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Pancreatic Neuroendocrine Tumor GARD

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.

MEN1, PCSK1, ATM, BRCA2, C11orf65, IGF2, SST, TP53, CDKN2A, SLC6A2, MTOR, EPHB1, POMC, GH1, GCGR, DAXX, ELK3, KRT19, SSTR2, CHGA, SSTR5, UCHL1, FZD4, GCM2, DLGAP1, DCLK1, SSTR4, INA, STK11, EIF2AK3, TFE3, THBD, CXCR4, PAX8, TSC1, TTR, TYMS, VEGFA, ABO, CNPY2, MRGPRX4, GPR166P, VN1R17P, MIR196A1, GADL1, MRGPRX1, GPRC6A, OXER1, GPR119, GPR151, MRGPRX3, SEMA3A, AZIN2, ACCS, STK33, LGR6, ACSS2, MEG3, NEUROG3, LPAR3, LILRB1, PLA2G15, RET, SLC2A3, INSM1, GRN, FFAR1, GHRH, GAST, FGFR4, F3, EGFR, DHCR24, CSF1, CRH, CHGB, CD44, CCK, CALCA, VPS51, ATRX, ASS1, ASCL1, ANGPT2, HSF1, PDX1, SLC2A2, KIT, SLC2A1, SEA, SDHB, SDHA, AKT1, PYGM, PTH, PTEN, PPY, PTPA, PGR, PCYT1A, PCNA, NFKB1, NEUROD1, MUC1, SMAD4, STMN1, KRAS, H3P10
- Neuroendocrine Tumor Of Pancreas Orphanet
  
  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.
Neuroendocrine Tumor GARD

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.

PRKAR1A, MEN1, CALCA, RUNX1T1, CDKN1B, CGA, CHGA, FN1, GAST, IGFBP3, PTH, RET, ADAM17, QRSL1, CDC73
- Endocrine Gland Neoplasm Wikipedia
  
  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 .
Neuroendocrine Tumor Wikipedia

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.

MEN1, CDKN1B, SSTR2, DAXX, ATRX, BRAF, TYMS, PTHLH, SSTR3, SSTR1, BAP1, MTOR, SST, GAST, SLC6A2, INSM1, CTNNB1, RET, PIK3CA, DNMT3A, POMC, EPHB1, PIK3CG, PIK3CD, CHGA, ELK3, CHEK2, PIK3CB, GRN, CD274, SMUG1, AKT1, GNA12, TP53, SYP, VEGFA, CDKN2A, ASCL1, BCL2, ENO2, NCAM1, GCG, MYCN, EGFR, MGMT, KIT, RASSF1, VHL, SCLC1, SSTR5, FOLH1, NKX2-1, KRAS, CALCA, CCND1, TAC1, PTPRF, VIP, NTS, PAX5, RHBDF2, GRP, IGF1, SDHD, GOT1, MAP2K7, CCK, ERBB2, DLL3, PPY, CXCL12, TP63, SMAD4, MUC1, INS, GCGR, CKAP4, NEUROD1, ISL1, MYC, NGF, SATB2, GLP1R, HSP90AA1, H3P10, HRAS, CHGB, CALR, NTRK1, TEK, DLK1, CDK4, CDX2, TGFA, UCHL1, RPE65, PGR, PDGFRA, CARTPT, CRH, UVRAG, SLC5A5, CXCR4, IGF1R, OTP, IL6, PHLDA3, TTF1, PAX8, TACR1, STK11, TRIM21, PLA2G15, SCG2, SQLE, SLC18A2, TERT, HDAC9, SLC2A1, PROM1, BCL2L11, NTSR1, PAX6, NAMPT, NOCT, INA, PLCB3, CD200, MKI67, PDX1, MAPK1, NES, HPSE, PTEN, STMN1, ABO, RIPK1, RORC, RAF1, IL1B, TRPV1, GATA3, ANGPT2, FOXM1, PTK2B, SDHAF2, ACCS, BDNF, EPAS1, EGF, ACSS2, MIB1, DNMT1, CCN2, TRPM8, CLDN4, CPE, CD34, CD44, FLNA, CEACAM5, B3GAT1, GH1, GIP, GHSR, GIPR, ADCY2, ALB, H3P28, TPPP2, H4C5, GGH, MIR1290, TMEM209, ELOA3, H4C13, H4C14, GPR151, SRPX, LGR5, TNFSF11, PSMG1, DCBLD2, H4-16, NRP1, MRGPRX4, SOCS1, H4C2, MIR3137, MRGPRX3, TNFRSF25, H3P12, CYYR1, AZIN2, DNER, AK6, MLIP, LMLN, NRP2, GPR68, MIR1246, H4C8, MAFK, MIR150, MIR155, MBOAT4, H4C9, MIR21, POTEKP, VN1R17P, SNORD95, GPR166P, ARID1A, EID3, SLC7A5, MIR375, H4C15, FZD4, MIRLET7C, OXER1, H4C12, HMGA2, H4C3, ARX, ELOA3B, GPRC6A, H4C11, H4C6, C17orf97, POTEM, MRGPRX1, ARMH1, H4C1, GADL1, ACTBL2, H4C4, BRI3, SQSTM1, ISYNA1, GHRL, ACOT7, KLF12, KRT20, SLC27A4, TET2, BCOR, EBNA1BP2, RALBP1, PGRMC1, LAMTOR1, FBXW7, MEG3, MAML3, TMEM127, NTNG1, ATRAID, KHDRBS1, DCTN4, SNORD61, NUP62, SNORD48, NTSR2, LPAR3, MAPK8IP2, SRRM2, BRD4, TRAM1, SPINK4, XIST, PPWD1, RBMS3, SETD1B, ZHX2, TNFSF13B, USE1, MAK16, UBE2Z, ONECUT2, FHL5, GCM2, DCLK1, ZBED1, ARHGEF2, PALB2, ALG9, SNED1, TET1, PDCD1LG2, TMPRSS13, MTA1, RPAIN, H1-10, EEF1E1, LGR6, PRMT5, NEUROD4, YAP1, SCML2, LANCL1, PAK4, RABEPK, ZNF197, CTNNBL1, PNO1, INSL5, EPB41L5, HDAC5, AKT3, CD302, GBA3, DCAF1, ATAT1, SERPINA3, VCL, CGA, ESR1, ERBB4, EPHB2, E2F1, DUSP2, DSG3, DPT, DPP4, DMBT1, DDC, DAD1, VCAN, CREB1, CRABP1, KLF6, CLU, FOXN3, CEACAM7, CEACAM3, ESR2, ETFA, EZH2, GHRH, HSPA4, AGFG1, HMOX1, HMGA1, GTF2H1, GSN, GNAS, GNA15, GFRA1, F3, GDNF, FSHR, FLT4, FLII, FLI1, FOXO1, FHIT, FGFR4, CGB3, CFL1, UQCRFS1, CDKN2C, FAS, APRT, APLP1, XIAP, APC, SLC25A6, SLC25A4, ANGPT1, ALK, AKT2, AFP, PARP1, ADCYAP1R1, ADCYAP1, ACVRL1, ACTN4, ACTG2, ACTG1, ACR, AQP4, ARF1, ATM, CASP3, CDK6, CD40LG, CD36, CD33, CCNE1, CCKBR, SERPINA6, CAV1, CA9, ATOH1, VPS51, C5, BRS3, BRCA2, DST, BAX, AVP, ATP4A, HTC2, HTR2A, TNC, IAPP, SDC1, SCT, SORT1, RNASE3, RARB, PTPRZ1, PTPRM, PTBP1, PSMD7, PSG2, PRKAR1A, PPP4C, POU4F1, PNN, PKD2, PITX2, PCYT1A, SERPINA5, PAX4, SDCBP, SDHB, SDHC, ST2, UBE2I, TPM3, TPH1, TNF, TM7SF2, TERC, TAT, STAT3, SSTR4, SEMA3F, SSR2, SOX11, SOX4, SOX2, SLPI, SLC3A2, SLC1A5, SFRP1, PAK3, PAK1, TNFRSF11B, KIF11, MDK, MAOA, LCN2, RPSA, L1CAM, KRT19, KRT7, KRT5, IL12A, MET, IL9, CXCL8, IL2, IL1A, IGFBP1, IGF2, IFNA13, IFNA1, MDM2, MFAP1, ODC1, MUTYH, NTRK2, NT5E, NRAS, NOTCH3, NPY, NOTCH1, NFKB1, NEFM, MUC4, CD99, NUDT1, COX2, MTAP, MST1R, MST1, MSMB, MMP7, MLH1, PTPRC
- Neuroendocrine Tumors Mayo Clinic
  
