1990

Total parenteral nutrition 1990. A review of its current status in hospitalised patients, and the need for patient-specific feeding.

The decision to initiate total parenteral nutrition (TPN) in hospitalised patients should be based on the presence of clinically significant starvation and dysfunction of the gastrointestinal tract. It must also take into account the clinical status of the patient, considering major treatment strategies and the need for prolonged hospitalisation, the benefits of feeding and the attendant risks of central venous alimentation. Recent evidence in surgical patients in intensive care provides the impetus for early parenteral feeding; withholding TPN and inducing a cumulative caloric deficit of greater than or equal to 10,000 calories has been associated with a survival disadvantage compared to those patients with a positive caloric balance. Moreover, the incidence of serious organ failure was consistently higher in the group with cumulative caloric deficits. Additional evidence favouring the provision of TPN exists, but the axiom 'if the gut works, use it' still prevails. Exceptions to this precept do exist, however, particularly in critically ill patients. The metabolic derangements encountered in these patients could be so severe that it may be impossible to correct the electrolyte and acid-base abnormalities via the enteral route. For example, such patients may have large potassium requirements and/or severe alkalaemia necessitating systemic acidification with hydrochloric acid, precluding enteral delivery due to gastrointestinal intolerance. In this setting, combined enteral feeding with 10 to 20 ml/h to maintain gut integrity (via a post-pyloric feeding tube) and TPN during the acute phases of illness is an exciting possibility. Once the decision to feed is made, the amount of nutrition prescribed may assume equal importance with respect to patient outcome. The frequent use of the Harris-Benedict equation, plus a multiplying factor for stress, may overestimate caloric requirements; this is particularly true during critical illness. The dangers of overfeeding may be just as harmful as not feeding at all. The use of indirect calorimetry provides the most accurate measurement of resting energy expenditure. However, in the absence of indirect calorimetry, modified equations to estimate caloric needs are available. Caution must be observed as caloric intakes exceeding the range of 25 to 35 kcal/kg may be dangerous, particularly in the severely ill patient with preexisting organ failure. The amount of protein and the 'calorie-mix' necessary for optimal nutritional support is open to debate. Recent evidence has demonstrated no additional benefit to nitrogen balance in severely septic patients when protein was given at a level exceeding 1.5 g/kg/day.(ABSTRACT TRUNCATED AT 400 WORDS)

Critical Care↗
PubMed1983

Relationship between morphological findings and function of the small intestine in familial amyloidosis with polyneuropathy.

Twenty-seven patients with familial amyloidosis with polyneuropathy were studied with regard to the morphology of the small intestine, and this was correlated to symptoms and malabsorption features. The mucosa was normal in all cases investigated by the dissecting microscope, the light microscope, and the scanning electron microscope. Amyloid was demonstrated in 83% of the cases by the presence of green birefringent material in the biopsy specimens stained with alkaline Congo red and examined in polarized light. Nineteen patients had steatorrhea, and 12 had pathological D-xylose test results. The degree of amyloid infiltration did not correlate with these data, nor did the symptomatic state correlate with the amount of amyloid in the biopsy specimens. The surface ultrastructure was normal when investigated by means of the scanning electron microscope in all patients except five in whom the glycocalyx was altered. As a group, however, those five did not differ in any respect from the rest of the patients. Rod-shaped microorganisms were shown to adhere to the surface in one patient. The results suggest that mechanisms other than bowel-wall deposition of amyloid cause the dysfunction of the gastrointestinal tract in familial amyloid polyneuropathy.

Adult↗
PubMed1999

[HMG-CoA reductase inhibitors: a brief review of their pharmacological properties and clinical efficacy in cardiovascular disease].

The results of recently published studies on primary and secondary prevention of coronary heart disease with HMG-CoA reductase inhibitors--statins--support their use in patients with primary hypercholesterolaemia or mixed hyperlipidaemia, with or without atherosclerotic vascular disease. From a pharmacological point of view, statins inhibit HMG-CoA reductase, reduce the endogenous synthesis of cholesterol and increase the apoB/apoE lipoprotein clearance from plasma. Recent studies confirm that HMG-CoA reductase inhibitors may also decrease hepatic production of VLDL and LDL-cholesterol. However, they have different pharmacokinetic properties and variable effectiveness with potential clinical implications. These drugs are generally well tolerated with a similar profile of adverse effects (gastrointestinal effects, hepatic dysfunction and myopathy). The knowledge of their pharmacodynamic and pharmacokinetic properties can lead to a rational use and greater understanding of their potential benefits.

Cerebrovascular Disorders↗
PubMed1999

[Specific COX-2 inhibitors: prospects of therapy with new analgesic and anti-inflammatory substances].

Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase (COX) activity, thereby suppressing the synthesis of proinflammatory prostaglandins. The identification and molecular-biological characterization of an inducible COX isoform (COX-2) in inflammatory cells led to the hypothesis that a selective inhibition of COX-2 would result in relief of inflammation and pain without causing the COX-1-dependent side effects (gastrointestinal ulceration, platelet dysfunction, kidney damage) of conventional NSAIDs. On the basis of data obtained in several laboratories by means of the "human whole blood assay" there is now convincing evidence that none of the currently available NSAIDs is a selective COX-2 inhibitor. Meanwhile, the specific COX-2 inhibitors celecoxib and rofecoxib are being tested worldwide in phase III clinical trials on patients with rheumatoid arthritis and osteoarthritis. However, the simple concept of COX-2 being an exclusively proinflammatory inducible enzyme cannot be upheld any longer. In addition, COX-2 is expressed constitutively in brain, spinal cord and kidney, as well as in numerous other organs. In the present review the perspectives and possible risks of specific COX-2 inhibitors are discussed, as well as additional indications for their implementation (e.g. colon cancer).

Analgesics↗
PubMed1999

Syndromes associated with immunodeficiency.

Immunodeficiency often has a genetic basis. Immune defects are the predominant manifestation in primary immunodeficiency disorders, and immune defects may also be associated with a number of other recognizable syndromes. There are 45 recognized primary immunodeficiency disorders, but immunodeficiency has been reported in 105 other syndromes. Abnormalities associated with these syndromes include growth deficiency (19 syndromes with disproportionate or proportionate short stature); specific organ system dysfunction (39 with gastrointestinal, dermatologic, or neurologic abnormalities); inborn errors of metabolism (17); miscellaneous anomalies (17); and chromosome anomalies (13). In most of these disorders, immunodeficiency is present in only a portion of the patients. However, in 49 syndromes, immunodeficiency is present in the vast majority. We review the clinical manifestations of each syndrome and delineate the associated immune defects. For most, the underlying mechanism linking the immune defect and other anomalies is unclear. Recognition of these conditions involving both the immune and other organ systems may facilitate accurate diagnosis and management, as well as yield information regarding genes critical for the development of the involved systems.

Chromosome Aberrations↗
PubMed1975

Postoperative metabolic alkalosis and acute renal failure: rationale for the use of hydrochloric acid.

Metabolic alkalosis secondary to chloride depletion, especially following gastrointestinal surgery and associated with acute renal failure, is a frequent clinical occurrence. Management of the resultant acid-base disturbance mandates chloride replacement. The presence of oliguria limits the choice of accompanying cation. The use of intravenous hydrochloric acid to correct and maintain proper chloride balance, secondary to external gastric fluid losses, is recommended as a straightforward approach. Two brief case synopses are presented. Both patients, florid examples of profound chloride depletion, required large amounts of intravenous hydrochloric acid. The options regarding the choice of chloride solution, hazards involved, and a simplified schema of replacement therapy are presented. Combined gastrointestinal and renal dysfunction create unusual biochemical and clinical alterations and may result in a complex management problem.

Acute Kidney Injury↗
PubMed2002

Report of a rare case of trauma-induced thyroid storm.

Thyroid storm is a potentially life-threatening endocrinologic emergency characterized by an exacerbation of a hyperthyroid state. Several inciting factors can instigate the conversion of thyrotoxicosis to thyroid storm; trauma is one such trigger, but it is rare. Patients with thyroid storm can manifest fever, nervous system disorders, gastrointestinal or hepatic dysfunction (e.g., nausea, vomiting, diarrhea, and/or jaundice), and arrhythmia and other cardiovascular abnormalities. Treatment of thyroid storm is multimodal and is best managed by the endocrinologist and medical intensivist. Initial medical and supportive therapies are directed at stabilizing the patient, correcting the hyperthyroid state, managing the systemic decompensation, and treating the underlying cause. Once this has been achieved, definitive treatment in the form of radioactive ablation or surgery should be undertaken. We describe a case of thyroid storm in a young man that was precipitated by a motor vehicle accident.

Accidents, Traffic↗
PubMed2003

Inorganic lead toxicology.

Lead is a health hazard for all humans. Especially children under the age of six are most at risk for lead poisoning. Lead toxicity causes hematological, gastrointestinal, and neurological dysfunction. Symptoms are usually noted with blood lead greater than 2 micromoles/L. Severe or prolonged exposure may also cause chronic nephropathy, hypertension, and reproductive impairment. Lead inhibits some enzymes, alters cellular calcium metabolism, stimulates synthesis of binding proteins in kidney, brain, and bone, and slows down nerve conduction. Acute lead poisoning is relatively infrequent and results from ingestion of acid soluble lead compounds or inhalation of lead vapors but chronic exposure to low levels of the metal is still a public health issue, especially among some minorities and socioeconomically disadvantaged groups. Lead has been used since prehistoric times, and has become widely distributed and mobilized in the environment. Exposure to and uptake of this non-essential element have consequently increased. Both occupational and environmental exposures to lead remain a serious problem in many developing and industrializing countries and a public health problem of global dimensions.

