scholarly journals PARACETAMOL POISONING – REVIEW

2019 ◽  
Vol 34 (4) ◽  
pp. 859-866
Author(s):  
Olimpiada Atmazhova ◽  
Evgenia Barzashka

Paracetamol (acetaminophen) is included in more than 200 medicines of various trade names, including numerous preparations for children used as analgesic and antipyretic drugs. Poisoning usually occurs after taking a large single dose of paracetamol or combination paracetamol-containing preparations, and as a result of prolonged use of paracetamol in smaller doses by persons with increased sensitivity, alcohol abuse, diet error, or in combination with drugs, which affect its metabolism in the liver. Paracetamol poisoning is among the intoxications that have a latent period. Clinical manifestations of acute poisoning develop in stages. The intensity of the initial symptoms does not always determine the outcome of the disease. Paracetamol poisoning is a common cause of liver damage and is a leading etiologic factor in acute liver failure. The worldwide spread of poisoning with this drug is epidemic.

2020 ◽  
pp. 14-17
Author(s):  
Irina A. Shkuratova ◽  
◽  
Lyudmila I. Drozdova ◽  
Aleksander I. Belousov ◽  

Mycotoxicological monitoring of forages shows that the problem of mycotoxicosis has been relevant for several decades. Minimal doses of mycotoxins in feed lead to a decrease in milk productivity, increased sensitivity to infectious and non-infectious diseases. When several mycotoxins enter the body simultaneously, a synergistic effect develops, causing a significant increase in toxicity. Feed contaminated with several types of fungi and their toxins is dangerous for dairy cattle. It was found that the feed mixture contained the types of associations of Aspergillus spp. fungi + Fusarium; Aspergillus spp. + Penicillium spp. + Mucor spp; Fusarium + Penicillium; Mucor spp. + Fusarium + Ustilaginales. Pathogenetic features of metabolic and morphological changes in highly productive cows with polymycotoxicosis were studied. Feeding food contaminated with various metabolites of mold fungi leads to the development of signs of chronic toxemia in animals. Clinical manifestations are the development of diarrhea and dehydration, with a decrease in milk productivity. Metabolic disorders feature the development of an inflammatory process, metabolic acidosis, hyperfermentonemia, with an increase in the amount of creatinine and urea in the blood serum. Metabolic signs indicate the development of hepatorenal syndrome due to structural disorders of the liver and kidneys. Histological signs of polymicotoxicosis are intracapillary and hemorrhagic glomerulonephritis, hepatocyte micronecrosis, and proliferation of connective tissue stroma cells, which leads to the development of atrophic cirrhosis in the interstitial and circular phases.


2014 ◽  
Vol 34 (2) ◽  
pp. 100-103 ◽  
Author(s):  
Ajaya Kumar Dhakal ◽  
D Shrestha ◽  
A Shakya ◽  
SC Shah ◽  
H Shakya

Introduction: Acute poisonings are one of the common cause of emergency visits and hospital admissions and is potentially preventable cause of childhood mortality and morbidity. The objectives of this study were to identify the common type of poisoning in children, to determine types of poisoning according to age and to find out the common age group in which the incidence of poisoning was high.Materials and Methods: It was a descriptive observational study done in a teaching hospital in Lalitpur, Nepal in patients aged 1 month to 18 years who visited the emergency department and were admitted to hospital with history of alleged poisoning from 2009 July to 2014 January.Results: Fifty patients were included. Drugs, kerosene and organophosphorus were most common cause of poisoning. Drugs and kerosene below 10 years of age and organophosphorus and drugs above 10 years of age were common types of poisoning. Maximum numbers (50%) of children with poisoning cases were below five year of age. Mean duration of hospital stay was 2.1days and mean age of poisoning was 7.8 years with a male(54%) predominance. Majority of poisoning occurred at home (84%) and 68% of patients were symptomatic at presentation to hospital with 84% of patients presenting to hospital within six hours.Conclusion: This study showed that drugs, kerosene and organophosphorus were most common forms of poisoning. Young children were most vulnerable for acute poisoning.DOI: http://dx.doi.org/10.3126/jnps.v34i2.10139J Nepal Paediatr Soc 2014;34(2):100-103 


2020 ◽  
Vol 33 (6) ◽  
pp. 793-802 ◽  
Author(s):  
Weijing Kong ◽  
Yan Meng ◽  
Liping Zou ◽  
Guang Yang ◽  
Jing Wang ◽  
...  

