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In Dogger Bank itch, sensitivity is acquired after repeated handling of the sea chervils that become entangled in fishing nets. [ citation needed ] The specific toxin responsible for the rash was determined to be the sulfur -bearing salt (2-hydroxyethyl) dimethylsulfoxonium chloride. [3] This salt is also found in some sea sponges and has potent in vitro activity against leukemia cells. [4] Treatment [ edit ] A study of two cases in 2001 suggests that the rash responds to oral ciclosporin . ... The sea chervil, abundant in the area, frequently came up with the fishing nets and had to be thrown back into the water. ... Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 978-0-7216-2921-6 . ^ Bonnevie, P. (1948). ... Comparative Biochemistry and Physiology B . 128 (1): 27–30. doi : 10.1016/S1096-4959(00)00316-X . CS1 maint: multiple names: authors list ( link ) ^ a b Bowers PW, Julian CG., PW; Julian, CG (2001).
A number sign (#) is used with this entry because pachyonychia congenita-4 (PC4) is caused by heterozygous mutation in the KRT6B gene (148042) on chromosome 12q13. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
Pachyonychia congenita (PC) is a rare genodermatosis predominantly featuring painful palmoplantar keratoderma, thickened nails, cysts and whitish oral mucosa. Epidemiology The prevalence is not known but approximately 1000 patients have been registered to date worldwide. Clinical description PC presents clinically as a spectrum of conditions. PC onset is variable with most cases manifesting soon after birth, others becoming clinically apparent only in late childhood and rarely in adulthood. The first signs of the disease usually are thickened nails or neonatal teeth.
Pachyonychia congenita (PC) is a rare inherited condition that primarily affects the nails and skin. The fingernails and toenails may be thickened and abnormally shaped . Affected people can also develop painful calluses and blisters on the soles of their feet and less frequently on the palms of their hands ( palmoplantar keratoderma ). Additional features include white patches on the tongue and inside of the mouth (leukokeratosis); bumps around the elbows, knees, and waistline (follicular hyperkeratosis); and cysts of various types including steatocystoma. Features may vary among affected people depending on their specific mutation.
For a phenotypic description and a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Inheritance Chong-Hai and Rajagopalan (1977) suggested autosomal recessive inheritance of pachyonychia congenita in a 4-year-old Malaysian girl with first-cousin parents, although they recognized new dominant mutation as a possibility. See also Sivasundram et al. (1985). INHERITANCE - Autosomal recessive HEAD & NECK Mouth - No oral leukoplakia SKIN, NAILS, & HAIR Skin - Horny papules (face, leg, buttocks) - No palmoplantar hyperkeratosis - No hyperhidrosis Nails - Episodic inflammatory swelling of nail bed - Recurrent shedding of nails - Hard,thickened nails (pachyonychia) - Subungual hyperkeratosis MISCELLANEOUS - See also pachyonychia congenita, type 3 (PC1, 167200 ) ▲ Close
A number sign (#) is used with this entry because pachyonychia congenita-3 (PC3) is caused by heterozygous mutation in the keratin-6a gene (KRT6A; 148041) on chromosome 12q13. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
A number sign (#) is used with this entry because of evidence that pachyonychia congenita-2 (PC2) is caused by heterozygous mutation in the KRT17 gene (148069) on chromosome 17q21. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). For a discussion of genetic heterogeneity of pachyonychia congenita, see 167200. Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita.
A number sign (#) is used with this entry because pachyonychia congenita-1 (PC1) is caused by heterozygous mutation in the keratin-16 gene (KRT16; 148067) on chromosome 17q21. Description Pachyonychia congenita (PC) is an autosomal dominant genodermatosis with the main clinical features of hypertrophic nail dystrophy, painful and highly debilitating plantar keratoderma, oral leukokeratosis, and a variety of epidermal cysts. Although the condition had previously been subdivided clinically into Jadassohn-Lewandowsky PC type 1 and Jackson-Lawler PC type 2, patients with PC were later found to have a mixed constellation of both types, leading to a classification of PC based on genotype (summary by Sybert, 2010; Eliason et al., 2012; McLean et al., 2011). Historical Classification of Pachyonychia Congenita Gorlin et al. (1976) suggested that 2 distinct syndromes are subsumed under the designation pachyonychia congenita. PC type 1, the Jadassohn-Lewandowsky type, shows oral leukokeratosis.