  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).
Postural Orthostatic Tachycardia Syndrome Due To Net Deficiency Orphanet

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.

SLC6A2, SLC12A2
- Orthostatic Intolerance Wikipedia
  
  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.
- Postural Orthostatic Tachycardia Syndrome Wikipedia
  
  Not to be confused with Pott disease . Condition in which a change from lying to standing causes an abnormally large increase in heart rate Postural orthostatic tachycardia syndrome Other names Postural tachycardia syndrome (POTS) Specialty Cardiology , Neurology Symptoms More often with standing: lightheadedness , trouble thinking , tachycardia , weakness, [1] palpitations , heat intolerance , acrocyanosis Usual onset Most common (modal) age of onset is 14 years [2] Duration > 6 months [3] Causes Antibodies against the Alpha 1 adrenergic receptor [4] [5] [6] Risk factors Family history [1] Diagnostic method An increase in heart rate by 30 beats/min with standing [1] Differential diagnosis Dehydration , heart problems, adrenal insufficiency , epilepsy , parkinson disease [7] Treatment Avoiding factors that bring on symptoms, increasing dietary salt and water, compression stockings , exercise, medications [1] Medication Beta blockers , Ivabradine , midodrine , and fludrocortisone . [1] Prognosis ~90% improve with treatment, [8] 25% of patients unable to work [9] Frequency ~ 500,000 (US) [7] Postural orthostatic tachycardia syndrome ( POTS ) is a condition in which a change from lying to standing causes an abnormally large (or higher than normal) increase in heart beat rate . [1] This occurs with symptoms that may include lightheadedness , trouble thinking, blurred vision , or weakness. [1] Other commonly associated conditions include Ehlers–Danlos syndrome , mast cell activation syndrome , irritable bowel syndrome , insomnia , chronic headaches , chronic fatigue syndrome , and fibromyalgia . [1] Contents 1 Causation 2 Signs and symptoms 2.1 Brain fog 3 Causes 3.1 Autoimmunity 3.2 Secondary 4 COVID-19 5 Diagnosis 5.1 Diagnostic criteria 5.2 Autoantibodies against G-protein coupled receptor 5.3 Orthostatic intolerance 5.4 Differential diagnoses 6 Treatment 6.1 Medication 7 Prognosis 8 Epidemiology 9 History 10 Notable cases 11 References 12 Further reading 13 External links Causation [ edit ] The causes of POTS are varied. [10] Often, it begins after a viral infection, surgery, or pregnancy. [8] Risk factors include a family history of the condition. [1] Diagnosis in adults is based on an increase in heart rate of more than 30 beats per minute within ten minutes of standing up that is accompanied by symptoms. [1] Low blood pressure with standing , however, does not occur. [1] Other conditions which can cause similar symptoms, such as dehydration , heart problems, adrenal insufficiency , epilepsy , and parkinson disease , must not be present. [7] Treatment may include avoiding factors that bring on symptoms, increasing dietary salt and water, small and frequent meals, [11] avoidance of immobilization, [11] compression stockings , exercise program, and medications. [12] [13] [1] [14] Medications used may include beta blockers , [15] pyridostigmine , [16] midodrine [17] or fludrocortisone . [1] More than 50% of people whose condition was triggered by a viral infection get better within five years. [8] About 80% have symptomatic improvement with treatment, but 25 percent of patients are still unable to work. [9] [8] Retrospective studies has shown that five years after diagnosis 19% had a full resolution of symptom. [18] It is estimated that 500,000 people are affected in the United States. [19] The average age of onset is 20 years old, and it occurs about five times more frequently in females. [1] Signs and symptoms [ edit ] In adults the primary symptom is an increase in heart rate of more than 30 beats per minute within ten minutes of standing up. [1] [20] The resulting heart rate is typically more than 120 beats per minute. [1] For people aged between 12 and 19, the minimum increase for diagnosis is 40 beats per minute. [21] This symptom is known as orthostatic (upright) tachycardia (fast heart rate). It occurs without any coinciding drop in blood pressure, as that would indicate orthostatic hypotension . [20] Certain medications to treat POTS may cause orthostatic hypotension. It is accompanied by other features of orthostatic intolerance —symptoms that develop in an upright position and are relieved by reclining. [20] These orthostatic symptoms include palpitations , light-headedness , chest discomfort, shortness of breath , [20] nausea, weakness or "heaviness" in the lower legs, blurred vision , and cognitive difficulties. [1] Symptoms may be exacerbated with prolonged sitting, prolonged standing, alcohol, heat, exercise, or eating a large meal. [ citation needed ] In up to one third of people with POTS, [1] fainting occurs in response to postural changes or exercise. [22] Migraine -like headaches are common, sometimes with symptoms worsening in an upright position ( orthostatic headache ). [22] 40-50% of patients with POTS develop acrocyanosis of extremities, a reddish-purple color in the legs and/or hands when they stand (indicative of blood pooling). [23] [22] [24] 48% of people with POTS report chronic fatigue and 32% report sleep disturbances . [25] [26] [27] [28] Others exhibit only the cardinal symptom of orthostatic tachycardia. [22] Additional symptoms are varied, and may include excessive sweating, a lack of sweating, heat intolerance, digestive issues such as bloating, nausea, indigestion, constipation, and diarrhea, a flu-like feeling, coat-hanger pain, forgetfulness, brain fog, and presyncope . [29] Brain fog [ edit ] One of the most disabling and prevalent symptoms in POTS is " brain fog ", [30] a term used by patient to describe the cognitive difficulties they experience. In one survey of 138 POTS patients, brain fog was defined as “forgetful” (91%), “difficulty thinking” (89%), and “difficulty focusing” (88%). Other common description was "Difficulty processing what others say" (80%), Confusion (71%), Lost (64 %), and "Thoughts moving too quickly" (40%) [31] The same survey described the most common triggers of brain fog to be fatigue (91%), lack of sleep (90%), prolonged standing (87%) and dehydration (86%). [ citation needed ] Neuropsychological testing has shown that a POTS-patient has reduced attention (Ruff 2&7 speed and WAIS-III digits forward), short-term memory ( WAIS-III digits back), cognitive processing speed ( Symbol digits modalities test ) and executive function ( Stroop word color and trails B ). [32] [33] [34] A potential cause for brain fog is a decrease in cerebral blood flow (CBF), especially in upright position. [35] [36] [37] Another theory is that interoception of excessive autonomic activity causes interoceptive prediction errors (PE) to occur. [38] A prediction error is the mismatch between a prior expectation and reality. [39] This would cause anxiety which then overwhelms the consciousness of pots-patient causing cognitive-affective symptoms.
- Orthostatic Intolerance OMIM
  
  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).
Pyoderma Gangrenosum Orphanet

Pyoderma gangrenosum (PG) is a primarily sterile inflammatory neutrophilic dermatosis characterized by recurrent cutaneous ulcerations with a mucopurulent or hemorrhagic exudate. Epidemiology The exact prevalence of PG is unknown. The incidence has been estimated to range between 1 and 3.3 in 330,000. ... Management and treatment The treatment of PG is a challenge. Randomized, double-blind prospective multicenter trials for PG are not available. ... The combinations of steroids with sulfa drugs or immunosuppressants are used as steroid sparing modalities. Rapid improvement of PG has been obtained by anti-tumor necrosis alpha therapy used in Crohn's disease. ... Prognosis Despite recent advances in therapy, the prognosis of PG remains unpredictable.

PSTPIP1, MEFV, NOD2, NLRP3, TCIRG1, SYN3, ELANE, GFI1, SRP54, GLI3, TNF, PAPPA, MTHFR, MAP6, JAK2, RAG1, MPO, JAK1, INSRR, DERL1, IL25, CD40, NELFCD, IL37, ACAD8, TRAF3IP2, CD40LG, USP15, CCR3, COL17A1, TYK2, GYPA, TIMP3, TG, IL5, SOAT1, CXCL8, PTPN6, CXCR1, NM, CXCR2, PRDM1, IL15, IL17A, LAD1, JAK3, ALB
- Pyoderma Gangrenosum Wikipedia
  
