Condylar hyperplasia: new histological data Centofanti, Antonio; Anastasi, Michel Runci; Pergolizzi, Simona ...
Italian journal of anatomy and embryology,
09/2023, Letnik:
127, Številka:
S1
Journal Article
Benign lesions of the mediastinum Gerber, Tiemo Sven; Porubsky, Stefan
Histopathology,
January 2024, 2024-Jan, 2024-01-00, 20240101, Letnik:
84, Številka:
1
Journal Article
Recenzirano
Odprti dostop
Mediastinal tumours represent a heterogeneous group of entities derived from the manifold structures located in or adjacent to the mediastinum. Due to the occurrence of some of these tumours in ...characteristic mediastinal compartments, an anatomical subdivision of the mediastinum in the prevascular (anterior), visceral (middle), and paravertebral (posterior) is helpful for the differential diagnosis. Benign anterior mediastinal tumours linked to an enlargement of the thymic gland mainly consist of thymic cysts and several types of thymic hyperplasia: true thymic hyperplasia, rebound hyperplasia, lymphofollicular hyperplasia, and so‐called thymic hyperplasia with lymphoepithelial sialadenitis (LESA)‐like features. Mature teratomas, ectopic (para)thyroid tissue, and benign thymic tumours such as thymolipoma or thymofibrolipoma represent further typical tumours of the anterior mediastinum. Pericardial, bronchogenic, or oesophageal duplication cysts predominate in the middle mediastinum, whereas neurogenic tumours and myelolipomas are characteristic findings in the posterior compartment. Vascular tumours, lipomas, adenomatoid tumours, Castleman disease, or mediastinitis are further examples of less frequent tumours or tumorous lesions affecting the mediastinum. This review focuses on benign mediastinal lesions with an emphasis on benign tumours of the thymus. Besides histology, characteristic epidemiological and clinical aspects prerequisite for the correct diagnosis and patient management are discussed.
Thymic hyperplasia with lymphoepithelial sialadenitis (LESA)‐like features as an example of a thymic tumorous lesion showing an association with non‐myasthenic autoimmune diseases and lymphomas.
Benign prostatic hyperplasia (BPH) as the leading cause of urination disorder is still a refractory disease, and there have no satisfied drugs or treatment protocols yet. With identifying excessive ...Zn2+, inflammation, and oxidative stress as the etiology of aberrant hyperplasia, an injectable sodium alginate (SA) and glycyrrhizic acid (GA)‐interconnected hydrogels (SAGA) featuring Zn2+‐triggered in situ gelation are developed to load lonidamine for reprogramming prostate microenvironment and treating BPH. Herein, SAGA hydrogels can crosslink with Zn2+ in BPH via coordination chelation and switch free Zn2+ to bound ones, consequently alleviating Zn2+‐arisen inflammation and glycolysis. Beyond capturing Zn2+, GA with intrinsic immunoregulatory property can also alleviate local inflammation and scavenge reactive oxygen species (ROS). Intriguingly, Zn2+ chelation‐bridged interconnection in SAGA enhances its mechanical property and regulates the degradation rate to enable continuous lonidamine release, favoring hyperplastic acini apoptosis and further inhibiting glycolysis. These multiple actions cooperatively reprogram BPH microenvironment to alleviate characteristic symptoms of BPH and shrink prostate. RNA sequencing reveals that chemotaxis, glycolysis, and tumor necrosis factor (TNF) inflammation‐related pathways associated with M1‐like phenotype polarization are discerned as the action rationales of such endogenous Zn2+‐triggered in situ hydrogels, providing a candidate avenue to treat BPH.
An injectable sodium alginate (SA) and glycyrrhizic acid (GA)‐interconnected hydrogel (SAGA) featuring Zn2+‐triggered in situ gelation is developed to capture Zn2+, alleviate local inflammation, scavenge ROS, inhibit glycolysis and chemotaxis, which are available to reprogram the microenvironment of benign prostatic hyperplasia (BPH) and shrinking prostate especially after entrapping lonidamine.