Characteristics [ edit ] Botellón usually begins around 11:00 p.m. and ends around 3:00 a.m. when many people move to a bar or club. ... Since botellón is usually a nighttime activity, Spain passed a law that prohibits stores to sell alcohol to the public after 10:00 p.m, hoping to persuade people to attend clubs or bars where alcohol must remain on site. [ citation needed ] However, the measure is a controversial one because people can still buy alcohol before the selling limit hour and consume it in public. ... One example of a macro-botellón was on 17 March 2006, "Half of Spain [met] on the net to organize a macro-botellón". [13] The macro-botellón was organized in cities around Spain, such as Madrid, Barcelona, Sevilla, Oviedo, Murcia, Vitoria, Málaga, Córdoba, Granada, and Jaén. [14] One of the purposes of the macro-botellón on 17 March 2006, near the Faro de Moncloa in Madrid, Spain, was to protest against the municipal restrictions on drinking alcohol in the streets. ... CS1 maint: archived copy as title ( link ) ^ "Media España se cita en la Red para celebrar un macrobotellón el 17 de marzo" . 2006-03-07. ^ http://www.20minutos.es/noticia/97295/0/macrobotellones/ciudades/espana/ | Literally translated from Spanish ^ "El Ayuntamiento "no consentirá" el macrobotellón que se prepara en Moncloa" . 2006-03-07.
The chalky grayish-white particles within the tumor mass correspond to foci of cartilage on histology; the semi-translucent membrane covering the lens in some tumors corresponds to spreading neoplastic cells. [4] [6] Tumor cells form a characteristic diktyomatous pattern, with folded cords and sheets resembling a fisherman's net. [3] In early development of the retina, the medullary epithelial cells acquire polarity, such that a basement membrane associated with the vitreous forms the internal limiting membrane on one side, while terminal bars form the outer limiting membrane on the other side. ... American Journal of Ophthalmology . 130 (3): 364–366. doi : 10.1016/S0002-9394(00)00542-0 . ^ a b c d e Vajaranant, Thasarat S.; Mafee, Mahmood F.; Kapur, Rashmi; Rapoport, Mark; Edward, Deepak P. ... American Journal of Ophthalmology . 133 (6): 841–843. doi : 10.1016/S0002-9394(02)01432-0 . ^ Janss, Anna J.; Yachnis, Anthony T.; Silber, Jeffrey H.; Trojanowski, John Q.; Lee, Virginia M.
Medulloepithelioma of the central nervous system is a rare, primitive neuroectodermal tumor characterized by papillary, tubular and trabecular arrangements of neoplastic neuroepithelium, mimicking the embryonic neural tube, most commonly found in the periventricular region within the cerebral hemispheres, but has also been reported in brainstem and cerebellum. It usually presents in childhood with headache, nausea, vomiting, facial nerve paresis, and/or cerebellar ataxia, and typically has a progressive course, highly malignant behavior and poor prognosis. Hearing and visual loss have also been observed.