  It can also be part of a syndromes such as PAPA syndrome . [ citation needed ] One hallmark of pyoderma gangrenosum is pathergy , which is the appearance of new lesions at sites of trauma, including surgical wounds. [10] Diagnosis [ edit ] Diagnosis of PG is challenging owing to its variable presentation, clinical overlap with other conditions, association with several systemic diseases, and absence of defining histopathologic or laboratory findings. ... It has been shown that up to 39% of patients who initially received a diagnosis of PG have an alternative diagnosis. [11] In light of this, validated diagnostic criteria have recently been developed for ulcerative pyoderma gangrenosum. [12] Diagnostic criteria [ edit ] In addition to a biopsy demonstrating a neutrophilic infiltrate, patients must have at least 4 minor criteria to meet diagnostic criteria. [12] These criteria are based on histology, history, clinical examination and treatment. [ citation needed ] Histology: Exclusion of infection (including histologically indicated stains and tissue cultures) Pathergy (ulcer occurring at sites of trauma, with ulcer extending past area of trauma) Personal history of inflammatory bowel disease or inflammatory arthritis History of papule, pustule, or vesicle that rapidly ulcerated Clinical examination (or photographic evidence) of peripheral erythema, undermining border, and tenderness at site of ulceration Multiple ulcerations (at least 1 occurring on an anterior lower leg) Cribriform or “wrinkled paper” scar(s) at sites of healed ulcers Decrease in ulcer size within 1 mo of initiating immunosuppressive medication(s) Treatment [ edit ] First-line therapy for disseminated or localized instances of pyoderma gangrenosum is systemic treatment by corticosteroids and ciclosporin .
- Pyoderma Gangrenosum Mayo Clinic
  
  Overview Pyoderma gangrenosum (pie-o-DUR-muh gang-ruh-NO-sum) is a rare condition that causes large, painful sores (ulcers) to develop on your skin, most often on your legs. The exact causes of pyoderma gangrenosum are unknown, but it appears to be a disorder of the immune system. People who have certain underlying conditions, such as inflammatory bowel disease or arthritis, are at higher risk of pyoderma gangrenosum. Pyoderma gangrenosum ulcers can develop quickly. They usually clear up with treatment, but scarring and recurrences are common. Symptoms Pyoderma gangrenosum usually starts with a small, red bump on your skin, which may resemble a spider bite.
- Pyoderma Gangrenosum GARD
  
  Pyoderma gangrenosum is a rare, destructive inflammatory skin disease of which a painful nodule or pustule breaks down to form a progressively enlarging ulcer. Lesions may occur either in the absence of any apparent underlying disorder or in association with other diseases, such as ulcerative colitis , Crohn's disease , polyarthritis (an inflammation of several joints together), gammopathy , vasculitis, leukemia, and other conditions. Each year in the United States, pyoderma gangrenosum occurs in about 1 person per 100,000 people. Pyoderma gangrenosum belongs to a group of autoinflammatory skin diseases called neutrophilic dermatoses . Neutrophils are a type of white blood cell or leukocyte which form an early line of defense against bacterial infections.
Neuroendocrine Neoplasm Of Esophagus Orphanet

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.
Pemphigoid Gestationis Orphanet

Clinical description Pemphigoid gestationis (PG) Pemphoid gestationis (PG) typically presents during the second or third trimesters, although onset during the first trimester and postpartum is possible. ... Recurrence in subsequent pregnancies is common (35-50%), and is typically more severe with earlier onset. PG is associated with the autoimmune Graves' disease in the mother. ... Etiology PG is caused by production of anti-BP180 IgG antibodies that result from antigen presentation by MHC class II molecules aberrantly expressed on amniochorionic stromal cells and on the trophoblast. PG is strongly associated with maternal MHC class II antigens haplotypes HLA-DR3 and HLA-DR4. Diagnostic methods Clinical and histological features are not specific to PG; therefore, additional tests are required for diagnosis.

COL17A1, DST, DSG1, DSG3, HLA-DRB1, CCL11, TGM2, RBM45
- Gestational Pemphigoid Wikipedia
  
  Gestational pemphigoid Other names Pemphigoid gestationis Micrograph of gestational pemphigoid showing the characteristic subepidermal blisters and abundant eosinophils . HPS stain . Specialty Obstetrics Gestational pemphigoid ( GP ) is an autoimmune blistering skin disease of pregnancy , [1] [2] [3] typically occurring in the second or third trimester. It was originally called herpes gestationis because of the blistering appearance, although it is not associated with the herpes virus . It is one of the pemphigoid ( pemphigus -like) diseases. Contents 1 Presentation 2 Causes 2.1 Risk 3 Diagnosis 3.1 Differential diagnosis 4 Treatment 5 See also 6 References 7 External links Presentation [ edit ] Diagnosis of GP becomes clear when skin lesions progress to tense blisters during the second or third trimester. The face and mucous membranes are usually spared. GP typically starts as a blistering rash in the navel area and then spreads over the entire body.
- Pemphigoid Gestationis GARD
  
  Pemphigoid gestationis (PG) is a pregnancy-associated, autoimmune skin disorder . ... Symptoms may improve at the end of pregnancy, but flares may occur during, or right after, delivery. While PG usually goes away on its own within weeks to months after delivery, it has been reported to persist for years in some cases. PG is caused by a woman's immune system producing autoantibodies and mistakenly attacking her own skin, but the trigger for autoantibody production is poorly understood.
Duodenal Ulcer, Hyperpepsinogenemic I OMIM

Human gastric mucosa contains 2 immunochemically distinct types of pepsinogens, I and II. Only pepsinogen I (PG I) is derived exclusively from the chief cells in the oxyntic glands of the gastric body and fundus. The level of PG I in the serum, as determined by radioimmunoassay, correlates with gastric secretory capacity, serves as a marker for the ulcer diathesis, and demonstrates heterogeneity, i.e., a bimodal distribution, in large groups of duodenal ulcer patients. Rotter et al. (1979) found autosomal dominant transmission of elevated serum PG I level in 2 large families with a prominent history of duodenal ulcer. An elevated PG I level identified genetically susceptible but clinically normal persons. About half of sibships with 2 or more cases of duodenal ulcer were found to segregate for high serum PG I. Rotter et al. (1982) did a variance component analysis of the distribution of serum pepsinogen I levels in normal individuals, using a maximum-likelihood method on entire pedigrees.
Familial Gastric Type 1 Neuroendocrine Tumor Orphanet

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).
Purple Glove Syndrome Wikipedia

