Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a group of patients with clinically diagnosed drug hypersensitivity the in vitro lymphocyte response to the suspected drug was assessed by the lymphocyte transformation test. The test gave positive results in all 15 patients with penicillin-induced immediate or accelerated allergic reactions and positive immediate skin-test reactivity to the major or the minor antigenic determinant of penicillin, or both, but in only 3 of the 12 patients with delayed-onset maculopapular rashes induced by penicillin, despite positive immediate reactivity to the skin-test reagents.Lymphocyte stimulation greater than five times the control level was demonstrated for five patients with penicillin-induced erythroderma, Stevens-Johnson syndrome or a serum-sickness-like illness, or with methicillin-induced interstitial nephritis, all of whom had negative reactions to the appropriate skin-test reagents. A low level of stimulation was seen in eight other skin-test-negative patients with possible allergic reactions induced by penicillins. However, in all subjects tested the stimulation was significantly greater than the mean for control subjects.For 9 of 11 patients with isoniazid-induced hepatitis or maculopapular rashes, but for only 8 of 31 patients with eruptions induced by a variety of drugs other than penicillins and isoniazid, significant stimulation occurred in the lymphocyte transformation test.It is concluded that the lymphocyte transformation test is useful in the detection of hypersensitivity to the penicillins (although in IgE-mediated reactions skin testing is clearly preferable) and isoniazid but is of limited value in the demonstration of hypersensitivity to other drugs.
 ...
PMID:Lymphocyte transformation studies in drug hypersensitivity. 44 3

In accordance with the system of viral species, viral disorders of the oral mucosa may be classified with regard to their intensity of affection. There are but few viral infections exclusively affecting the oral mucosa like e.g. 1. Glossitis papulosa of Michelson, representing a special form of vaccinia inoculata, 2. Gingivo-stomatitis herpetica and 3. warts of the mucosa or condyloma-like papillomas of the oral mucosa including oral papillomatosis, that, itself shows morphological and clinical similarities to laryngeal papilloma. A second group of disorders mainly affecting the oral mucosa includes the "Aphthoid of Pospischill and Feyrter", Zahorsky's herpangina and other viral infections by the Coxsackie group, like vesicular stomatitis. The 3rd group represents viral infections of other organs in which affection of the oral mucosa is a prerogative, e.g. smallpox, varicella, foot-and-mouth disease and pharyngo-conjunctival fever. A 4th group includes those viral infections of the organs in which co-affection of oral mucosa occurs frequently or once in a while (at occasions). Here, we find eczema vaccinatum, herpes zoster, herpes simplex of the oral mucosa mostly on the hard palate, eczema herpeticatum, post-herpetic Erythema exsudativum multiforme, Mononucleosis infectiosa Pfeiffer, viral flu, German measles, parotitis epidemica, rubeola and ECHO-exanthema. A 5th and last group is made up by viral infections of other organs, in which affection of the oral mucosa hardly occurs at all. This group contains paravaccinal Ecthyma contagiosum, poliomyelitis, viral infection of the city of Marburg and some Arbovirus infections. Relatively few viral disorders never co-exist with lesions on the oral mucosa like e.g. Virus-hepatitis or some viral encephalitides. Groups 1 and 2, most important of all, are presented in detail regarding clinics, diagnostics, differential-diagnosis and therapy. The disorders within the other 3 groups are discussed only regarding their importance in the field of ENT-related symptoms of the oral mucosa. A number of pictures and tables completes important clinical details and give further hints to their differential-diagnosis.
 ...
PMID:[Virus diseases of the mouth mucosa]. 83 Jan 6

The Stevens-Johnson syndrome is rarely associated with hepatitis and neither entity is commonly seen following the use of ampicillin or cephalexin. An infant is described in whom both entities appeared simultaneously following therapy with these drugs.
 ...
PMID:Stevens-Johnson syndrome with hepatitis following therapy with ampicillin and cephalexin. 105 88

Between September 1976 and May 1989, 12 cases of uveitis attributed to the systemic use of sulfonamide derivatives were reported to the National Registry of Drug-Induced Ocular Side Effects and the US Food and Drug Administration. We evaluated these reports in addition to one case previously reported in the literature and one patient seen at the Uveitis Clinic, Oregon Health Sciences University, Portland. The patients' median age was 34 years. Twelve of 14 patients were treated with trimethoprim-sulfamethoxazole. All patients for whom the location of the eye disease was specified presented with an iritis. Six reports included a description of ocular symmetry, with all patients having bilateral inflammation. Of the nine patients for whom data on the duration of drug use was available, seven experienced adverse effects within 8 days of beginning trimethoprim-sulfamethoxazole therapy and four showed effects within 24 hours. Three patients had histories of rechallenge with trimethoprim-sulfamethoxazole, and in each case acute iritis recurred within 24 hours of reinstitution of therapy. Five patients had additional evidence of an adverse reaction manifested as Stevens-Johnson syndrome, erythema multiforme, diffuse macular or vesicular rashes, stomatitis, glossitis, conjunctival and scleral injection, and granulomatous hepatitis. The consistent presentation including bilateral, anterior inflammation and the recurrence with rechallenge strongly indicate a cause-effect relationship. Although uveitis secondary to sulfonamides is a rarely diagnosed clinical event, recognition of the distinct presentation of this entity is important in the differential diagnosis of uveitis.
 ...
PMID:Systemic sulfonamides as a cause of bilateral, anterior uveitis. 178 69