Medulloepithelioma Histopathology of medulloepithelioma showing characteristic neural tube like strands. Specialty Neurosurgery , oncology Medulloepithelioma is a rare, primitive, fast-growing brain tumour thought to stem from cells of the embryonic medullary cavity . [1] Tumours originating in the ciliary body of the eye are referred to as embryonal medulloepitheliomas, [1] or diktyomas . [2] A highly malignant undifferentiated primitive neuroepithelial tumour of children, medulloepithelioma may contain bone , cartilage , skeletal muscle , and tends to metastasize extracranially. [2] Contents 1 Signs and symptoms 2 Diagnosis 2.1 Classification 3 Treatment 4 Prognosis 5 Epidemiology 6 References 7 External links Signs and symptoms [ edit ] Medulloepithelioma have been reported to occur in the cerebral hemispheres , brainstem , cerebellum , and peripheral sites . [3] [4] [5] [6] Due to rapid growth of the tumour, patients typically present with increased intracranial pressure , seizures , and focal neurologic signs . [7] Diagnosis [ edit ] Neuronal differentiation, ranging from neuroblasts to ganglion cells, is seen in some medulloepitheliomas. Imaging studies such as Computerized Tomography (CT) and Magnetic Resonance Imaging (MRI) can aid diagnosis . Medulloepithelioma appears isodense or hypodense with variable heterogeneity and calcification on non-contrast CT scan, and enhances with contrast. [3] This radiographical finding is consistent with a primitive neuroectodermal tumour, especially in children. [6] Blood studies and imaging studies of the abdomen may be used to detect metastases. [6] Needle aspiration biopsy can be used to aid diagnosis. [6] Definitive diagnosis requires histopathological examination of surgically excised tumour tissues. Histologically, medulloepithelioma resemble a primitive neural tube and with neuronal, glial and mesenchymal elements. [8] [9] Flexner-Wintersteiner rosettes may also be observed. [10] Immunohistochemically , neural tube-like structures are vimentin positive in the majority of medulloepitheliomas. [11] Poorly differentiated medulloepitheliomas are vimentin negative.
Waterhouse et al. [3] recommend: Time zones Local time to avoid light at destination Local time to seek light at destination East 6h 03:00–09:00 11:00–17:00 East 7h 04:00–10:00 12:00–18:00 East 8h 05:00–11:00 13:00–19:00 East 9h 06:00–12:00 14:00–20:00 Travelling east by 10 hours or more is usually best managed by assuming it is a 14-hour westward transition and delaying the body clock. [3] A customised jet lag program can be obtained from an online jet lag calculator.
. ^ "Deaths in the district of Inveresk and Musselburgh in the County of Edinburgh" . Statutory Deaths 689/00 0032 . ScotlandsPeople . Retrieved 11 April 2015 . External links [ edit ] Classification D ICD-O : 8011/0, 8011/3 Wikimedia Commons has media related to Epithelioma .
The Lancet . 156 (4011): 89–95. doi : 10.1016/S0140-6736(00)65681-7 . ^ a b c d Weisse, ME (31 December 2000). ... The Lancet . 357 (9252): 299–301. doi : 10.1016/S0140-6736(00)03623-0 . PMID 11214144 . S2CID 35896288 . ^ Dukes-Filatov disease at Who Named It?
The Lancet . 156 (4011): 89–95. doi : 10.1016/S0140-6736(00)65681-7 . ^ Weisse, Martin E (31 December 2000). ... The Lancet . 357 (9252): 299–301. doi : 10.1016/S0140-6736(00)03623-0 . PMID 11214144 . S2CID 35896288 . ^ Powell, KR (January 1979). ... The Journal of Pediatrics . 78 (6): 958–67. doi : 10.1016/S0022-3476(71)80425-0 . PMID 4252715 . ^ Morens, David M; Katz, Alan R; Melish, Marian E (31 May 2001). ... The Lancet . 357 (9273): 2059. doi : 10.1016/S0140-6736(00)05151-5 . PMID 11441870 . S2CID 35925579 .
A rare staphylococcal toxemia caused by epidermolytic toxins of Staphylococcus aureus and characterized by the appearance of widespread erythematous patches, on which large blisters develop. Upon rupture of these blisters, the skin appears reddish and scalded. The lesions typically begin in the face and rapidly expand to other parts of the body. The disease may be complicated by pneumonia and sepsis. It most commonly affects newborns and infants.