Adrenocortical hyperplasia: A multifaceted disease Bourdeau, Isabelle; Parisien-La Salle, Stéfanie; Lacroix, André
Baillière's best practice & research. Clinical endocrinology & metabolism,
20/May , Letnik:
34, Številka:
3
Journal Article
Recenzirano
Adrenocortical hyperplasia may develop in different contexts. Primary adrenal hyperplasia may be secondary to primary bilateral macronodular adrenocortical hyperplasia (PBMAH) or micronodular ...bilateral adrenal hyperplasia (MiBAH) which may be divided in primary pigmented nodular adrenocortical disease (PPNAD) and isolated micronodular adrenocortical disease (i-MAD). Both lead to oversecretion of cortisol and potentially to Cushing's syndrome. Moreover, adrenocortical hyperplasia may be secondary to longstanding ACTH stimulation in ACTH oversecretion as in Cushing's disease, ectopic ACTH secretion or glucocorticoid resistance syndrome and congenital adrenal hyperplasia secondary to various enzymatic defects within the cortex. Finally, idiopathic bilateral adrenal hyperplasia is the most common cause of primary aldosteronism. We will discuss recent findings on the multifaceted forms of adrenocortical hyperplasia.
Summary Obstructive sleep apnea (OSA) is a condition of intermittent nocturnal upper airway obstruction. OSA increases sympathetic drive which may result in clinical and biochemical features ...suggestive of pheochromocytoma. We present the case of a 65-year-old male with a 2.9-cm left adrenal incidentaloma on CT, hypertension, symptoms of headache, anxiety and diaphoresis, and persistently elevated 24-h urine norepinephrine (initially 818 nmol/day (89–470)) and normetanephrine (initially 11.2 µmol/day (0.6–2.7)). He was started on prazosin and underwent left adrenalectomy. Pathology revealed an adrenal corticoadenoma with no evidence of pheochromocytoma. Over the next 2 years, urine norepinephrine and normetanephrine remained significantly elevated with no MIBG avid disease. Years later, he was diagnosed with severe OSA and treated with continuous positive airway pressure. Urine testing done once OSA was well controlled revealed complete normalization of urine norepinephrine and normetanephrine with substantial symptom improvement. It was concluded that the patient never had a pheochromocytoma but rather an adrenal adenoma with biochemistry and symptoms suggestive of pheochromocytoma due to untreated severe OSA. Pseudo-pheochromocytoma is a rare presentation of OSA and should be considered on the differential of elevated urine catecholamines and metanephrines in the right clinical setting. Learning points Obstructive sleep apnea (OSA) is a common condition among adults. OSA may rarely present as pseudo-pheochromocytoma with symptoms of pallor, palpitations, perspiration, headache, or anxiety. OSA should be considered on the differential of elevated urine catecholamines and metanephrines, especially in patients with negative metaiodobenzylguanidine (MIBG) scan results.
To update the congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency clinical practice guideline published by the Endocrine Society in 2010.
The writing committee presents updated ...best practice guidelines for the clinical management of congenital adrenal hyperplasia based on published evidence and expert opinion with added considerations for patient safety, quality of life, cost, and utilization.
Summary Congenital adrenal hyperplasia is a group of autosomal recessive disorders encompassing enzyme deficiencies in the adrenal steroidogenesis pathway that lead to impaired cortisol biosynthesis. ...Depending on the type and severity of steroid block, patients can have various alterations in glucocorticoid, mineralocorticoid, and sex steroid production that require hormone replacement therapy. Presentations vary from neonatal salt wasting and atypical genitalia, to adult presentation of hirsutism and irregular menses. Screening of neonates with elevated 17-hydroxyprogesterone concentrations for classic (severe) 21-hydroxylase deficiency, the most common type of congenital adrenal hyperplasia, is in place in many countries, however cosyntropin stimulation testing might be needed to confirm the diagnosis or establish non-classic (milder) subtypes. Challenges in the treatment of congenital adrenal hyperplasia include avoidance of glucocorticoid overtreatment and control of sex hormone imbalances. Long-term complications include abnormal growth and development, adverse effects on bone and the cardiovascular system, and infertility. Novel treatments aim to reduce glucocorticoid exposure, improve excess hormone control, and mimic physiological hormone patterns.
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