A woman with a history of drug allergy, renal impairment and carcinoma of the breast with pulmonary micrometastases developed haemolytic anaemia and Stevens-Johnson syndrome following the use of mefenamic acid, paracetamol (acetaminophen) and furosemide (frusemide). In addition there was severe cholestatic hepatitis in the absence of clinical evidence of sepsis, biliary obstruction or recurrent metastases. The rash resolved on steroid therapy but the patient eventually died from both renal and liver failure. Acute tubular necrosis with a background of chronic tubulointerstitial nephritis was also found at autopsy. Although in the presence of multiple drug therapy the causative agent cannot be identified with absolute certainty, the association of these severe idiosyncratic hepatic and dermatological reactions with haemolytic anaemia strongly suggests mefenamic acid as the most likely culprit.
 ...
PMID:A case of Stevens-Johnson syndrome, cholestatic hepatitis and haemolytic anaemia associated with use of mefenamic acid. 206 63

The toxicities of antimalarial drugs vary because of the differences in the chemical structures of these compounds. Quinine, the oldest antimalarial, has been used for 300 years. Of the 200 to 300 compounds synthesised since the first synthetic antimalarial, primaquine in 1926, 15 to 20 are currently used for malaria treatment, most of which are quinoline derivatives. Quinoline derivatives, particularly quinine and chloroquine, are highly toxic in overdose. The toxic effects are related to their quinidine-like actions on the heart and include circulatory arrest, cardiogenic shock, conduction disturbances and ventricular arrhythmias. Additional clinical features are obnubilation, coma, convulsions, respiratory depression. Blindness is a frequent complication in quinine overdose. Hypokalaemia is consistently present, although apparently self-correcting, in severe chloroquine poisoning and is a good index of severity. Recent toxicokinetic studies of quinine and chloroquine showed good correlations between dose ingested, serum concentrations and clinical features, and confirmed the inefficacy of haemodialysis, haemoperfusion and peritoneal dialysis for enhancing drug removal. The other quinoline derivatives appear to be less toxic. Amodiaquine may induce side effects such as gastrointestinal symptoms, agranulocytosis and hepatitis. The main feature of primaquine overdose is methaemoglobinaemia. No cases of mefloquine and piperaquine overdose have been reported. Overdose with quinacrine, an acridine derivative, may result in nausea, vomiting, confusion, convulsion and acute psychosis. The dehydrofolate reductase inhibitors used in malaria treatment are sulfadoxine, dapsone, proguanil (chloroguanide), trimethoprim and pyrimethamine. Most of these drugs are given in combination. Proguanil is one of the safest antimalarials. Convulsion, coma and blindness have been reported in pyrimethamine overdose. Sulfadoxine can induce Lyell and Stevens-Johnson syndromes. The main feature of dapsone poisoning is severe methaemoglobinaemia which is related to dapsone and to its metabolites. Recent toxicokinetic studies confirmed the efficacy of oral activated charcoal, haemodialysis and haemoperfusion in enhancing removal of dapsone and its metabolites. No overdose has been reported with artemesinine, a new antimalarial tested in the People's Republic of China. The general management of antimalarial overdose include gastric lavage and symptomatic treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Clinical features and management of poisoning due to antimalarial drugs. 330 66

