scholarly journals Clinical Features of Sporotrichosis

2021 ◽  
Vol 7 (2) ◽  
pp. 1-4
Author(s):  
Ana San Juan Romero ◽  

Sporotrichosis is a mycosis caused by Sporothrixschenckii complex. Generallyoccurs by traumatic inoculation. It has a wide variety of clinical presentations and can affect the skin, lungs, bones, joints and other organs. The paper reviews the current scientific literature data on sporotrichosisand the different clinical presentations. Results: Sporotrichosis is classified as primary cutaneous disease, with three main clinical presentations: lymphocutaneous, fixed-cutaneous and disseminated; and the systemic disease. The predominant form is lymphangitic sporotrichosis, which represents 60-80% of cases in Mexico.

‘Uveitis’ provides the reader with a practical approach to the assessment and management of this group of intraocular inflammatory conditions. After outlining the relevant anatomy and physiology of the uveal tract, the chapter addresses the key clinical presentations of uveitic diseases before discussing each syndrome in more detail. Using a patient-centred approach the key clinical features, investigations and treatment (medical and surgical) are described for each condition. Emphasis is given to the association of some forms of uveitis with systemic disease, and the need for appropriate investigation.


‘Sclera’ provides the reader with a practical approach to the assessment and management of scleral disease. After outlining the relevant anatomy and physiology of this structure, the chapter addresses the key clinical presentations arising from scleral disease, notably episcleritis, anterior scleritis and posterior scleritis. Using a patient-centred approach the key clinical features, investigations and treatment (medical and surgical) are described for each condition. Emphasis is given to the possible association with systemic disease, and the need for appropriate investigation.


Author(s):  
Alastair K.O. Denniston ◽  
Philip I. Murray

‘Sclera’ provides the reader with a practical approach to the assessment and management of scleral disease. After outlining the relevant anatomy and physiology of this structure, the chapter addresses the key clinical presentations arising from scleral disease, notably episcleritis, anterior scleritis and posterior scleritis. Using a patient-centred approach the key clinical features, investigations and treatment (medical and surgical) are described for each condition. Emphasis is given to the possible association with systemic disease, and the need for appropriate investigation.


Author(s):  
Alastair K.O. Denniston ◽  
Philip I. Murray

‘Uveitis’ provides the reader with a practical approach to the assessment and management of this group of intraocular inflammatory conditions. After outlining the relevant anatomy and physiology of the uveal tract, the chapter addresses the key clinical presentations of uveitic diseases before discussing each syndrome in more detail. Using a patient-centred approach the key clinical features, investigations and treatment (medical and surgical) are described for each condition. Emphasis is given to the association of some forms of uveitis with systemic disease, and the need for appropriate investigation.


Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 785
Author(s):  
Mila Glavaški ◽  
Lazar Velicki

Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiovascular disease with a prevalence of 1 in 500 people and varying clinical presentations. Although there is much research on HCM, underlying molecular mechanisms are poorly understood, and research on the molecular mechanisms of its specific clinical presentations is scarce. Our aim was to explore the molecular mechanisms shared by HCM and its clinical presentations through the automated extraction of molecular mechanisms. Molecular mechanisms were congregated by a query of the INDRA database, which aggregates knowledge from pathway databases and combines it with molecular mechanisms extracted from abstracts and open-access full articles by multiple machine-reading systems. The molecular mechanisms were extracted from 230,072 articles on HCM and 19 HCM clinical presentations, and their intersections were found. Shared molecular mechanisms of HCM and its clinical presentations were represented as networks; the most important elements in the intersections’ networks were found, centrality scores for each element of each network calculated, networks with reduced level of noise generated, and cooperatively working elements detected in each intersection network. The identified shared molecular mechanisms represent possible mechanisms underlying different HCM clinical presentations. Applied methodology produced results consistent with the information in the scientific literature.


