China
Africa
Explore chapters and articles related to this topic
Digital Deformities in Rheumatoid Arthritis
Published in J. Terrence Jose Jerome, Clinical Examination of the Hand, 2022
There is hyperextension of DIP. This is not only due to excessive traction of the extensor apparatus, but also to a voluntary compensatory extension of the patient, to put the end of the affected finger at the same level as the others.
Case 26
Published in Andrew Solomon, Julia Anstey, Liora Wittner, Priti Dutta, Clinical Cases, 2021
Andrew Solomon, Julia Anstey, Liora Wittner, Priti Dutta
A urine dip does not show any evidence of infection, proteinuria or haematuria. Given his history, the emergency department doctor suspects spontaneous bacterial peritonitis so runs some initial blood tests (Table 26.9), as well as sending some ascitic fluid for analysis.
The Interstitial Pneumonias
Published in Lourdes R. Laraya-Cuasay, Walter T. Hughes, Interstitial Lung Diseases in Children, 2019
The onset of DIP is usually insidious. There may be a preceding viral-like illness. Cough has been described, also there is difficulty of breathing, cyanosis, and failure to gain weight during the first month of life. This is followed by progressive hypoxia and death from respiratory failure before 4 months of age despite intensive drug and supportive treatment.50 Dyspnea, tachypnea and growth retardation were the prominent findings of 28 patients reviewed by Stillwell and associates.51 Cough and cyanosis were present in 63% of the patients. The characteristic cough was dry and nonproductive. Clubbing was reported in 26%. Only 11 cases had febrile onset.
Immunopathogenesis and therapeutic potential of macrophage influx in diffuse parenchymal lung diseases
Published in Expert Review of Respiratory Medicine, 2020
Ritu Kulshrestha, Himanshu Dhanda, Apoorva Pandey, Amit Singh, Raj Kumar
DIP is characterized by accumulation of granular-pigmented alveolar macrophages in alveolar lumens and septa secondary to active or passive exposure to tobacco smoke. This light brown pigment, called ‘smoker’s macrophages’ comprises mainly of aluminum silicate (kaolinite) [107]. Such a histologic pattern of DIP may also occur in pneumoconiosis, rheumatologic disease, drug-associated ILD and other inhaled agents, including marijuana smoke [108]. BAL fluid examination of DIP patients reveals a nonspecific increase in eosinophil, neutrophil, lymphocyte, and macrophage counts [109]. Wojtan et al., in 2016, quantified the CD40 and CD163 antigen staining in BALF of DIP patients. They identified three populations of cells: small cells with strong antigen expression (+++), large cells with weak (+), and cells with no expression (–). DIP patients showed a very low proportion of small cells with strong CD40 (M1 phenotype) and CD163 (M2 phenotype) reaction and an elevated proportion of large cells with weak reaction in the BALF [17]. M1 macrophages produced proinflammatory cytokines such as TNF-α and IL-12 and displayed cytotoxic properties while M2 macrophages released inflammatory mediators such as IL-10 and were involved in angiogenesis and wound healing [17,110]. This dual polarization of human alveolar macrophages was seen to progressively increase with smoking severity [111] and remains to be evaluated for progression of DIP.
Acute pancreatitis secondary to the use of the anabolic steroid trenbolone acetate
Published in Clinical Toxicology, 2019
Vidhya Kumar, Danny Issa, George Smallfield, Doumit Bouhaidar
Drug-induced pancreatitis (DIP) is rare, with a reported incidence of 0.1–2% of all causes of AP [5]. The mechanism of injury is dependent on the medication-specific characteristics and not completely understood. The diagnosis of DIP, such as other medication-induced conditions, is almost always clinically based and difficult to confirm [6]. This is particularly the case when the origin of DIP is unknown and linked to illicit drugs. Excluding all other causes of pancreatitis implies the diagnosis of DIP. Causality assessment scales can be used to categorize the strength of the relationship between the adverse event and the medication. When re-challenge with the drug causes a similar clinical picture, diagnosis is affirmed.
Smoking-associated interstitial lung disease: update and review
Published in Expert Review of Respiratory Medicine, 2020
Yaser T Dawod, Noah E Cook, William B Graham, Farah Madhani-Lovely, Choua Thao
DIP is relatively uncommon, with the age of onset between 40 and 60 years and a 2:1 male to female predominance. Prevalence of smoking among reported cases is as high as 60–87% [45]. DIP was first described histologically in 1965, with large desquamated epithelial cells filling the alveoli; there were later identified as alveolar macrophages (smoker macrophages) [46]. Diffuse involvement of distal air spaces with these distinctive macrophages, along with mild interstitial thickening and the lack of excessive fibrosis and honeycombing, is characteristic of the disease [47].