However in some cases, a pancreatic NET occurs outside of the pancreas. A NET arises from cells that produce hormones, so the tumor can also produce hormones. ... Pancreatic NETs are called either functional or nonfunctional. A functional pancreatic NET causes specific symptoms because it makes extra hormones, such as gastrin, insulin, or glucagon. ... Pancreatic NETs can be hard to diagnosis, often not identified until 5 to 10 years after they begin to grow. Most pancreatic NETs are not inherited and occur sporadically in people with no family history of NETs.
Pancreatic endocrine tumor, also known as pancreatic neuroendocrine tumor (PNET), describes a group of endocrine tumors originating in the pancreas that are usually indolent and benign, but may have the potential to be malignant. They can be functional, exhibiting a hormonal hypersecretion syndrome, but can be non-functional presenting with non-specific symptoms and include insulinoma, glucagonoma, VIPoma, somatostatinoma (SSoma), PPoma and Zollinger-Ellison syndrome (ZES, or gastrinoma) and other ectopic hormone producing tumors (such as GRFoma) (see these terms). Epidemiology Prevalence in the U.S. is estimated at 1/4,000-1/3,300 and 1/37,000 in Japan, but this is likely an underestimate due to a low detection rate. Clinical description PNETs, when functional, usually present in the 5th decade of life as various hypersecretion syndromes. These include insulinoma presenting with hyperinsulinemic hypoglycemia; glucagonoma with necrolytic migratory erythema, diabetes mellitus, and thomboembolisms; VIPoma with watery diarrhea, hypokalemia and or hypo/achlorhydia; SSoma with diabetes mellitus, cholelithiasis, steatorrhea and hypochlorhydria; and ZES with severe peptic ulcer disease.
A neuroendocrine tumor (NET) is a rare type of tumor that arises from specialized body cells called neuroendocrine cells . ... Pancreatic neuroendocrine tumors (also called islet cell tumors) - NETs that typically arise in the pancreas, although they can occur outside the pancreas. A p heochromocytoma is another, rarer type of NET that usually develops in the adrenal gland , but can also arise in other parts of the body. ... Functional NETs produce a specific set of symptoms due to the production of excess hormones, while non-functional NETs generally do not cause specific symptoms. In many cases, a person has no symptoms until the tumor spreads to the liver and/or impairs the function of an organ or system. This can make NETs very hard to diagnose. The majority of NETs are not inherited and occur sporadically in people with no family history of NETs.
Endocrine gland neoplasm Specialty Oncology , endocrinology An endocrine gland neoplasm is a neoplasm affecting one or more glands of the endocrine system . Examples include: Adrenal tumor Pituitary adenoma The most common form is thyroid cancer . [1] Condition such as pancreatic cancer or ovarian cancer can be considered endocrine tumors, or classified under other systems. Pinealoma is often grouped with brain tumors because of its location. [ citation needed ] See also [ edit ] Multiple endocrine neoplasia References [ edit ] ^ "Thyroid cancer" . Archived from the original on 2007-12-20 . Retrieved 2007-12-22 . External links [ edit ] Classification D ICD - 10 : C73 - C75 D34 - D35 MeSH : D00470 v t e Overview of tumors , cancer and oncology Conditions Benign tumors Hyperplasia Cyst Pseudocyst Hamartoma Malignant progression Dysplasia Carcinoma in situ Cancer Metastasis Primary tumor Sentinel lymph node Topography Head and neck ( oral , nasopharyngeal ) Digestive system Respiratory system Bone Skin Blood Urogenital Nervous system Endocrine system Histology Carcinoma Sarcoma Blastoma Papilloma Adenoma Other Precancerous condition Paraneoplastic syndrome Staging / grading TNM Ann Arbor Prostate cancer staging Gleason grading system Dukes classification Carcinogenesis Cancer cell Carcinogen Tumor suppressor genes / oncogenes Clonally transmissible cancer Oncovirus Carcinogenic bacteria Misc. Research Index of oncology articles History Cancer pain Cancer and nausea v t e Tumours of endocrine glands Pancreas Pancreatic cancer Pancreatic neuroendocrine tumor α : Glucagonoma β : Insulinoma δ : Somatostatinoma G : Gastrinoma VIPoma Pituitary Pituitary adenoma : Prolactinoma ACTH-secreting pituitary adenoma GH-secreting pituitary adenoma Craniopharyngioma Pituicytoma Thyroid Thyroid cancer (malignant): epithelial-cell carcinoma Papillary Follicular / Hurthle cell Parafollicular cell Medullary Anaplastic Lymphoma Squamous-cell carcinoma Benign Thyroid adenoma Struma ovarii Adrenal tumor Cortex Adrenocortical adenoma Adrenocortical carcinoma Medulla Pheochromocytoma Neuroblastoma Paraganglioma Parathyroid Parathyroid neoplasm Adenoma Carcinoma Pineal gland Pinealoma Pinealoblastoma Pineocytoma MEN 1 2A 2B This article about a neoplasm is a stub .