The clinical, radiographic and microbiological data of 47 patients with Mycoplasma pneumoniae infection admitted to three Norfolk hospitals during a 20-month period between 1982 and 1983 have been reviewed. Thirty-nine presented with pneumonia and eight with non-pulmonary infection. The M. pneumoniae specific IgM test was positive in 42 of 45 patients tested (89 per cent); in 39 the levels were diagnostic on admission. Cold agglutinins were detected in 27 (57 per cent) and a fourfold rise in complement fixation titre was demonstrated in 13 (29 per cent). Sputum culture was positive in 12 (26 per cent). The extrapulmonary manifestations observed were haemolytic anaemia (17 per cent), Stevens Johnson syndrome (4.1 per cent), neurological abnormalities (4.1 per cent), arthritis (2.1 per cent), hepatitis (2.1 per cent) and pericarditis (2.1 per cent). One patient with multilobe pneumonia, pericardial effusion and haemolytic anaemia died. Six patients presented with a history of illness longer than a month; in three the clinical and radiographic picture suggested chronic disease (pulmonary tuberculosis, lymphoma and unresolving pneumonia). There were no distinctive clinical or radiographic features of M. pneumoniae infection. Diagnosis, therefore, relies on serological tests of which the most useful is the rapid, specific IgM test, positive in 86 per cent of the admission sera.
 ...
PMID:The clinical spectrum and diagnosis of Mycoplasma pneumoniae infection. 373 68

We report 2 patients who had serious adverse effects after taking sulindac. One of these patients developed toxic hepatitis and Stevens-Johnson/toxic epidermal necrolysis syndrome which resulted in death. Such fatal reaction to sulindac therapy has not been reported previously. There was temporal relation of ingestion of sulindac to 2 episodes of acute pancreatitis in the 2nd patient, strongly suggesting drug induction. Recent reports of similar side effects with other nonsteroidal antiinflammatory drugs suggest that these drugs may have potentially more serious toxicity than has been recognized.
 ...
PMID:Hepatitis, toxic epidermal necrolysis and pancreatitis in association with sulindac therapy. 622 35

Carbamazepine therapy is occasionally complicated by hypersensitivity reactions, the mechanism of which is poorly understood. It has been suggested that affected individuals may have a genetically-determined defect of microsomal epoxide hydrolase. The aim of this study was to determine whether a single genetic mutation or pattern of mutations could be used to predict individual susceptibility to carbamazepine-hypersensitivity. DNA was isolated from 10 carbamazepine-hypersensitive patients and 10 healthy volunteers. The patients had developed various forms of toxicity with carbamazepine, including toxic epidermal necrolysis, Stevens-Johnson syndrome, hepatitis and pneumonitis. The technique of polymerase chain reaction single-strand conformation polymorphism analysis (PCR-SSCP) was used to screen for mutations in all nine exons of the microsomal epoxide hydrolase gene. Any new mutations detected by this method were characterised by direct sequencing of the DNA. In addition, in the most severely affected patient, we sequenced all nine exons of the gene. There was a higher frequency of mutations in the hypersensitive group when compared with the controls, but there was no consistent mutation (or pattern of mutations) in the microsomal epoxide hydrolase gene which was common to the hypersensitive group. DNA sequencing of all nine exons of the microsomal epoxide hydrolase gene from the most severely affected patient showed the sequence to be "wild-type," when compared to the previously published sequences. The results of this study suggest that a single mutation within the coding region of the microsomal epoxide hydrolase gene cannot be the sole determinant of the predisposition to carbamazepine hypersensitivity.
 ...
PMID:Genetic analysis of microsomal epoxide hydrolase in patients with carbamazepine hypersensitivity. 750 83

Severe skin adverse drug reactions can result in death, but the rate of such events is fortunately low. The incidences of Stevens-Johnson syndrome and toxic epidermal necrolysis range from 1.2 to 6 per million per year and 0.4 to 1.2 per million per year, respectively. Stevens-Johnson syndrome is fatal in about 5% and toxic epidermal necrolysis in 30% of cases. Drugs implicated in these diseases are the sulphonamides, anticonvulsants, allopurinol, pyrazolone derivatives, oxicams and chlormezanone. The principles of symptomatic treatment are the same as for burns, and patients with extensive skin detachment should be transferred to an intensive care unit or a burn centre. Hypersensitivity syndrome is characterised by mucocutaneous eruption and fever with frequent lymphadenopathy, hepatitis and eosinophilia. Drugs implicated are mainly anticonvulsants and sulphonamides. The mortality rate of such a reaction has been estimated to be about 8%. Corticosteroid therapy has been widely used in hypersensitivity syndrome, despite the lack of controlled studies. Drug-induced vasculitis and serum sickness may also be life-threatening when the kidney, liver, gastrointestinal tract or nervous system are involved. In angioedema, congestion may involve mucous membranes and therefore impair swallowing and ventilation. Drugs associated with angioedema include penicillins, radiographic contrast agents and ACE inhibitors. Severe forms of angioedema necessitate epinephrine (adrenaline) subcutaneous injection and possibly resuscitative efforts. Corticosteroids and/or antihistamines are used to block or reduce prolonged or late phase reactions. Prompt recognition and withdrawal of the suspected drug is essential in severe drug-induced skin reactions.
 ...
PMID:Drug-induced severe skin reactions. Incidence, management and prevention. 852 20


1 2 3 4 Next >>