Purple glove syndrome Specialty Dermatology Purple glove syndrome (PGS) is a poorly understood skin disease in which the extremities become swollen , discoloured and painful. [1] PGS is potentially serious, and may require amputation . PGS is most common among elderly patients and those receiving multiple large intravenous doses of the epilepsy drug phenytoin . [2] Compartment syndrome is a complication of PGS.
Skin Cancer In Horses Wikipedia

XIV Congress. ^ a b c d e Valentine, Neoplasia , pg. 147. ^ a b Knottenbelt and McGarry, Sarcoids. , pg. 400. ^ a b c Valentine, "Neoplasia" pg. 149. ^ a b c d Torrontegui, B.O.; S. ... Retrieved August 11, 2011 . ^ Pascoe and Knottenbelt, Equine sarcoids. , pg. 247 ^ Pascoe and Knottenbelt. Equine sarcoids. , pg. 249. ^ a b c Pascoe and Knottenbelt. Equine sarcoids. pg. 251. ^ a b Knottenbelt, Derek C.; Donald F. ... Squamous cell carcinoma. , pg. 433. ^ Knight, C.G.; J. S. Munday; J. ... Pg. 148 ^ Rooney and Robertson. [1] , pg. 305 ^ Fleury, Catherine; Frederic Bérard; Agnés Leblond; Christine Faure; Nathalie Ganem; Luc Thomas (February 2000).
Malaria Wikipedia

The mosquitoes remain on the wall until they fall down dead on the floor. Insecticide treated nets [ edit ] A mosquito net in use. Mosquito nets help keep mosquitoes away from people and reduce infection rates and transmission of malaria. Nets are not a perfect barrier and are often treated with an insecticide designed to kill the mosquito before it has time to find a way past the net. Insecticide-treated nets are estimated to be twice as effective as untreated nets and offer greater than 70% protection compared with no net. [73] Between 2000 and 2008, the use of ITNs saved the lives of an estimated 250,000 infants in Sub-Saharan Africa. [74] About 13% of households in Sub-Saharan countries owned ITNs in 2007 [75] and 31% of African households were estimated to own at least one ITN in 2008. ... That number increased to 20.3 million (18.5%) African children using ITNs in 2007, leaving 89.6 million children unprotected [76] and to 68% African children using mosquito nets in 2015. [77] Most nets are impregnated with pyrethroids , a class of insecticides with low toxicity . ... According to the WHO and UNICEF, deaths attributable to malaria in 2015 were reduced by 60% [77] from a 2000 estimate of 985,000, largely due to the widespread use of insecticide-treated nets and artemisinin-based combination therapies. [74] In 2012, there were 207 million cases of malaria.