Clinical Features Lisch et al. (1992) described 5 family members and 3 unrelated patients (4 males, 4 females), aged 23 to 71 years, with bilateral or unilateral, gray, band-shaped, and feathery opacities that sometimes appeared in whorled patterns. Retroillumination showed that the opacities consisted of intraepithelial, densely crowded, clear microcysts. Light and electron microscopy disclosed diffuse vacuolization of the cytoplasm of epithelial cells in the affected area. Visual acuity was so reduced in 3 patients that abrasion of the corneal epithelium was performed. The corneal abnormalities recurred within months, with the same reduction in visual acuity as before.
Lisch epithelial corneal dystrophy (LECD) is a very rare form of superficial corneal dystrophy characterized by feather-shaped opacities and microcysts in the corneal epithelium arranged in a band-shaped and sometimes whorled pattern, occasionally with impaired vision. Epidemiology Exact prevalence of this form of corneal dystrophy is not known but very few cases have been reported to date. LECD has been documented in one German family and in rare sporadic cases in Germany and the USA. Clinical description Lesions generally develop in childhood. Epithelial opacities are slowly progressive and painless blurred vision sometimes occurs after 60 years of age. Etiology The exact cause is unknown but appears to be genetic. The gene related to Lisch epithelial corneal dystrophy has been mapped to the short arm of the X chromosome (Xp22.3).
H&E stain Specialty Endocrine oncology Neuroendocrine tumors ( NETs ) are neoplasms that arise from cells of the endocrine ( hormonal ) and nervous systems . ... G1 and G2 neuroendocrine neoplasms are called neuroendocrine tumors (NETs) – formerly called carcinoid tumours. ... Unsourced material may be challenged and removed. ( November 2015 ) ( Learn how and when to remove this template message ) NETs from a particular anatomical origin often show similar behavior as a group, such as the foregut (which conceptually includes pancreas, and even thymus, airway and lung NETs), midgut and hindgut ; individual tumors within these sites can differ from these group benchmarks: Foregut NETs are argentaffin negative. ... Bone metastasis is uncommon. Hindgut NETs are argentaffin negative and rarely secrete 5-HT, 5-HTP, or any other vasoactive peptides. ... Not all cells are immediately killed; cell death can go on for up to two years. [ citation needed ] PRRT was initially used for low grade NETs. It is also very useful in more aggressive NETs such as Grade 2 and 3 NETs [83] [84] provided they demonstrate high uptake on SSTR imaging to suggest benefit.
Overview Neuroendocrine tumors are cancers that begin in specialized cells called neuroendocrine cells. Neuroendocrine cells have traits similar to those of nerve cells and hormone-producing cells. Neuroendocrine tumors are rare and can occur anywhere in the body. Most neuroendocrine tumors occur in the lungs, appendix, small intestine, rectum and pancreas. There are many types of neuroendocrine tumors. Some grow slowly and some grow very quickly. Some neuroendocrine tumors produce excess hormones (functional neuroendocrine tumors).