Acute Disease↗
PubMedDate not supplied

[Inorganic lead stimulates endothelin secretion in the MDCK cell line].

BACKGROUND: Lead (Pb) is an environmental toxin whose acute intoxication causes haematological, gastrointestinal and neurological dysfunctions. Moreover it is well-established that prolonged exposure to low levels of inorganic Pb compounds is closely related to hypertension in experimental animals and occupationally exposed humans. Previous reports have suggested that endothelins (ETs), a family of peptides with potent vasoconstrictive properties, might be involved in the pathogenesis of lead-induced hypertension. In vivo studies demonstrated that rats chronically exposed to Pb low levels exhibited blood pressure elevation coupled with an increase of ET-3 concentration in plasma and urine in comparison with control animals. OBJECTIVE: Since kidney is one of the target organs of lead injury, as well as the site of production/action of ETs, we investigated the effects of an inorganic Pb compound (Pb chloride) on the synthesis and secretion of these peptides, using, as in in vitro model, a renal-derived cell line (MDCK). METHODS: The ETs assays in culture media of sub-confluent cell cultures exposed to different concentration of PbCl2 were performed by Enzyme linked Immunoassay (EIA), using two experimental procedures: a) cultures were exposed to 1100 and 200 microM PbCl2 for 30 min, next cells received Pb-free culture medium up to 24 h (pulse/chase experiment); b) cultures were fed continuously up to 24 h with treatment media containing the same PbCl2 concentrations (pulse experiment). Concomitantly, the Pb influence on cell viability was evaluated by different cytotoxicity assays (LDH release, DAPI staining and cell density assays). The mRNA expression of ET-1 was evaluated in pulse experiments by RT-PCR analysis before and after cell exposure to PbCl2. The Pb2+ cellular content of parallel MDCK cell cultures was assessed by AAS analysis. RESULTS: In our experimental conditions, the administration of PbCl2 to sub-confluent MDCK cell cultures did not significantly affect cell viability. Either in pulse or in pulselchase experiments, the ETs content, evaluated in culture media of cells exposed to 100 microM PbCl2, significantly increased. On the contrary, cell treatment with 1 or 200 microM PbCl2 did not modify the ETs secretion. Because the amounts of ETs released in culture media were similar in both kinds of experiment, our results suggest that the metal induces the ETs secretion already after 30 min of cell exposure to the toxicant. Moreover, the ET-3 EIA specific assay did not reveal any immunoreactivity, excluding the involvement of this isoform in the Pb-induced secretion of ETs. Additionally, our results seem to exclude any Pb-induced up-regulation of ET-1 transcripts. The Pb2+ quantification in cell extracts demonstrated that the uptake of the metal is dose- and time-dependent and, in pulse experiments, it was maximum after six hours from the beginning of treatments, then the intracellular Pb2+ content decreased. This last phenomenon suggests the involvement of an ATP-dependent transporter in the mechanism of Pb cell excretion. Moreover, the ETs cell release in culture media of MDCK cells appears to depend on the intracellular content of Pb ions reached within 30 min of treatment. CONCLUSION: Our results indicate that there is a range of PbCl2 doses (100 microM) at which MDCK cells enhance their ETs secretion. Lower doses (1 microM) of Pb salt seem to be ineffective to stimulate ETs release, while, doses equivalent to 200 microM seem to inhibit this phenomenon.

Cell Line↗
PubMed1990

Clinical evaluation of a newly developed enteric nutrient given to the neurosurgical patients with disturbances of consciousness.

An enteric nutrient 'SAN-ET-A', rich in protein and electrolytes, was given to 8 patients with disturbances of consciousness. Although the adminstered dosage had a calorie content so low that basal metabolism was barely maintained, the level of serous proteins increased following administration. Electrolyte imbalance was not found, and the patients did not suffer from severe renal or liver dysfunctions. No notable gastrointestinal troubles occurred except in one case. It is concluded that a low dosage of SAN-ET-A was sufficient to maintain the patients in good nutritional condition. Furthermore, it is suggested that this nutrient can be safely given for a long period.

Aged↗
PubMed1987

Zinc-induced hemolytic anemia in a dog.

A dog ingested a zinc nut that was retained in the stomach and caused a life-threatening hemolytic crisis with renal, gastrointestinal, and hepatic dysfunction. The dog was stabilized by blood transfusion and was anesthetized, and the zinc nut was removed with a fiberoptic endoscope. With continued supportive care, the dog recovered. Metallic zinc is found in high concentrations in nuts, bolts, and pennies. Zinc toxicosis should be considered in cases of unexplained hemolytic anemia.

Anemia, Hemolytic↗