Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among drug exanthemata (AE) are included allergic reactions of the cutaneous system which are of a cutaneous vascular type after hematogenous supply of the allergen, which run an immunological course according to the early, Arthus or late type. They are manifested morphologically as urticaria (monosymptomatic or a partial symptom of an anaphylactic or serum sickness syndrome), as macular or maculopapular exanthema (9 days AE) predominantly after ampicillin, as a fixed AE, as Lyell's disease (fatal in about 30% of cases), as erythema multiforme-like AE, as purpura (allergic vasculitis, "carbromal purpura"), as rare lichenoides or nodose AE and as erythematodes-like drug reactions.
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PMID:[Drug-induced allergic skin reactions of a cutaneous vascular type (author's transl)]. 80 98

Antibiotic therapy of bacterial meningitis is being reevaluated due to reports of ampicillin-resistant strains of Hemophilus influenzae type b. The infant reported had a relapse of H. influenzae type b meningitis after an excellent clinical and bacteriologic response to an initial course of combined antibiotic therapy including chloramphenicol. This relapse is postulated to be due to localized cerebral vasculitis which was not treated for a sufficient period of time during the initial course of therapy. The patient responded well to a second course of penicillin and chloramphenicol. Since the use of pencillin and chloramphenicol will be increasing, the clinician should be aware that bacteriologic relapse of H. influenzae type b meningitis may occur with chloramphenicol therapy.
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PMID:Relapse of Hemophilus influenzae type b meningitis after combined antibiotic therapy: report of a case. 108 7

A patient with hypocomplementemic urticarial vasculitic syndrome (HUV) is presented. This is an immunological pathology, limited to skin or multisystemic, that requires a differential diagnosis with erythematosus systemic lupus on the same occasions. The ever-present symptom is skin participation, such as urticaria-angioedema or fixed exanthema; biopsy shows necrotizing venulitis with polymorphonuclear infiltration and leukocytoclastic powder. Typical laboratory data are: diminished C3, C4 and C1q; C1 inhibition can be low or normal; the more characteristic finding is the presence of C1q associated immunocomplexes. Leukocytoclastic necrotizing vasculitis was found in the skin biopsy. During the course of illness (three years) the patient presented moderate cutaneous symptoms and asthma, without other systemic participation. During this period, antihistamines and, occasionally, corticoids were administered with improvement. Moreover, the patient presented urticaria related to ampicillin ingestion, and furthermore, the presence of anaphylaxis to beta-lactam was diagnosed in vivo and specific IgE was found in the laboratory study. This feature was previously observed by other authors; however, we cannot determine why the IgE-mediated allergy to beta-lactam and a complement pathology like HUV are related.
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PMID:Hypocomplementemic urticarial vasculitic syndrome, asthma and anaphylactic reaction with ampicillin. 166 67

Autopsy tissue specimens of 69 cases of hypersensitivity myocarditis were studied to determine drug association, spectrum of histologic findings, distribution of infiltrates, and correlation between degree of infiltrates and cardiac symptoms. Hypersensitivity myocarditis was defined by the presence of eosinophils, a mixed lymphohistiocytic infiltrate along natural planes of separation, and an absence of fibrosis or granulation tissue in areas of infiltrate. Commonly implicated drugs were methyldopa, hydrochlorothiazide, ampicillin, furosemide, digoxin, tetracycline, aminophylline, phenytoin, benzodiazepines, and tricyclic antidepressants. Histiocytes composed the predominant cell type (in addition to eosinophils and lymphocytes). Lymphocytes were predominantly T cells in 12 cases studied immunohistochemically. Small foci of myocyte necrosis were present in 37 cases, and they correlated with the degree of infiltrate. A nonnecrotizing vasculitis was present in 28 cases. The right ventricle was involved in all but three cases. Cardiac arrhythmias or unexplained death occurred in 29 patients and did not correlate with the degree of myocardial infiltrate or presence of necrosis. Eosinophils were present in the livers of 30 of 58 patients, and their presence correlated with the degree of cardiac infiltration. A causative association between histologic findings and drugs is difficult to prove because of the common usage of many of the drugs implicated, multiple drug use, and the absence of clinical criteria of hypersensitivity. Symptoms do not appear related to the degree of infiltrate. In more than half the cases, infiltrates may be missed by endomyocardial biopsy due to focality of lesions.
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PMID:Hypersensitivity myocarditis. 186 86