ICAM1, FCGR2B, HBB, CD36, NOS2, FCGR2A, TNF, CR1, G6PD, CRP, HP, ACKR1, GYPA, SLC4A1, GYPB, NCR3, TIRAP, GYPC, LTBR, CISH, IFNG, HMOX1, PKLR, ABO, ANK1, AQP4, ATP2B4, HBG2, CYTB, ENOSF1, MSMB, MST1, ZNF536, LINC00944, SMARCB1, DHODH, PDR, TREML4, ZNF804A, OR51F1, OR51B5, CDH13, PROCR, SPATA3, OR51N1P, DHFR, DDT, RECQL4, FAM155A, IGHG3, IL4, MMP26, IL6, IL10, TLR9, HLA-DRB1, CSMD1, HBE1, DNAJC5, TMPRSS13, KLHL3, HDGFL2, TLR4, ATAD1, LMLN, TENM3-AS1, MECP2, POMGNT2, MBL2, TFRC, TGFB1, MIF, HLA-B, HAMP, DHPS, SERPINA3, TLR2, IL1B, FOXP3, FHL5, ACOT7, POTEKP, POTEM, GEM, KIR3DL1, RN7SL263P, ACTG2, ACTG1, ACTB, ACTBL2, HBA2, CYP2B6, HSPA4, LSAMP, TRAP, FCGR3B, HSP90AA1, IL1A, LAMP3, CD81, OR10A4, CCL5, ABCB1, FAS, CD40LG, TEP1, CXCL8, IARS1, HLA-G, CTLA4, HBA1, INSRR, ANGPT2, TYMS, CFH, GSTP1, IFNAR1, AGT, GYPE, FCGR3A, TXN, IL13, HSPB3, APOE, MTCO2P12, ISYNA1, FCGR2C, FYB1, VDR, HLA-A, GSTM1, GSR, ATR, MBL3P, LAIR1, PNP, IL12B, MNAT1, IL1RN, CYP2D6, IGF1, CD55, ACHE, DECR1, COX2, IL3, CCL2, MAPK1, NLRP3, FBXW7, HAVCR2, THBD, VPS51, EMP1, ITGA2B, PTGS2, ANC, IL10RA, XPO1, VNN1, PLEK, UMPS, IL2, IL2RA, TPPP, VWF, ISG20, ADAMTS13, IRF1, IL7R, AIMP2, IL12RB1, CLEC11A, METAP2, CDK5R1, ING1, IL18R1, PGD, HAP1, H6PD, PRDX5, GRAP2, CXCL9, MMP9, MPO, TAP1, CCL4L2, COX1, EBI3, ITGAX, COX3, TLR6, CXCL11, MTHFR, NFKB2, NFYA, NOS1, TBC1D9, ORC1, MCF2, AKAP13, RNF19A, TLR7, NT5C3A, IRAK4, KIR2DS1, CCL4, KIR3DL2, ICOS, COQ2, PSIP1, PECAM1, TPT1, RNASE3, ARTN, TP53, POLDIP2, PDCD1, TLR1, AHSA1, UBL4A, AQP3, AGRP, H3C9P, CYP2C8, CYP2C19, GTF2H4, CRK, RNA18SN5, ANXA2, H3P37, CASP1, NANP, CCL4L1, MAPK14, CXCR3, GNAS, GLO1, FCN2, SMIM10L2B, FKBP4, CD27, FOXO3, RBM45, HM13, IL33, HK1, CCR5, IFNA13, IFNA1, H3P42, DNAJB1, CHIT1, CYP3A4, SMIM10L2A, EGF, CHI3L1, CAT, EPHA2, NSFL1C, ADRB2, MYMX, COX8A, GAPDH, ABCB6, NR1I3, TREML1, PUM3, FMN1, TICAM2, TRIM13, BMS1, FZD4, RABEPK, LANCL1, FUT9, TNFSF13B, DCTN6, CXCR6, ARL6IP5, MRGPRX1, ZNRD2, ASPM, KAT5, RAB7B, CIB1, SEMA3C, ARMH1, STING1, CFDP1, CPQ, MYLK4, DLC1, AKR1A1, PIEZO1, TMPRSS11D, HDAC9, CARTPT, DEFB4B, TIMELESS, SPHK1, TMED7-TICAM2, PSC, VNN2, PROM1, UPK3B, H3P23, H3P28, TNFRSF11A, TNFRSF18, TP63, PDXK, CNTNAP1, DHX16, STK24, H3P19, LOH19CR1, WASHC1, WASH6P, LPAR2, MIR146A, APOBEC3B, SPAG6, CLOCK, ATG5, MIR142, AIM2, ABCG2, PCSK9, MIR155, NCF1, PPIG, MIR29A, VN1R17P, GPR166P, CD163, MIR451A, CXADRP1, ARHGEF2, CERS1, SPINK5, MASP2, GEMIN4, ACD, TLR8, MPPE1, MCPH1, HSPA14, RNF34, TMED7, ARMC9, PPP1R2C, IL22, TRAF3IP2, A1CF, PDCD1LG2, SLC44A4, SGSM3, MCAT, HPGDS, B3GAT1, ROPN1L, PHGDH, RAB14, IL23A, ABCG4, IFIH1, CFC1, BTNL2, MARCHF1, POLE4, CMC2, TMED9, ACKR3, PDXP, RHOF, AICDA, POLD4, RBM25, TOLLIP, TREM1, LGR6, ADA2, BACH2, ERAP1, GOLPH3, PARS2, KRT88P, TRIM5, IL17RE, CHP1, GPR151, NRSN1, EIF5AL1, CD160, APCDD1, ERFE, OXER1, DNAJB1P1, DSTN, GPRC6A, CCNI, ADIRF, EBNA1BP2, TMED2, EHD1, RNPS1, HPSE, SEPTIN9, SCLT1, NT5C2, SLC25A21, LEO1, NLRP12, TIMD4, CDCA5, DBA2, CARD16, PTPMT1, CGAS, RAB39B, TADA1, MRGPRX3, MRGPRX4, PGLS, PANX1, SPO11, LPAR3, CBX5, POFUT2, SPPL3, NBEAL2, LUC7L, PTPRC, FGF23, EIF5, FLT3LG, FLT1, FECH, FBN2, FBN1, FANCD2, F3, EPO, ENO2, ADGRE1, ELK4, ELF4, EIF5A, EIF4G2, CXADR, EGR3, EDNRA, EDN1, S1PR3, RCAN1, ATN1, DNMT1, DEFB4A, DHX9, ACE, DBP, CYP1A2, CYC1, GABPA, GCHFR, GDF1, GPR42, IL4R, IL1R1, IGFBP1, IFNGR1, IFNB1, IFNA2, IFI27, IDE, HTN3, HSPA9, HSD11B1, HRES1, HPRT1, HPR, HPGD, HMGB1, HLA-DOA, UBE2K, HGF, SERPIND1, HBG1, GTF3A, GSTT1, GSN, GPX1, GPT, GRK5, CYBB, CTSL, IL9, ANXA1, C3, BSG, BRS3, BRCA2, PRDM1, BCL2, BAX, ASPA, ASIP, ARR3, NUDT2, ANXA7, ANXA4, ANPEP, CSH2, AMBP, ALOX5, ALB, AHR, AFP, ADSL, ADRA2B, ADRA1A, ADORA2A, ADH1B, ADA, ACP1, ACACA, CAST, CASR, CD1B, CD1C, CSH1, CSF1R, CSF1, CS, CRYZ, CREM, CR2, CLDN4, CPB1, CNTF, CCR4, CLU, ERCC8, CTSC, CEL, CDC25C, CD69, CD68, CD40, ENTPD1, CD34, CD28, CD19, CD14, CD9, CD1E, CD1D, IL5, IL12A, FOSL1, SELE, SPTA1, SPP1, SPINK1, SPG7, SOD3, SOD1, SMN1, SLC16A1, SLC11A1, SLC6A7, SLC2A1, SGCG, SET, SEA, ABCA1, SDC1, CXCL5, CCL22, CCL18, CCL3L1, CCL3, CCL1, SAFB, SORT1, RPS19, RBP2, RANBP2, PEX19, SSR2, SSTR4, DENND2B, STAT6, DDX39B, PRRC2A, PFBI, RAB7A, CXCR4, MOGS, ZBTB16, TRPV1, VCP, USP1, TYRP1, TTR, TTPA, TRPC1, TRP-AGG2-5, TPO, TPH1, TNFRSF1B, TLR3, TGFB2, TRBV20OR9-2, TCN2, HNF1A, TADA2A, ADAM17, TAC1, STK3, PTPRH, PTHLH, IL15, KIR3DS1, MAL, MAF, LTB, LTA, LMAN1, LEPR, LDLR, LCN2, LBR, RPSA, LAG3, KRT13, KNG1, KIR2DS5, PSMD9, KIR2DL3, KIR2DL2, KDR, KCNG1, KARS1, ITPA, ITGB2, ITGAM, ITGAL, CXCL10, IDO1, ILF3, IL18, MAP2, MAP6, MEFV, MVD, PSMD7, PSMD2, PSMB9, PSEN1, PSAP, PRSS1, PROC, MAP2K1, PRKG1, PRKAR1A, PPP1R1A, PPARG, SEPTIN4, PLP1, PGM1, PGAM1, P2RX7, SLC22A18, TNFRSF11B, OMD, ODC1, NOS3, NQO2, NFE2L2, NEK2, MYD88, MYC, H3P5
- Malaria, Susceptibility To OMIM
  