2005 ◽  
Vol 41 (3) ◽  
pp. 179-184 ◽  
Author(s):  
Jennifer L. Strasser ◽  
Eleanor C. Hawkins

Epistaxis was retrospectively evaluated in 35 dogs. Systemic disease was diagnosed in seven dogs and intranasal disease in 29. Nineteen dogs with intranasal disease had neoplasia. Dogs with neoplasia were older (mean 10.0 years) than dogs with nonneoplastic intranasal disease (mean 5.6 years). Signs persisting for >1 month occurred more often in dogs with intranasal than systemic disease. Unilateral epistaxis did not distinguish intranasal from systemic disease. Only dogs with intranasal disease had facial deformity, decreased airflow, or regional sub-mandibular lymphadenopathy. Dogs with systemic disease had a lower packed cell volume (mean 31.8%) than dogs with intranasal disease (mean 42.7%).


Author(s):  
Richard A. Watts ◽  
Eleana Ntatsaki

The vasculitides are a group of relatively rare conditions with a broad spectrum of clinical presentations that can cause significant morbidity and mortality. Classification of the vasculitic syndromes is done according to the size of the vessels affected and also the presence of anti-neutrophil cytoplasmic antibodies (ANCA). Vasculitides can be either primary or secondary to an underlying systemic disease, malignancy, or infection. This chapter covers the spectrum of the secondary vasculitides; some of the non-ANCA-associated primary vasculitides and miscellaneous types of vasculitic syndromes. Secondary vasculitis can occur in the background of systemic rheumatic diseases such as rheumatoid arthritis, spondyloarthropathies, or other connective tissue diseases. Vasculitis can also present in relation to precipitants such as drugs (propylthiouracil, hydralazine, leucotriene antagonists) or vaccines. Infection (bacterial, mycobacterial, viral, and fungal) has been associated with vasculitis either as a trigger or as a consequence of iatrogenic immunosuppression. Infection-related vasculitis can affect all types and sizes of vessels. Certain forms of vasculitis such as cryoglobulinaemia are closely associated with viral infections and more specifically with HCV infection. There are forms of vasculitis, which appear to be isolated or localized to a single organ, or site (skin, gastrointestinal, genital, and primary central nervous system vasculitis) that may be histologically similar to systemic syndromes, but have a different prognosis. Other conditions that may mimic vasculitis and miscellaneous conditions such as Cogan’s syndrome and relapsing polychondritis are also discussed.


Author(s):  
Wolfgang L. Gross ◽  
Julia U. Holle

The primary ANCA-associated vasculitides are granulomatosis with polyangiitis (Wegener’s, GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA, Churg-Strauss syndrome, CSS). They predominantly affect small (and medium-sized) vessels and share a variable association with ANCA (anti-neutrophil cytoplasm antibody) directed against neutrophil proteinase 3 (PR3, mainly in GPA) and myeloperoxidase (MPO, mainly in MPA and CSS). Crescentic necrotizing glomerulonephritis and alveolar haemorrhage due to pulmonary capillaritis represent classical (vasculitic) organ manifestations of the ANCA-associated vasculitides (AAV). MPA occurs as a ’pure’ small (to medium-size) vessel vasculitis, whereas GPA and CSS are characterized by additional distinct clinical and pathological features. In GPA, granulomatous lesions of the upper and/or lower respiratory tract are a hallmark of the disease. Granulomatous lesions may be large in appearance and occur as space-consuming, infiltrating, and destructive inflammatory masses. GPA is believed to follow a stagewise course with an initial localized form, restricted granulomatous lesions of the upper and/or lower respiratory tract without clinical signs of vasculitis, and a consecutive generalization to systemic vasculitis which may be either non-organ-threatening (early systemic) or organ- and life- threatening (generalized GPA). Rarely, patients arrest in the localized stage and do not progress to systemic disease. In EGPA asthma, hypereosinophilia and eosinophilic organ infiltration (e.g. eosinophilic myocarditis) are typical features of the disease apart from vasculitis. Similarly to GPA, EGPA follows a stagewise course: asthma and eosinophilia may precede full-blown disease for several months or years. Recent cohort studies suggest different phenotypes in EGPA (predominantly vasculitic and MPO-ANCA-positive and predominantly with eosinophilic organ infiltration, usually ANCA-negative). This chapter focuses on the clinical features of the primary AAV and their outcome.


