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)

A 38-year-old patient with chronic alcoholism was on chemotherapy for acute myelomonocytic leukemia and developed purpuric and erythematous papules. Skin biopsy showed a vasculitis. Subsequent autopsy revealed disseminated tuberculosis with a poor cellular response. This case calls attention to the lack of tuberculoid granulomatous reaction is anergic patients and to the need of pathologists to suspect tuberculosis when necrotizing vasculitis in the skin is encountered in a patient with decreased immunological competence.
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PMID:Nongranulomatous septic vasculitis due to miliary tuberculosis. A pitfall in diagnosis for the pathologist. 724 71

Fournier's gangrene represents an acute severe necrotizing inflammatory process affecting the scrotum and penis. It has an associated mortality of 30-50%. In most cases, aetiological factors can be identified, such as diabetes mellitus, chronic alcoholism and perianal, perirectal or periurethral infection. The disease is characterized by a polybacterial infection, and the classic treatment includes surgical removal of the necrotic tissue and the use of broad-spectrum antibiotics. We report a case of Fournier's gangrene, histologically characterized by a necrotizing vasculitis, in which surgical resection of the necrotic tissue and antibiotic treatment failed to halt progression of the disease, whereas complete remission was achieved by high-dose corticosteroid therapy. This suggests that Fournier's gangrene is related to some form of localized vasculitis, and represents a local Shwartzman phenomenon.
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PMID:Systemic corticosteroids are important in the treatment of Fournier's gangrene: a case report. 757 98

We report the first known case of native valve endocarditis due to Corynebacterium striatum and review 51 previously reported cases of native valve endocarditis due to non-diphtheriae corynebacteria. Of the 52 patients with corynebacterial endocarditis, 11 (21%) had no predisposing conditions and 27 (52%) had structural heart disease; endocarditis in the remaining 14 patients (27%) was associated with noncardiac predisposing factors including injection drug use, chronic hemodialysis, vasculitis, alcoholism, liver transplantation and hemodialysis, a peritoneovenous shunt, and prior aspiration of a noninfected bursa. The mortality rate associated with corynebacterial endocarditis was 31%. The majority of corynebacteria in this series were sensitive to penicillin, erythromycin, gentamicin, and vancomycin. Non-diphtheriae corynebacteria are capable of producing acute valvular damage, even in patients without conditions that are predisposing for endocarditis. The occurrence of bacteremia due to non-diphtheriae corynebacteria in the appropriate clinical setting should alert physicians to the possible diagnosis of endocarditis. Empirical antibiotic therapy with vancomycin, with or without an aminoglycoside, should be initiated pending antibiotic susceptibility testing.
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PMID:Native valve endocarditis due to Corynebacterium striatum: case report and review. 757 55

Neuromyositis defined as the association of dermatomyositis or polymyositis and a neuropathy without any found cause is a very controversial entity because of the possibility of, in one hand, muscular modifications caused by neurological involvement and, on the other hand, neurogenic type manifestations caused by polymyositis. The study of 4 cases seen in an Internal Medicine department and the review of the literature allowed us to show that the concept of neuromyositis corresponds to a clinico-pathological reality when the diagnosis is based on the association of definite criteria of both primary muscle and nerve involvement excluding muscular abnormalities that could be the consequence of nerve involvement and vice versa. The criteria, most relevant when associated are: a) for muscular involvement: high increase of muscular enzyme over 6 times the superior limit of the normal values, pseudomyotonic electrical discharges, perifascicular atrophy, intense inflammatory infiltrates and massive necrosis, b) for neurological involvement: early abolition of tendinous reflexes in a patient without notable muscular atrophy and with little or no myalgia, sensitive abnormalities in areas other than those of muscular involvement, especially when they are intense, early weakness of distal muscles, decrease of nerve conduction speed, target fibers and lesions of nerve trunks (and albuminocytological dissociation in the particular case of polyradiculoneuritis). Once the diagnosis of neuropathy settled, it is necessary to exclude an usual cause (alcoholism, diabetes...) before concluding to neuromyositis. When we apply these restrictive (but nevertheless necessary for the validity of diagnosis) criteria, only 6 cases of the literature respond to this entity. It is a peripheral neuropathy in 5 cases (like two of ours) and a polyradiculoneuritis in one case (like our two others). Among these 6 cases, there is a vasculitis in two, frequency much higher to what is observed in adult polymyositis, which suggest a possible causative role of vascular involvement in neuropathy arising. In the other cases we can just give pathogenic hypothesis making the neuropathy and the polymyositis the result of the same process (immunological disturbance, paraneoplastic origin, viral disease). In one of our four patients, who have shown an HTLV-I infection by polymerase chain reaction in situ hybridization was positive in muscle which suggest a direct pathogenic role of the virus. HTLV-I infection should be considered as a possible cause of neuromyositis especially in endemic areas.
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PMID:[Do neuromyosites exist?]. 802 85