Scores of drugs in common clinical use are capable of inflicting various degrees of damage to the kidney. Similarly, a large number of widely employed chemicals may adversely affect renal tissue as part of their toxic potential. A xenobiotic may damage the kidney by more than one mechanism. For example, NSAIDs may cause decreased renal perfusion, interstitial nephritis, primary glomerulopathy and/or altered potassium homeostasis. A large number of drugs and chemicals inflict their damage on the renal tubular cell secondary to intracellular accumulation to concentrations substantially higher than in the plasma or in other tissues. These include aminoglycosides, mercury and carbon tetrachloride and cephaloridine. Drug-induced interstitial nephritis is characterised by inflammatory lesions of the renal interstitium developed after at least 7 to 10 days of therapy. The immunological nature of this reaction is suggested by the associated fever, maculopapular rash and arthralgia observed in some of the patients. Although eosinophilia, eosinophiluria, and raised blood IgE levels are characteristic, immunoglobulins are not deposited in renal tissue, and the basic mechanism has not been elucidated. Renal biopsy demonstrates oedema and interstitial inflammatory reaction, mainly with lymphocytes, monocytes, eosinophils and plasma cells. Less frequent, vasculitis of small vessels or granulomatous reaction may develop, leading to necrotising glomerulonephritis. The drugs most commonly causing acute interstitial nephritis are methicillin, ampicillin, cephalosporins, rifampicin (rifampin), sulphonamides, phenindione and allopurinol. Other penicillins, NSAIDs, phenytoin, thiazides and frusemide (furosemide) are less frequently associated with this syndrome. Drugs and chemicals may affect renal function by pharmacologically decreasing glomerular filtration rate and/or renal blood flow. These include the NSAIDs, radiological contrast media and cyclosporin. Normal renal function depends upon an intact glomerular apparatus. Many drugs and chemicals are capable of damaging the glomerulus, causing its increased permeability to large molecules such as proteins. Several drugs including d-penicillamine, thiopronine, captopril, pyrithioxine and methimazole, are believed to exert their damage through their sulfhydryl group which bind with high affinity to glomerular structures. A variety of xenobiotics or their metabolites may be deposited in the renal tubule causing obstruction of urine flow and a secondary damage to tubular epithelium. Sulphonamides, methotrexate and ethylene glycol are good examples.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The nephrotoxic potential of drugs and chemicals. Pharmacological basis and clinical relevance. 265 51

Inadequacy of the routine methods for therapy of infectious allergic vasculitides and the necessity of sanitizing the foci of infection have prompted the application of endolymphatic administration of antibiotics. Studies of ampicillin pharmacokinetics have demonstrated that a single endolymphatic injection in a dose of 1 x 10(6) U is sufficient to maintain the therapeutic concentration of the drug in the blood serum for 24 hrs. Ampicillin has been injected into the lymph vessels of both soles in the above dose once daily for 5-7 days to 10 patients suffering from allergic vasculitis for a long time. The pathologic elements regressed by the end of the course of therapy in all the cases; only two patients have developed relapses in several months, that have been rapidly arrested.
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PMID:[Endolymphatic antibiotic therapy of allergic vasculitis]. 271 14

Recently, advances in identifying the etiologic agent, improving antibiotic therapy, and understanding the pathogenesis of complications of bacterial meningitis have been made. The acute and long-term sequelae and their courses have been documented. Acridine orange staining of the cerebrospinal fluid may identify bacteria in children with partially treated meningitis when gram-staining is not helpful. Monoclonal antibodies for meningococcus group B antigen have been developed and may prove useful for testing cerebrospinal fluid. Several newer cephalosporins have been shown to have excellent in vitro activity against the bacteria commonly associated with meningitis. They are indicated in the treatment of infants between 4 and 8 weeks of age, children in septic shock, children with liver disease, and children with infection with gram-negative enteric agents or bacteria resistant to ampicillin and chloramphenicol. Vasculitis and cerebral infarction may result in some of the complications, such as seizures and hemiparesis, noted in children, and their consequences can be documented by various neuroimaging procedures. The prognosis for ataxia is good, while that for sensorineural deafness is poor. The majority of children will have neither intellectual deficits nor difficulty with academic achievement. An effective vaccine against Haemophilus influenzae type b has been developed and is recommended for children between 18 and 60 months of age.
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PMID:Update on bacterial meningitis. 328 49