2020 ◽  
Vol 21 (10) ◽  
pp. 3448 ◽  
Author(s):  
Lars Schlotawa ◽  
Laura A. Adang ◽  
Karthikeyan Radhakrishnan ◽  
Rebecca C. Ahrens-Nicklas

Multiple sulfatase deficiency (MSD, MIM #272200) is an ultra-rare disease comprising pathophysiology and clinical features of mucopolysaccharidosis, sphingolipidosis and other sulfatase deficiencies. MSD is caused by impaired posttranslational activation of sulfatases through the formylglycine generating enzyme (FGE) encoded by the sulfatase modifying factor 1 (SUMF1) gene, which is mutated in MSD. FGE is a highly conserved, non-redundant ER protein that activates all cellular sulfatases by oxidizing a conserved cysteine in the active site of sulfatases that is necessary for full catalytic activity. SUMF1 mutations result in unstable, degradation-prone FGE that demonstrates reduced or absent catalytic activity, leading to decreased activity of all sulfatases. As the majority of sulfatases are localized to the lysosome, loss of sulfatase activity induces lysosomal storage of glycosaminoglycans and sulfatides and subsequent cellular pathology. MSD patients combine clinical features of all single sulfatase deficiencies in a systemic disease. Disease severity classifications distinguish cases based on age of onset and disease progression. A genotype- phenotype correlation has been proposed, biomarkers like excreted storage material and residual sulfatase activities do not correlate well with disease severity. The diagnosis of MSD is based on reduced sulfatase activities and detection of mutations in SUMF1. No therapy exists for MSD yet. This review summarizes the unique FGE/ sulfatase physiology, pathophysiology and clinical aspects in patients and their care and outlines future perspectives in MSD.


2020 ◽  
Vol 2 (9) ◽  
pp. 1401-1406 ◽  
Author(s):  
Valerio Spuntarelli ◽  
M. Luciani ◽  
E. Bentivegna ◽  
V. Marini ◽  
F. Falangone ◽  
...  

Abstract Due to its extreme virulence, COVID-19 virus has rapidly spread, developing a severe pandemic. SARS-COV-2 mostly affected the respiratory tract, causing a severe acute lung failure. Although the infection of airways, COVID-19 can be associated with chronic and systemic damages still not so much known. The purpose of this research is to collect recent evidence in literature about systemic diseases caused by COVID-19. The format of the present article has features of a systematic case-based review (level of evidence), and it is structured as a case series report (patients of our COVID-19 Medicine Ward have been selected as cases). Data for this review have been selected systematically, taking evidence only from indexed journals and databases: PubMed, Scopus, MEDLINE, and Cochrane systems. Papers chosen included systematic reviews, case series, clinical cases, meta-analysis studies, and RCTs. We start collecting studies since 2003. The main keywords used were “COVID-19” “OR” “SARS” “OR” “SARS – COV 2” “AND” “systemic disease” / “nephropathy” / “cardiac pathology” / “central nervous system.” Clinical cases belong to our COVID-19 Medicine Ward. One of the most severe COVID-19 clinical presentations includes cardiovascular problems, like myocarditis, pericarditis, and acute hearth failure. Cytokine release syndrome caused by COVID-19 develops severe acute kidney failure. It is still unknown the way coronavirus damages the liver, brain, and reproductive system. Considering the majority of the new studies about this pathology, it issues that COVID-19 is considered to be a multi-organ disease.


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