  A reduction in mortality greater than that attributable directly to malaria had been observed after the prevention of malaria by insecticides, chemoprophylaxis, and insecticide-impregnated bed nets. Previous observations that direct malaria mortality cannot account for observed hemoglobin S gene frequencies suggest that the findings of this study may apply equally to other malaria resistance genes. ... Although the relative strength of the protection is less than that of the sickle-cell variant, the greater frequency of the DQB1 (see HLA-DQB1; 604305) polymorphism makes the net effect on resistance to malaria comparable.
- Malaria Orphanet
  
  A life-threatening parasitic disease caused by Plasmodium ( P. ) parasites that are transmitted by Anophles mosquito bites to humans and is typically clinically characterized by attacks of fever, headache, chills and vomiting.
- Malaria GARD
  
  Malaria is a serious and sometimes fatal disease caused by a parasite that commonly infects a certain type of mosquito which feeds on humans. Infection with malaria parasites may result in a wide variety of symptoms, ranging from absent or very mild symptoms to severe disease and even death. People who get malaria are typically very sick with high fevers, shaking chills, and flu-like illness. In general, malaria is a curable disease if diagnosed and treated promptly and correctly. Treatment depends on many factors including disease severity, the species of malaria parasite causing the infection and the part of the world in which the infection was acquired.
- Malaria Mayo Clinic
  
  To reduce malaria infections, world health programs distribute preventive drugs and insecticide-treated bed nets to protect people from mosquito bites. The World Health Organization has recommended a malaria vaccine for use in children who live in countries with high numbers of malaria cases. Protective clothing, bed nets and insecticides can protect you while traveling. ... Sprays containing permethrin are safe to apply to clothing. Sleep under a net. Bed nets, particularly those treated with insecticides, such as permethrin, help prevent mosquito bites while you are sleeping.
Gastrinoma Wikipedia

Specialty General surgery Gastrinomas are neuroendocrine tumors (NETs), usually located in the duodenum or pancreas, that secrete gastrin and cause a clinical syndrome known as Zollinger-Ellison syndrome (ZES). [1] A large number of gastrinomas develop in the pancreas or duodenum, with near-equal frequency, and approximately 10% arise as primary neoplasms in lymph nodes of the pancreaticoduodenal region (gastrinoma triangle). [2] Most gastrinomas are sporadic (75%–80%), whereas approximately 20% to 25% are associated with multiple endocrine neoplasia type 1(MEN-1). [3] Over 50% of gastrinomas are malignant and can metastasize to regional lymph nodes and liver. ... The normal levels of gastrin are 150 pg/mL ( > 72.15 pmol/L); therefore elevated levels of > 1000 pg/mL (> 480 pmol/L) would establish the diagnosis of gastrinoma. [12] Another test that can be conducted is the secretin stimulated test, [4] which is useful in patents who have the sign and symptoms of gastrinoma but the gastrin levels are below < 1000 pg/mL.

MEN1, GAST, CHGA, SST, SCT, CDKN2A, ACTB, SCTR, GRPR, GRP, ERBB2, POTEF, CASR, MET, NMBR, POMC, PYGM, S100B, BBS2, ATP4A, ATP12A, SSTR5, TCF3, TNFRSF1B, TP53, VIP, KHSRP, PSIP1, SIGLEC7, NMB, CUX1, EGF, SMAD4, EGFR, CDKN2D, CDKN2B, GFAP, GH1, FFAR1, CDH1, CD44, HCLS1, HGF, APC, IGF1, IGF1R, IGFBP1, IL2RB, HRH2
- Zollinger-Ellison Syndrome Orphanet
  
  If the FSG level is elevated less than 10 fold and the gastric pH is <2, secretin stimulation (abnormal: increase >120 pg/ML) and basal acid (abnormal: >15 mEq/hr-basal) tests need to be done.
- Zollinger-Ellison Syndrome GARD
  
  Zollinger-Ellison syndrome (ZES) is a condition in which tumors called gastrinomas in the pancreas and duodenum (part of the small intestine) cause high levels of the hormone gastrin in the blood. High levels of gastrin then cause production of too much stomach acid. Signs and symptoms may include abdominal pain, peptic ulcers , vomiting blood, and diarrhea. The tumors are sometimes cancerous and may spread to other areas of the body. In most cases, the cause of ZES is unknown. However, about 25-30% of gastrinomas are caused by an inherited condition called multiple endocrine neoplasia type 1 (MEN1) .
Inflammatory Bowel Disease 24 OMIM

The mean +/- standard error of the mean (SEM) serum DCR3 concentration increased from 84 +/- 37 pg/ml in healthy controls to 4,333 +/- 1,637 pg/ml in individuals with IBD carrying the major allelic variants, and 11,793 +/- 2,452 pg/ml in individuals with IBD carrying the minor allelic variants, (P less than 0.05 for IBD vs control, and within IBD for major vs minor allelic variants).
Fear Of Medical Procedures Wikipedia

