To the syringomyelia clinic

1937 ◽  
Vol 33 (3) ◽  
pp. 363-366
Author(s):  
A. I. Sheiman ◽  
A. I. Nestereva
Keyword(s):  
Clinical Manifestations

The clinic of syringomyelia is currently well studied. Even 30 years ago, Schlesinger presented a classification of this disease with various complexes of clinical manifestations. In recent years, the literature on this issue has become even more enriched both in relation to the clinic and etiopathogenesis (Margulis, Bremer, Preobrazhensky, Genneberg, etc.).

Use of photodynamic therapy for photodamage skin (review of literature)

2019 ◽  
Vol 1 (7) ◽  
pp. 19-23
Author(s):  
S. I. Surkichin ◽  
N. V. Gryazeva ◽  
L. S. Kholupova ◽  
N. V. Bochkova
Keyword(s):  
Photodynamic Therapy ◽  
Comparative Evaluation ◽  
Clinical Manifestations ◽  
Light Sources ◽  
Review Of Literature ◽  
Photosensitizing Agents ◽  
Selection Of

The article provides an overview of the use of photodynamic therapy for photodamage of the skin. The causes, pathogenesis and clinical manifestations of skin photodamage are considered. The definition, principle of action of photodynamic therapy, including the sources of light used, the classification of photosensitizers and their main characteristics are given. Analyzed studies that show the effectiveness and comparative evaluation in the selection of various light sources and photosensitizing agents for photodynamic therapy in patients with clinical manifestations of photodamage.

scholarly journals Classification of lymphoid neoplasms: the microscope as a tool for disease discovery

Blood ◽  
2008 ◽  
Vol 112 (12) ◽  
pp. 4384-4399 ◽  
Author(s):  
Elaine S. Jaffe ◽  
Nancy Lee Harris ◽  
Harald Stein ◽  
Peter G. Isaacson
Keyword(s):  
Molecular Mechanisms ◽  
Nk Cell ◽  
Clinical Manifestations ◽  
Lymphoid Cells ◽  
World Health ◽  
International Studies ◽  
Lymphocyte Function ◽  
Lymphoid Neoplasms

AbstractIn the past 50 years, we have witnessed explosive growth in the understanding of normal and neoplastic lymphoid cells. B-cell, T-cell, and natural killer (NK)–cell neoplasms in many respects recapitulate normal stages of lymphoid cell differentiation and function, so that they can be to some extent classified according to the corresponding normal stage. Likewise, the molecular mechanisms involved the pathogenesis of lymphomas and lymphoid leukemias are often based on the physiology of the lymphoid cells, capitalizing on deregulated normal physiology by harnessing the promoters of genes essential for lymphocyte function. The clinical manifestations of lymphomas likewise reflect the normal function of lymphoid cells in vivo. The multiparameter approach to classification adopted by the World Health Organization (WHO) classification has been validated in international studies as being highly reproducible, and enhancing the interpretation of clinical and translational studies. In addition, accurate and precise classification of disease entities facilitates the discovery of the molecular basis of lymphoid neoplasms in the basic science laboratory.

The Epidemilogy of Chronic Venous Ulcer: Some Unanswered Questions

2000 ◽  
Vol 15 (3-4) ◽  
pp. 106-109
Author(s):  
C. V. Ruckley
Keyword(s):  
Chronic Venous Insufficiency ◽  
Venous Insufficiency ◽  
Varicose Veins ◽  
Clinical Manifestations ◽  
Epidemiological Studies ◽  
Therapeutic Interventions ◽  
Venous Disease ◽  
Clinical Classification ◽  
Age Related