The risk factors of stroke in young adults and in the whole population are the same in general, but there are some special risk factors in young adults. They are congenital or early acquired diseases which are complicating with early stroke. We studied the risk factors of cerebrovascular insults in 150 patients, 20-49 years old (Table 1). This was 26.04 percent of all patients that were hospitally treated in the urgent neurological department over one year. However, twenty years ago, this percent was 20.20 [2]. We found that arterial hypertension was dominant both among young adults (47.99 percent) and in the whole population (Table 2) [1-3]. Essential hypertension was the most frequent, and renal and thyreotoxical hypertensions were rare. The atherogenic level of low density and high density lipoproteins (LDL/HDL) was present in 14.66 percent of young adult patients [3]. Diabetes mellitus, a known risk factor of stroke, was found in 5.33 percent of our studied patients, especially in the juvenile form [1-3]. Besides juvenile diabetes mellitus, we found other risk factors that were characteristic of young adults: systemic lupus erythematosus (3.33 percent), which began at an early vital age, and numerous cerebrovascular complications appeared during the first five years of illness [7]. In this group of young adults, we found no other type of vasculitis, which also can be a risk factor of stroke. Great risk factors of stroke in young adults were arterial-venous malformation, brain aneurysm and congenital muscular hypoplasia of the carotide and middle caliber cerebral arteries-multiple progressive intracranial arterial occlusion or Nishimoto Takeuchi disease or Moya Moya disease, which were found in 3.99 percent of our patients. These diseases were complicated by cerebrovascular haemorrhagic or ischaemic insults over the young vital period [9]. The similar was with congenital or early acquired (rheumatic fever) heart valve defects (3.99 percent in our group), with early cerebrovascular complications due to cardiogenic thromboembolism mechanisms [10]. In 2 percent of patients the stroke was the consequence of anticoagulant therapy. These were the patients with operated heart valve defects (haemodynamic risk factor was eliminated, but haemorrheological risk factor was evident) [2, 3]. Also, disturbances of cardiac rhythm were risk factors of stroke in 2 percent of our patients. The mechanism of stroke originated is cardiogenic thromboembolism or global hypotension and the following ischaemia in the border brain zone [11]. All these risk factors were present in a relatively small number of patients, but they were "strong" risk factors of stroke, especially in young adults. On the other hand, there were nicotinism, alcoholism and obesity. They were present in a greater percent (25.33; 15.66; 18.66 percent), but their influence was slow and indirect by haemorrheologic mechanism (the increasing aggregation of platelets, reduced flexibility of red and white blood cells, changed prostacycline-prostaglandin relation in endothelial and blood cells, viscosity of blood, LDL/HDL) [2, 3, 12, 13]. A prolonged psychogenic stress (8.66 percent in our group) was, also, a risk factor of stroke. It induced increase in catecholamine level, arterial hypertension, constriction of blood vessels, endothelial cell damages, increased aggregation of platelets, changed prostacycline-prostaglandin relation, metabolism of lipids and polysaccharides) [2, 3]. We found no abuse of ephedrine [16] or cocaine [15] as risk factors of stroke in our group, although it was described in litterature. Also, we found no postoperative thromboemolism (foramen ovale apertum). Ischaemic cerebrovascular insults dominated (77.34 percent) in our group of patients. In one article (Canada) [17] haemorrhagic insults were dominant in young adults. In our opinion, the number of our patients was not adequated, as haemorrhagic stroke is also treated in neurosurgical departments. The mor
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PMID:[Risk factors for stroke in young people]. 910 54

