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Alexander P Rozin

Publications and source records attributed to Alexander P Rozin.

2 recordsLinked to original sources

From molecular mimicry to cross-reactivity or pathogen expansion? A hypothesis.

Very recently, several studies have convincingly demonstrated the role of infection in the development of the antiphospholipid syndrome. Cross antibody-mediated reactivity due to molecular mimicry between endothelial glycoproteins and microbial products was considered as an important pathogenic mechanism. However, another consequence of the molecular mimicry may be proposed. Similar tissues have less likelihood of being rejected and have a greater chance of being accepted by the host. According to this principle, pathogens with common-to-host antigens may attach readily and not be eliminated. A direct expansion of such pathogens may involve new territories. The targets of the approach 1, "from molecular mimicry to cross-reactivity," are T-B cells system inhibition-modulation. The targets of approach 2, "from molecular mimicry to pathogen expansion," are pathogens, enforcement of barriers, elimination techniques, and preventive strategy.

Antiphospholipid Syndrome↗

Fever due to aortitis.

We report a case of vasculitis with predominant aortic involvement. Vasculitis of large vessels has a limited number of tools for diagnosis and follow-up. A 78-year-old woman was referred to the internal medicine department with a 2-month history of fever of unknown origin (FUO), night sweats, weight loss and markedly elevated ESR and CRP. The results of an extended routine investigation found no infection, malignancy, hypersensitivity or autoimmune disorder. The patient did not suffer from claudication; systolic blood pressure difference between arms was 20 mm Hg. Temporal artery biopsies were negative. 2-18F-Fluorine-2-deoxy-D -glucose positron emission tomography (FDG PET) scan imaging demonstrated intense FDG uptake along the aorta and in the brachio-cephalic and carotid arteries consistent with arteritis. A high dose of corticosteroid therapy (1 mg/kg) was instituted with further tapering. The therapy was followed by complete resolution of the symptoms and pathological FDG uptake on repeated FDG PET. Second-line therapy was not added because of positive conversion of Mantaux test followed by rifampicin prophylaxis. FDG PET should be a part of the work-up of FUO when routine investigation fails to determine its etiology. FDG PET is useful both for diagnosis and assessment of response to therapy for large-vessel vasculitis.

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