A rare, genetic, primary orthostatic disorder characterized by dizziness, palpitations, fatigue, blurred vision and tachycardia following postural change from a supine to an upright position, in the absence of hypotension. A syncope with transient cognitive impairment and dyspnea may also occur. The norepinephrine transporter deficiency leads to abnormal uptake and high plasma concentrations of norepinephrine.
Human disease Orthostatic intolerance ( OI ) is the development of symptoms when standing upright which are relieved when reclining . [1] There are many types of orthostatic intolerance. OI can be a subcategory of dysautonomia , a disorder of the autonomic nervous system [2] occurring when an individual stands up. [3] There is a substantial overlap between syndromes of orthostatic intolerance on the one hand, and either chronic fatigue syndrome (CFS) or fibromyalgia (FM) on the other. [4] It affects more women than men (female-to-male ratio is at least 4:1), usually under the age of 35. [5] Orthostatic intolerance occurs in humans because standing upright is a fundamental stressor and requires rapid and effective circulatory and neurologic compensations to maintain blood pressure , cerebral blood flow , and consciousness . When a human stands, approximately 750 mL of thoracic blood is abruptly translocated downward. People who suffer from OI lack the basic mechanisms to compensate for this deficit. [1] Changes in heart rate , blood pressure, and cerebral blood flow that produce OI may be caused by abnormalities in the interactions between blood volume control, the cardiovascular system , the nervous system and circulation control system . [6] Contents 1 Signs and symptoms 1.1 Acute OI 1.2 Chronic OI 2 Causes 3 Diagnosis 4 Management 5 Notable case 6 See also 7 References 8 External links Signs and symptoms [ edit ] Orthostatic intolerance is divided, roughly based on patient history, in two variants: acute and chronic . Acute OI [ edit ] Patients who suffer from acute OI usually manifest the disorder by a temporary loss of consciousness and posture , with rapid recovery (simple faints , or syncope ), as well as remaining conscious during their loss of posture.
The American Journal of the Medical Sciences . 317 (2): 124–133. doi : 10.1016/s0002-9629(15)40486-0 . ISSN 0002-9629 . ^ Novak P (2016). ... Clinical Autonomic Research . 16 (6): 390–5. doi : 10.1007/s10286-006-0373-0 . PMID 17036177 . The two drugs had similar potencies; combination therapy was not significantly better than monotherapy. ^ a b Freitas J, Santos R, Azevedo E, Costa O, Carvalho M, de Freitas AF (October 2000). ... Oxford University Press. doi : 10.1093/med/9780198784906.001.0001/med-9780198784906-chapter-472 . ISBN 978-0-19-182714-3 . ^ Ruzieh M, Dasa O, Pacenta A, Karabin B, Grubb B (2017).
A number sign (#) is used with this entry because of evidence that orthostatic intolerance is caused by heterozygous mutation in the gene encoding the norepinephrine transporter (SLC6A2; 163970) on chromosome 16q12. One such family has been reported. Clinical Features Orthostatic intolerance is a syndrome characterized by adrenergic symptoms that occur when an upright posture is assumed: the heart rate increases by at least 30 beats per minute, without orthostatic hypotension (Jacob et al., 1997). Most patients with orthostatic intolerance are women between the ages of 20 and 50 years (Low et al., 1995). This syndrome, first described by Da Costa (1871), has been called soldiers heart (Fraser and Wilson, 1918), neurocirculatory asthenia (Wooley, 1976), and mitral valve prolapse syndrome (Boudoulas et al., 1980). It is similar in many respects to chronic fatigue syndrome (Schondorf and Freeman, 1999).
Clin Dermatol . 19 (1): 69–71. doi : 10.1016/S0738-081X(00)00215-7 . PMID 11369491 . ^ "Drugs that call for extra caution. ... New York: Simon Schuster. p. 56. ISBN 978-0-684-87309-1 . ^ M.d. Kamath, Bob (30 May 2007). ... Kendall Hunt Publishing. p. 25. ISBN 978-0-7872-8701-6 . ^ Ashton CH (2002).