Azathioprine is employed for its immunosuppressive properties, as a steroid-sparing agent or as monotherapy. Its most traditional clinical indications are connective tissue diseases, vasculitis, post-transplant, and immunobullous dermatoses. The main disadvantages of azathioprine therapy are a delayed onset of action (6-8 weeks), and rare profound bone marrow toxicity. Susceptibility to bone marrow toxicity is due to a genetically determined metabolic defect (1 in 300). Patients at risk of such toxicity may be identified by a Thiopurine methyltransferase enzyme assay. We have undertaken a retrospective study, looking at the use of azathioprine as monotherapy for non-bullous inflammatory dermatoses. We studied a total of 24 patients (10 male, 14 female). The dermatoses comprised: atopic eczema (10), pompholyx (6), plaque psoriasis (6), and chronic actinic dermatitis (2). All patients had severe refractory disease warranting systemic second line therapy. The mean age was 49.4 years (range 17-86 years). The starting dose of azathioprine was 100-150 mg/day, and the maintenance dose 50-100 mg/day. The mean duration of treatment was 33.5 months(range 1-132 months). Eighteen patients (75%) showed a good to excellent sustained clinical response to azathioprine. This response rate was evenly represented in the 4 dermatoses studied. The adverse reactions encountered were raised MCV (6), leucopenia (2), raised hepatic enzymes (6), and dyspepsia (4). Azathioprine had to be discontinued due to adverse reactions in 2 patients (dyspepsia, raised hepatic enzymes) followed by normalization. Other factors that potentially contributed to the observed adverse events were present in 5 patients: alcoholism (2), erythromycin toxicity (1), and malabsorption (2). Our study demonstrates the efficacy of azathioprine monotherapy for severe atopic eczema, pompholyx, plaque psoriasis, and chronic actinic dermatitis. Furthermore, azathioprine is a low cost and generally well tolerated drug.
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PMID:Azathioprine in dermatological practice. An overview with special emphasis on its use in non-bullous inflammatory dermatoses. 1059 68

Aspiration of oro-pharyngeal secretions and gastric content is the most frequent cause of formation of primary lung abscess. A compromised mental status (e.g. alcoholism, sedatives, stroke) and esophageal dysfunction (e.g. herniation, vomiting) are important risk factors. Aspiration pneumonia presents as a subacute disease and is usually not distinguishable from other causes of pneumonia, until typical radiological signs of cavitation and putrid sputum appear 8 to 14 days after the initial event of aspiration. Anaerobic bacteria play a pivotal role in an almost exclusively mixed spectrum of causative organisms. Aerobic pathogens are also frequently isolated, but whether they are an active part of infection or merely represent colonizers remains unclear in many instances. Differential diagnosis includes bronchial neoplasms, either as necrotizing carcinoma or as the cause of poststenotic cavernous pneumonia, other infectious diseases like tuberculosis, Pneumocystis carinii pneumonia or endocarditis with septic metastases, and lung artery embolism or vasculitis (M. Wegener). Fiberoptic bronchoscopy is extremely helpful in determining cause and etiology of the disease and should be carried out in all patients presenting with cavernous lung lesions. Bacteriological sampling should be performed using protected specimen brushing (PSB) technique. Broncho-alveolar lavage might serve as a less expensive but also less sensitive alternative measure. Since anaerobic bacteria resemble ubiquitous commensals of the oral cavity, sputum is of no use in anaerobic culture. Principal therapeutic strategy is antibiotic therapy for an extended period, usually four weeks to four months, unless radiologic changes and as well laboratory as clinical indicators of infection are completely resolved. Clindamycin, optionally supplemented with a second or third generation cephalosporin and Ampicillin/Sulbactam proved equally effective in treating aspiration pneumonia and primary lung abscess. The role of Moxifloxacin and other new flouroquinolones with their favorable pharmacodynamics is currently evaluated. Provided that antibiotics are prescribed for a sufficient period of time and patients' compliance is ensured, surgical procedures are limited to a negligible number of complications, e.g. recurrent severe hemoptysis, empyema or broncho-pleural fistula.
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PMID:[Diagnosis and therapy of abscess forming pneumonia]. 1169 90