Objective: To highlight gaps in knowledge concerning the epidemiology of chronic venous insufficiency and to indicate what future studies are required. Methods: Existing classifications are compared. Limitations of epidemiological studies are defined. Data from published series and from the Edinburgh Vein Study are presented. Synthesis: The Basle 1978 classification of chronic venous insufficiency (CVI) is a purely clinical classification in which the earliest grade is corona phlebectatica. The Porter 1988 classification of CVI attempted to correlate clinical grades with sites of venous incompe-tence. However, a consistent relationship does not exist. The CEAP classification separates the clinical grades (which do not include corona phlebectasia) from the anatomical segments. The CEAP clinical classification covers a range of venous manifestations but is not consistent. There is a need for further consideration of classifications. Published selected series of patients show that the frequency of incompetence in both deep and superficial systems increases in proportion to the severity of the clinical manifestations of venous disease. To understand the significance of these data we need to know the patterns of venous incompetence in the general population. Data from 1566 subjects between the ages of 18 and 64 years in the Edinburgh Vein Study, a randomly selected cross-section of members of the Edinburgh population, showed that the prevalence of CVI was age-related and was present in 9.2% of men and 6.6% of women. Men had a significantly higher frequency of reflux in the deep system than women. In order to direct therapeutic interventions where they are most appropriate we need to know which patients with the early stages of varicose veins progress to CVI and which patients with early CVI progress to the serious skin complications. Conclusions: Key information concerning the natural history of venous disease and its evolution in relation to haemodynamic abnormalities awaits the findings of longitudinal-cohort epidemiological studies which include the duplex scanning of large populations.

SYSTEMIC LUPUS ERYTHEMATOSUS AND SYNDROMES POSSIBLY RELATED

PEDIATRICS ◽  
1957 ◽  
Vol 19 (6) ◽  
pp. 1109-1123
Author(s):  
M. A. Ogryzlo ◽  
H. A. Smythe
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Serum Proteins ◽  
Clinical Manifestations ◽  
Electrophoretic Pattern ◽  
Chemotherapeutic Agents ◽  
Systemic Lupus ◽  
Relationship Of ◽  
The Relationship

Attention is drawn to the difficulties that may be encountered in the positive identification and classification of many patients suspected of suffering from systemic lupus erythematosus. Much of this is due to a lack of specific criteria, either clinical or pathologic, for the diagnosis of the disease. The problem has been made more difficult by the recognition of a number of other syndromes that bear a superficial resemblance to systemic lupus erythematosus, yet differ in clinical manifestations, natural course, prognosis and other respects. A feature common to the group is the presence of the L.E. cell phenomenon. The related conditions differ from lupus enythematosus in that the L.E. phenomenon may only be demonstrable intermittently especially during severe exacerbations of the disease, while at the same time disturbances in the electrophoretic pattern of the serum proteins may be much more profound. In systemic rheumatoid disease the prognosis without steroid therapy is better than in systemic lupus erythematosus, although the morbidity may be great. The reactions which follow administration of certain chemotherapeutic agents are of considerable interest, particularly in view of the similarity to lupus erythematosus and rheumatoid arthritis, and the reversibility on withdrawal of the offending agent. The relationship of these syndromes to each other and to classical systemic lupus erythematosus has not yet been resolved, and inclusion of them under the diagnosis of systemic lupus erythematosus at this time must be regarded as premature.

Scleroderma and Related Disorders

2017 ◽  
Author(s):  
Kristine Phillips
Keyword(s):  
Differential Diagnosis ◽  
Antinuclear Antibodies ◽  
Clinical Course ◽  
Clinical Manifestations ◽  
Diagnosis And Treatment ◽  
Localized Scleroderma ◽  
Eosinophilic Fasciitis ◽  
Tomographic Images ◽  
Computed Tomographic

Scleroderma spectrum diseases are a heterogeneous group of disorders that are distinguished by abnormalities of the connective tissue in the skin and, in some cases, other organs. Each disorder may be characterized by the extent of cutaneous and internal involvement, as well as histopathologic features of skin biopsy. Scleroderma spectrum diseases include systemic scleroderma, localized scleroderma, and eosinophilic fasciitis. This chapter reviews the classification, epidemiology, etiology, pathophysiology and pathogenesis, diagnosis, differential diagnosis, treatment, outcome measures, management, and clinical course of scleroderma as well as the definition and classification, etiology/genetics, differential diagnosis, and treatment of localized scleroderma. Also discussed are the definition and classification, epidemiology, etiology/genetics/pathogenesis, diagnosis, differential diagnosis, and treatment of eosinophilic fasciitis. Tables review the classification of—and antinuclear antibodies in—scleroderma as well as the key assessments and interventions in scleroderma management. Figures illustrate the disease's presentation and clinical manifestations, including several images of scleroderma of the hands; face, palmar, and buccal telangiectasias in a patient with scleroderma; a radiograph demonstrating calcinosis of the elbow; Raynaud’s phenomenon; high-resolution computed tomographic images of diffuse cutaneous scleroderma, scleroderma and severe pulmonary hypertension, and limited cutaneous scleroderma; plus an esophagram demonstrating hypomotility. This review contains 11 highly rendered figures, 3 tables, and 72 references.