Acute cytomegalovirus infection was associated with two episodes of morbilliform eruption in a patient receiving ampicillin therapy. Shortly after the eruption cleared, the patient died. Histologic examination of the skin indicated a cytomegalovirus infection of the vascular endothelium with luminal obliteration, stasis, vasculitis, and thrombus formation.
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PMID:Cytomegalic inclusion disease of the skin. 626 99

Infective endocarditis has variable clinical presentations and may present with rheumatologic manifestations. Infective endocarditis due to high level aminoglycoside resistant enterococci represents a severe therapeutic challenge as none of the currently recommended treatment regimens are bactericidal against these isolates. In this report, a case of infective endocarditis with double aetiology, high level aminoglycoside resistant Enterococcus faecalis together with methicillin-resistant coagulase-negative staphylococci (MR-CNS), presenting with leukocytoclastic vasculitis and rapidly progressive glomerulonephritis, has been presented. A 48-years-old woman was admitted to our hospital with malaise and non-pruritic purpural rush on her lower extremities. On admission she had no fever or leukocytosis. Skin biopsy showed leukocytoclastic vasculitis and steroid therapy was started. On 12th day of admission rapidly progressive glomerulonephritis was diagnosed and she received plasmapheresis and haemodialysis support. Transthoracic echocardiography (TTE) demonstrated 1 x 1.5 cm vegetation on the mitral valve. An initial diagnosis of infective endocarditis was made and empirical treatment with vancomycin and gentamicin was started. All blood cultures yielded high level aminoglycoside resistant E. faecalis and additionally two of them yielded MR-CNS. Vancomycin was administered in combination with high dose ampicillin and repeated blood cultures taken after administration of ampicillin, revealed no growth. The patient remained afebrile, renal functions improved and a repeat TTE done on 20th day of ampicillin therapy showed waning of the vegetation. On 42nd day of treatment repeat TTE showed new vegetation on the mitral valve and severe valve insufficiency, so the patient was scheduled for mitral valve replacement. She was treated for 12 weeks with vancomycin and ampicillin and recovered successfully. In conclusion; infective endocarditis should be considered in the differential diagnosis of leukocytoclastic vasculitis and rapidly progressive glomerulonephritis. Physicians should document their treatment outcomes and experience with high level aminoglycoside resistant enterococcal infective endocarditis, which is a therapeutic challenge, so that the best therapeutic options can be identified.
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PMID:[Infective endocarditis due to high level aminoglycoside resistant Enterococcus faecalis and methicillin resistant coagulase-negative staphylococci presenting with rheumatic manifestations]. 1882 97

Leptospirosis is a zoonotic disease that occurs worldwide. Various clinical manifestations of leptospirosis can be seen. In this article, we present a case with acute renal failure, severe vasculitis and hyperbilirubinemia occurring simultaneously with leptospirosis. A 45-year-old male patient presented with fever, myalgia, jaundice and reddish skin lesions and anuria. Physical examination findings were icteric sclera, large tender hepatomegaly, and lower extremities' cutaneous necrosis due to vasculitis. Hemodialysis was started. Kidney biopsy revealed degenerative changes of proximal tubules, some of them containing bile casts. Microscopic agglutination test was positive and consistent with leptospirosis. Intravenous ampicillin and oral tetracycline were started. Methylprednisolone 60 mg per day was given for skin vasculitis. Hemodialysis therapy was discontinued. All clinical findings gradually regressed.
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PMID:Leptospirosis With Acute Renal Failure and Vasculitis: A Case Report. 3149 71


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