A group of esophageal epithelial neoplasms characterized by neuroendocrine differentiation, comprising well-differentiated neuroendocrine tumors (NETs), poorly differentiated neuroendocrine carcinomas (NECs), and mixed neuroendocrine-non-neuroendocrine neoplasms, an umbrella category including mixed adenoneuroendocrine carcinoma. ... NECs may also arise in other parts of the esophagus. On endoscopy, NETs usually appear as small polypoid or nodular submucosal masses, while NECs are large, infiltrative, and ulcerated. Patients most commonly present with dysphagia, pain, weight loss, and sometimes melena. Metastatic NETs may be associated with carcinoid syndrome.
Avoiding mosquito bites, such as by using insecticide -treated mosquito bed nets , also reduces the transmission of lymphatic filariasis. [19] [22] The Carter Center 's International Task Force for Disease Eradication declared lymphatic filariasis one of six potentially eradicable diseases. [19] According to medical experts, the worldwide effort to eliminate lymphatic filariasis is on track to potentially succeed by 2020. [23] For similar-looking but causally unrelated podoconiosis , international awareness of the disease will have to increase before elimination is possible. ... Andrews' Diseases of the Skin: clinical Dermatology . Saunders Elsevier. ISBN 978-0-7216-2921-6 . ^ a b Pfarr KM, Debrah AY, Specht S, Hoerauf A (November 2009). ... Anatomy & Physiology: The Unity of Form and Function . McGraw-Hill. ISBN 978-0-07-287506-5 . ^ a b c "Parasites - Lymphatic Filariasis" . cdc.gov . ... Wallingford: CAB International. pp. 1–848. ISBN 0-85198-689-7 . ^ Grove, David I (2014). ... Oxford: Oxford University Press. pp. 1–602. ISBN 978-0-19-964102-4 . ^ Burma D.P. (2010).
Lymphatic filariasis is a parasitic disease caused by microscopic, thread-like worms that only live in the human lymph system , which maintains the body's fluid balance and fights infections. It is spread from person to person by mosquitoes. Most infected people are asymptomatic and never develop clinical symptoms. A small percentage of people develop lymphedema , which may affect the legs, arms, breasts, and genitalia; bacterial infections that cause hardening and thickening of the skin, called elephantiasis; hydrocele (swelling of the scrotum) in men; and pulmonary tropical eosinophilia syndrome . Treatment may include a yearly dose of medicine, called diethylcarbamazine (DEC); while this drug does not kill all of the adult worms, it prevents infected people from giving the disease to someone else.
Lymphatic filariasis (LF) is a severe form of filariasis (see this term), caused by the parasitic worms Wuchereria bancrofti , Brugia malayi and Brugia timori , and the most common cause of acquired lymphedema worldwide. LF is endemic to tropical and subtropical regions. The vast majority of infected patients are asymptomatic but it can also cause a variety of clinical manifestations, including limb lymphedema, genital anomalies (hydrocele, chylocele), elephantiasis in later stages of the disease (frequently in the lower extremities), and tropical pulmonary eosinophilia (nocturnal paroxysmal cough and wheezing, weight loss, low-grade fever, adenopathy, and pronounced blood eosinophilia). Renal involvement (hematuria, proteinuria, nephritic syndrome, glomerulonephritis), and mono-arthritis of the knee or ankle joint have also been reported.
A rare neoplastic disease characterized by occurrence of atypical and aggressive gastric type 1 neuroendocrine tumors (NET) in early adulthood. The tumors often show nodal infiltration requiring total gastrectomy. ... Patients present high serum gastrin concentrations and iron-deficiency anemia (rather than megaloblastic anemia, which is a typical feature in patients with sporadic gastric type 1 NET, where the tumor usually arises on the background of autoimmune atrophic gastritis).