Osteonecrosis is a clinical entity characterized by death of bone marrow and trabecular bone as a result of disruption of blood supply to the bone (1,2). Other aspects of this condition include avascular necrosis, aseptic necrosis, and osseous ischemic necrosis of bones. Osteonecrosis is classified into two main forms; post-traumatic and nontraumatic. The post-traumatic form of osteonecrosis usually develops as a result of traumatic displacement of bone fragments, which leads to impaired blood supply and ischemia to the affected bone. Osteonecrosis of the femoral head is common following fracture of the femoral neck. A variety of systemic diseases and clinical conditions are associated with nontraumatic osteonecrosis. These include autoimmune rheumatic diseases, alcoholism, pregnancy, Gaucher's disease, thrombophilia, corticosteroid therapy, Sickle-cell anemia, pancreatitis, inflammatory bowel diseases, and use of cytotoxic drugs and others. Idiopathic forms of osteonecrosis have also been reported (2-4). Among the rheumatic diseases, osteonecrosis is strongly associated with systemic lupus erythematosus (SLE) (5). However, osteonecrosis has been diagnosed in patients with primary antiphospholipid syndrome (APS) (6), rheumatoid arthritis (7), and systemic vasculitis (8). This article reviews the causes, clinical and epidemiological features, diagnosis, and treatment options for osteonecrosis among patients with SLE.
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PMID:Osteonecrosis in patients with SLE. 1279 57

The paper deals with hemorrhagic stroke (HS) pathogenesis and diagnosis in young people. Among cerebrovascular diseases in the young acute hemorrhagic strokes take noticeable place. Arterial hypertension, diabetes mellitus, smoking, alcoholism are among risk factors of subarachnoidal hemorrhage (SAH). Massive hemorrhages occur in the rupture of arterial aneurysms and arteriovenous malformations. HS in the young may be caused by blood diseases, i.e. leukemias, hemophilias, idiopathic thrombocytopenic purpura, coagulopathies; vasculitis in diffuse diseases of the connective tissue; non-inflammatory arteriopathies; drug addiction. Genetic predisposition to HS development is discussed with focus to such diseases as a family form of moya-moya disease, glucocorticoid-depressed hyperaldosteronism, elastic pseudoxanthoma, Marfan's syndrome, renal olycystosis, Sturge-Veber syndrome. It is recommended to use wider updated methods of neurovisualization (CT, MRT, angiography) in diagnosis of HS. The conclusion is made that HS diagnosis, especially in the young, needs a multidisciplinary approach with active participation of neurologist, neurosurgeon, therapist, endocrinologist, hematologist.
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PMID:[Specific features of pathogenesis and diagnosis of hemorrhagic stroke in young patients]. 1511 67

Bartonella species are an important cause of culture-negative endocarditis, with recognized risk factors of alcoholism, homelessness, cat exposure, and pre-existing valvular disease. We report a case of Bartonella henselae endocarditis in a 36-year-old woman with complex congenital heart disease who presented with a 7-month history of hemolytic anemia, leukocytoclastic vasculitis, and recurrent fevers. Transesophageal echocardiogram revealed vegetations on the patient's native aortic valve and in the right ventricular to pulmonary artery conduit and associated bioprosthetic valve. Diagnosis of B. henselae was confirmed with serum antibody and polymerase chain reaction (PCR) testing and tissue stains. The patient was treated successfully with surgical resection and prolonged antimicrobial therapy with ceftriaxone, gentamicin, and doxycycline. A review of the literature suggests prosthetic valves and complex congenital heart disease are risk factors for Bartonella endocarditis, and a high index of suspicion with antibody and PCR testing can expedite diagnosis and improve outcomes.
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PMID:Bartonella endocarditis in complex congenital heart disease. 1837 22


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