AbstractObjectivesSanfilippo syndrome (Mucopolysaccharidosis III, MPS III) is a rare autosomal recessive hereditary disease, which is caused by lysosomal enzyme deficiency. This study was operated to investigate clinical and molecular characteristics of patients with MPS III, which will improve the diagnosis and treatment of MPS III.MethodThirty four patients with MPS III were assessed using clinical evaluation, questionnaire, and scoring system.ResultsAmong the 34 patients, 14 had MPS IIIA, 19 had MPS III B, and one had MPS III C. Speech delay (100%) and intellectual disability (100%) were the most prevalent clinical manifestations in this cohort, followed by hyperactivity (94.12%), hirsutism (91.18%), enlarged head circumference (73.52%), repeated diarrhea (67.64%), sparse teeth (67.64%), and Mongolian spots (64.71%). There were two clinical manifestations that were significantly different between IIIA and IIIB: Hepatosplenomegaly and serrated teeth. The most common initial symptoms at diagnosis were speech delay (52.94%), hyperactivity (35.29%), and mental retardation (29.41%). Genetic analysis of 25 patients was conducted, which identified 12 novel mutations.ConclusionWhen language retardation, mental retardation, and rough facial features occurred, MPS III should be considered. At same time, more examination should be operated, such as examination of changes in cranial magnetic resonance imaging of cerebral cortex atrophy. Hepatosplenomegaly and serrated teeth could be used clinically to preliminarily distinguish IIIA from IIIB.


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1284.1-1285
Author(s):  
A. S. Lundberg ◽  
B. A. Esbensen ◽  
E. M. Hauge ◽  
A. De Thurah

Background:Early treatment, before three months from symptom onset of rheumatoid arthritis (RA), is essential to increase the likelihood of remission and to prevent permanent joint damage (1). However, it has been shown that only 20% of the patients are seen within the first three months, and the median delay in general practice has been estimated to 4 months (range 2–9) (2).Objectives:To explore the barriers in diagnosing RA from the general practitioners’ (GPs) perspective.Methods:We conducted a qualitative study based on focus group interviews. We recorded the interviews digitally and transcribed verbatim. The transcribed interviews were analyzed based on content analysis (3), by using Nivo 12. Sample size was determined by thematic saturation.Results:In total ten GPs participated in three different focus groups. 40 % were female, mean age was 53 years (range 37-64), and mean year since specialist authorization as GP was 16 years (range 5-23). 60 % of the GPs worked in a practice located within the referral area of a university hospital; the remaining within the referral area of a regional hospital.Four themes emerged in the analysis: 1) When the patient is not a text book example, referring to the difficulty of identifying relevant symptoms among all clinical manifestations from the joints as described by the patients, 2)The importance of maintaining the gatekeeper function, referring to the societal perspective, and the GPs responsibility to refer the right patients to secondary care, 3)Difficulties in referral of patients to the rheumatologist,referring to perceived differences in the collaboration with rheumatologists. The GPs experienced that it was sometimes difficult to be assisted by rheumatologists, especially when the clinical picture was not ‘clear cut’. Finally, (4)Para-clinical testing, can it be trusted?referring to challenges on the evaluation of especially biomarkers.The overarching theme was:Like finding a needle in a haystack, covering the GPs difficulties in detecting RA among the many patients in general practice who appear to be well and at the same time have symptoms very similar to RA.Conclusion:The GPs experienced that RA was a difficult diagnosis to make. The immediate challenge was that RA patient’s initial symptoms often resembled those of more common and less serious conditions, and that investigative findings such as biomarkers can be negative at the early state of the disease. At the same time, the collaboration with rheumatologists was sometimes seen as a hurdle, when the clinical picture was not ‘clear cut’.In order to facilitate earlier diagnosis of RA in general practice, the GPs and rheumatologists need to focus on these barriers by strengthening mutual information and collaboration.Physicians should remain vigilant to patients who have conditions that do not resolve as expected with treatment, who have symptoms that persist, or who do not look well despite negative investigative findings.References:[1]Aletaha D, et al. JAMA, Oct 2018.[2]Kiely P, et al. Rheumatology, Jan 2009.[3]Braun V. Qualitative research in psychology. 2006, 3(2), 77-101Disclosure of Interests:Anne Sofie Lundberg: None declared, Bente Appel Esbensen: None declared, Ellen-Margrethe Hauge Speakers bureau: Fees for speaking/consulting: MSD, AbbVie, UCB and Sobi; research funding to Aarhus University Hospital: Roche and Novartis (not related to the submitted work)., Annette de Thurah Grant/research support from: Novartis (not relevant for the present study)., Speakers bureau: Lily (not relevant for the present study).


Author(s):  
A. N. Grebenyuk ◽  
V. N. Bykov

Introduction. Carbon monoxide (CO) remains one of the most common causes of acute poisoning and death, both in everyday life and in emergency situations, especially in fires.Material and methods. The paper summarizes information about the regulatory effects, mechanisms of toxic action, pathogenesis and clinical picture of intoxication, as well as predictors of the severity of CO poisoning.Results. The main mechanism of the toxic effect of CO is due to its ability to bind to the protohemal iron of hemoglobin (Hb) to form carboxyhemoglobin (HbCO). The toxicity of CO may also be enhanced by impaired functions of the myoglobin of the myocardium and skeletal muscles, mitochondrial cytochrome oxidase, and iron-containing enzymes of the antioxidant system. The leading link in the pathogenesis of acute CO intoxication is a violation of the oxygen transport function of hemoglobin and the associated development of hemic and tissue hypoxia. CO-induced cell and tissue damage due to the induction of mitochondrial dysfunction, oxidative stress, free radical hyperproduction, lipid peroxidation, inflammation, and apoptosis also play a role in the pathogenesis of intoxication.Conclusion. The mechanism of toxic action of CO, associated primarily with the formation of carboxyhemoglobin and the development of hypoxia, determines the clinical manifestations of acute intoxication, which depend on the concentration of CO and the duration of exposure, but are almost always associated with the central nervous system and cardiovascular system.


Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 153-158 ◽  
Author(s):  
James N. George ◽  
Richard H. Aster

AbstractAlthough drugs are a common cause of acute immune-mediated thrombocytopenia in adults, the drug etiology is often initially unrecognized. Most cases of drug-induced thrombocytopenia (DITP) are caused by drug-dependent antibodies that are specific for the drug structure and bind tightly to platelets by their Fab regions but only in the presence of the drug. A comprehensive database of 1301 published reports describing 317 drugs, available at www.ouhsc.edu/platelets, provides information on the level of evidence for a causal relation to thrombocytopenia. Typically, DITP occurs 1 to 2 weeks after beginning a new drug or suddenly after a single dose when a drug has previously been taken intermittently. However, severe thrombocytopenia can occur immediately after the first administration of antithrombotic agents that block fibrinogen binding to platelet GP IIb-IIIa, such as abciximab, tirofiban, and eptifibatide. Recovery from DITP usually begins within 1 to 2 days of stopping the drug and is typically complete within a week. Drug-dependent antibodies can persist for many years; therefore, it is important that the drug etiology be confirmed and the drug be avoided thereafter.


PEDIATRICS ◽  
1974 ◽  
Vol 53 (4) ◽  
pp. 540-542
Author(s):  
Arnold P. Gold

The most poorly understood and most frequently misdiagnosed seizure state of childhood is psychomotor epilepsy. Difficulties in diagnosis are related to the variety of possible clinical manifestations which characteristically differ from one child to another. In addition, psychomotor epilepsy can occur at any age, even during infancy. Therefore, the child's ability to verbalize the perceptive and affective sensations of this seizure state is obviously limited by his chronologic age. The diagnostic dilemma is further complicated as physicians tend to confuse psychomotor seizures and petit ma! epilepsy. INCIDENCE AND ETIOLOGY The terms psychomotor and temporal lobe epilepsy are often used synonymously and interchangeably. At times the seizure state may also be called uncinate epilepsy, epileptic automatisms or epileptic fuges. However, not all psychomotor seizures are associated with temporal lobe lesions, nor is temporal lobe pathology always productive of psychomotor epilepsy. Abnormalities and electrical foci from areas other than the temporal lobe can produce this seizure state. For these reasons, the term psychomotor epilepsy is preferred, and temporal lobe epilepsy, if used, should be restricted to those psychomotor seizures that result from primary temporal lobe pathology. Ten to 20% of children in most pediatric seizure clinics have psychomotor epilepsy. Focal lesions are often considered to be the responsible etiologic factor, but diffuse encephalopathies, above all in children, are more commonly encountered. Prolonged febrile convulsions, perinatal trauma and hypoxia, craniocerebral trauma or meningoencephalitis can be the specific etiologic condition. Expansive lesions including neoplasms, vascular malformations, cysts and abscesses must be considered, especially when there is clinical or electrical evidence of a focal lesion.


2019 ◽  
Author(s):  
Lynnette Nieman

Cushing syndrome is a condition with protean manifestations that are caused by chronic exposure to excess glucocorticoids. Treatment with supraphysiologic doses of glucocorticoids is the most common cause. Pathologic hypercortisolism may result from autonomous adrenal production or as a result of the action of excessive adrenocorticotropic hormone (ACTH) production by a tumor, which stimulates adrenal cortisol production. Primary adrenal forms include unilateral adenoma or carcinoma or, rarely, bilateral hyperplasia and/or nodules. This chapter covers the epidemiology, etiology, pathophysiology, and diagnosis of Cushing syndrome. Clinical manifestations, physical examination findings, and laboratory tests, including tests of the blood and other body fluids, imaging studies, and biopsy, are discussed. The differential diagnosis, treatment options, complications, and prognosis are described. Tables outline clinical features and causes of Cushing syndrome, abnormalities associated with primary adrenal causes of Cushing syndrome, diagnostic accuracy of screening tests, endogenous hypercortisolism without Cushing syndrome, and medical therapy for Cushing syndrome. Figures illustrate the causes of Cushing syndrome and a comparison of the hypothalamic-pituitary-adrenal axis in patients with ACTH-dependent Cushing syndrome and those with pseudo–Cushing syndrome. Algorithms show the evaluation of possible Cushing syndrome and evaluation of the causes of Cushing syndrome. Second-line treatments for Cushing syndrome when surgery fails or is not possible are also detailed. This chapter contains 5 figures, 7 tables, 50 references.


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