China
Africa
Explore chapters and articles related to this topic
The Mediastinum (including pre-and para-spinal lines, neural tumours, and pneumomediastinum).
Published in Fred W Wright, Radiology of the Chest and Related Conditions, 2022
Mediastinal fibrosis may be associated with prior radiotherapy, sarcoidosis, tuberculosis, chronic fungus infection (especially histoplasmosis which is more common in the USA - see p. 19.45), other fibrosing conditions such as Riedel's thyroiditis, retroperitoneal fibrosis (involving the ureters and/or aorta and pelvis), biliary cirrhosis (or fibrosis of the common bile duct), fibrosis of the pancreas or salivary glands, pseudo-tumour of the orbit, lymphoid granuloma, pulmonary hyalinising granuloma, or as part of a widespread disease complex such as rheumatoid or amyloid. In some cases it may be associated with drugs such as methysergide or practalol. In others there is an abnormal immune response as shown by a raised IGg. Sometimes it follows an auto-immune or inflammatory response in adipose tissue - Weber Christian disease (see Mitchinson, 1965 & 1970). It may also follow repeated trauma (Goodwin, 1972) or past syphilis (see Illus. SYPHILIS MEDIASTINITIS & ps. 19.49 - 50) and may be stimulated by foreign materials e.g. silicone gel. Some cases appear to be idiopathic.
Unexplained Fever Associated with Diseases of the Gastrointestinal Tract
Published in Benedict Isaac, Serge Kernbaum, Michael Burke, Unexplained Fever, 2019
The differential diagnosis is quite extensive and includes tuberculosis, sarcoidosis, systemic lupus erythematosus, polyarteritis nodosa, giant cell arteritis, adult Still’s disease, Weber-Christian disease, infective endocarditis, and thyrotoxicosis, as well as other conditions causing prolonged fever.
The peritoneum, omentum, mesentery and retroperitoneal space
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
The term ‘misty mesentery’ indicates a pathological increase in mesenteric fat attenuation at CT (Figure61.11). It is frequently observed on multidetector CT (MDCT) scans performed during daily clinical practice, and may be caused by various pathological conditions, including oedema, inflammation (especially in association with pancreatitis), haemorrhage, neoplastic infiltration (especially otherwise occult lymphoma) or sclerosing mesenteritis. In patients with acute abdominal disease, misty mesentery may be considered a feature of the underlying disease. Otherwise, it may represent an incidental finding on MDCT performed for other reasons. Follow-up scans may be required to dictate whether further investigation is required depending on progression or resolution. It should be noted that the term ‘mesenteric panniculitis’ is frequently used synonymously with ‘misty mesentery’. Correctly this term should be reserved for the mesenteric manifestation of Weber-Christian disease; isolated lipodystrophy and mesenteric lipogranuloma. It is a very rare (200-300 cases reported worldwide) benign inflammatory or fibrotic change in the mesentery of the bowel.
Advances in diagnosis and potential therapeutic options for familial chylomicronemia syndrome
Published in Expert Opinion on Orphan Drugs, 2018
Lane B. Benes, Eric J. Brandt, Michael H. Davidson
The diagnosis of FCS requires a combination of clinical manifestations and serum lipid markers. Genetic testing affords opportunity for a more specific diagnosis. FCS can be considered a single disease with a multitude of clinical presentations with monogenic or polygenic forms. Those that present with monogenic forms as homozygous or compound heterozygous loss-of-function mutations of LPL or one of LPL’s four cofactors (APOC2, GPI-HBP1, LMF1, or APOA5) tend to present at younger ages compared to polygenic forms that present later [1,17,18]. Polygenic forms typically require an exacerbating factor to institute an additional ‘hit’ on the LPL cascade that leads to clinically detectable manifestations and serum lipid abnormalities [16–18]. There are many exacerbating factors, including type 1 or 2 diabetes mellitus, hypothyroidism, obesity, high fat diet, alcohol use, pregnancy, nephrotic syndrome, multiple myeloma, lupus, lymphoma, Nelson syndrome, Weber–Christian disease, and medications (estrogens, glucocorticoids, beta-blockers, bile acid sequestrants, thiazide diuretics, sertraline, isotretinoin, and some antiretrovirals) [5,16,17]. Due to the heterogeneity of genotypes and phenotypes, there is considerable variation in the initial presentation of FCS patients; some may present early with acute pancreatitis, while others are not diagnosed until a screening lipid panel shows severe hypertriglyceridemia.