Gastroparesis

2015 ◽  
Author(s):  
Braden Kuo ◽  
Laurence Guay
Keyword(s):  
Multiple Sclerosis ◽  
Nervous System ◽  
Gastric Emptying ◽  
Clinical Manifestations ◽  
Gastrointestinal Dysmotility ◽  
Inflammatory Conditions ◽  
Gastric Physiology ◽  
Neuromuscular Apparatus ◽  
Pharmacologic Treatments

The gastric phase of digestion requires a tightly coordinated neuromuscular apparatus to permit appropriate timing for each step. Dysregulations in this apparatus may be related to the Cajal cells, the intrinsic enteric nervous system, the extrinsic nervous system, the muscle cells, or any combination of structures and may lead to abnormal gastric emptying, referred to as gastroparesis. Gastroparesis is idiopathic in 35 to 49.4% of cases but may also be related to diabetes, autoimmune and inflammatory conditions, multiple sclerosis, use of certain medications, and infections, among other factors. This review describes the epidemiology, etiology, pathophysiology, clinical manifestations, diagnosis, treatment, and prognosis of gastroparesis. The figure shows symptom mechanisms related to gastric physiology in gastroparesis patients. Tables list the physiopathologic mechanisms and symptoms associated with defective gastric physiologic phenomena, the classification of gastroparesis according to affected structures, and pharmacologic treatments for gastrointestinal dysmotility. This review contains 1 highly rendered figure, 3 tables, and 56 references.

The molecular classification of the clinical manifestations of Crohn's disease

2002 ◽  
Vol 122 (4) ◽  
pp. 854-866 ◽  
Author(s):  
Tariq Ahmad ◽  
Alessandro Armuzzi ◽  
Mike Bunce ◽  
Kim Mulcahy–Hawes ◽  
Sara E. Marshall ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Clinical Manifestations ◽  
Molecular Classification

scholarly journals Classification of gastrointestinal stromal tumor syndromes

2018 ◽  
Vol 25 (2) ◽  
pp. R49-R58 ◽  
Author(s):  
Priya Gopie ◽  
Lin Mei ◽  
Anthony C Faber ◽  
Steven R Grossman ◽  
Steven C Smith ◽  
...  
Keyword(s):  
Interstitial Cells Of Cajal ◽  
Clinical Manifestations ◽  
Incidence Rates ◽  
Wild Type ◽  
Mesenchymal Tumors ◽  
Therapeutic Implications ◽  
The Past ◽  
High Incidence ◽  
Cells Of Cajal

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract, thought to derive from neoplastic outgrowth of the interstitial cells of Cajal. Building on recent advances in recognition, classification and diagnosis, the past two decades have seen a changing paradigm with molecular diagnostics and targeted therapies.KITandPDGFRAmutations account for 85–90% of GIST carcinogenesis. However, the remaining 10–15% of GISTs, which until recently were calledKIT/PDGFRAwild-type GISTs, have been found to have one of the several mutations, including in theSDHA,B,C,D,BRAFandNF1genes. Though most of such GISTs are sporadic, a number of families with high incidence rates of GISTs and other associated clinical manifestations have been reported and found to harbor germline mutations inKIT,PDGFRA,SDHsubunits andNF1. The goal of this review is to describe the mutations, clinical manifestations and therapeutic implications of syndromic and inherited GISTs in light of recent studies of their clinicopathologic range and pathogenesis.

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