. ^ a b c d Specific Phobias: Clinical Applications of Evidence-Based Psychotherapy pg 5 ^ Diagnostic and Statistical Manual for Mental Disorders (DSM-IV; American Psychiatric Association, 1994) ^ Phobic Disorders and Panic in Adults: A guide to Assessment and Treatment pg 79 ^ Fears, Phobias, and Rituals: Panic, Anxiety and their Disorders pg 376 ^ Phobic Disorders and Panic in Adults: A guide to Assessment and Treatment pg 82 ^ a b Fears, Phobias, and Rituals: Panic, Anxiety and their Disorders pg 377 ^ Fears, Phobias, and Rituals: Panic, Anxiety and their Disorders pg 378 ^ Phobic Disorders and Panic in Adults: A guide to Assessment and Treatment pg 84 ^ Phobic Disorders and Panic in Adults: A guide to Assessment and Treatment pg 98-102 ^ Schmid, Markus; Wolf, Robert C; Freudenmann, Roland W; Schönfeldt-Lecuona, Carlos (2009-11-18). ... USA Today Magazine, 01617389, Feb96, Vol. 124, Issue 2609 ^ a b Fear of Cataract Operation in Aged Persons, Ritva Fagerstro:m Psychological Reports, 1993, 72, 1339-1346, pg.1339 ^ Fear of Cataract Operation in Aged Persons, Ritva Fagerstro:m Psychological Reports, 1993, 72, 1339-1346pg.1339 (Paddison, Strain, Strain & Strain, 1989) ^ Fear of Cataract Operation in Aged Persons, Ritva Fagerstro:m Psychological Reports, 1993, 72, 1339- 1346, pg. 1340 ^ Fear of Cataract Operation in Aged Persons, Ritva Fagerstro:m Psychological Reports, 1993, 72, 1339-1346, pg. 1342 ^ a b Fear of Cataract Operation in Aged Persons, Ritva Fagerstro:m Psychological Reports, 1993, 72, 1339-1349, pg. 1344 ^ Fear of Cataract Operation in Aged Persons, Ritva Fagerstro:m Psychological Reports, 1993, 72, 1339-1349, pg. 1345 ^ a b c Dental fear: Comparisons Between Younger and Older Adults, M. Michelle Rowe, PhD American Journal of Health Studies: 20(4) 2005 pg. 219-224 ^ a b c d Dental Fear in Children- a proposed model, H.R.
Abarognosis Wikipedia

Notes [ edit ] ^ Dorland 2011, baragnosis ^ Black 1995, pg. 14 ^ abarognosis , Drugs.com , retrieved 2013-03-21 ^ "abarognosis" , The American Heritage® Stedman's Medical Dictionary , Houghton Mifflin , retrieved 2013-03-21 ^ Campbell 2012, pg. 554 Sources [ edit ] Black, Peter McLaren; Rossitch, Eugene (1995), "Neurological Diagnosis" , Neurosurgery: An Introductory Text (Google eBook), Oxford University Press , ISBN 9780195044492 , retrieved 2013-02-21 Buck, Carol J. (2013), "Section Index to Diseases and Injuries" , 2013 ICD-9-CM for Physicians (Google preview), Vol. 2 (Professional ed.), Elsevier Health Sciences , ISBN 9781455775033 , retrieved 2013-03-21 Campbell, William W. (2012), "36: Sensory Localization" , DeJong's The Neurologic Examination (Google eBook) (7th ed.), Lippincott Williams & Wilkins , ISBN 9781469817521 , retrieved 2013-03-21 Dorland (2011), Dorland's Illustrated Medical Dictionary (Google eBook) (32nd ed.), Elsevier Health Sciences, ISBN 9781455709854 , retrieved 2013-03-21 External links [ edit ] Classification D ICD - 9-CM : 781.99
Pancreatic Neuroendocrine Tumor Wikipedia

PanNETs are a type of neuroendocrine tumor , representing about one third of gastroenteropancreatic neuroendocrine tumors (GEP-NETs). Many PanNETs are benign , while some are malignant . ... However, morphological imaging alone is not sufficient for a definite diagnosis [14] [16] On biopsy , immunohistochemistry is generally positive for chromogranin and synaptophysin . [17] Genetic testing thereof typically shows altered MEN1 and DAXX / ATRX . [17] Staging [ edit ] The 2010 WHO classification of tumors of the digestive system grades all the neuroendocrine tumors into three categories, based on their degree of cellular differentiation (from well-differentiated "NET G1" through to poorly-differentiated "NET G3"). ... Combinations of several medicines have been used, such as doxorubicin with streptozocin and fluorouracil (5-FU) [12] and capecitabine with temozolomide. [ citation needed ] Although marginally effective in well-differentiated PETs, cisplatin with etoposide has some activity in poorly differentiated neuroendocrine cancers (PDNECs), [12] particularly if the PDNEC has an extremely high Ki-67 score of over 50%. [8] : 30 Several targeted therapy agents have been approved in PanNETs by the FDA based on improved progression-free survival (PFS): everolimus (Afinitor) is labeled for treatment of progressive neuroendocrine tumors of pancreatic origin in patients with unresectable, locally advanced or metastatic disease. [20] [21] The safety and effectiveness of everolimus in carcinoid tumors have not been established. [20] [21] sunitinib (Sutent) is labeled for treatment of progressive, well-differentiated pancreatic neuroendocrine tumors in patients with unresectable locally advanced or metastatic disease. [22] [23] Sutent also has approval from the European Commission for the treatment of 'unresectable or metastatic, well-differentiated pancreatic neuroendocrine tumors with disease progression in adults'. [24] A phase III study of sunitinib treatment in well differentiated pNET that had worsened within the past 12 months (either advanced or metastatic disease) showed that sunitinib treatment improved progression-free survival (11.4 months vs. 5.5 months), overall survival , and the objective response rate (9.3% vs. 0.0%) when compared with placebo. [25] Genetics [ edit ] Pancreatic neuroendocrine tumors may arise in the context of multiple endocrine neoplasia type 1 , Von Hippel–Lindau disease , neurofibromatosis type 1 (NF-1) or tuberose sclerosis (TSC) [26] [27] Analysis of somatic DNA mutations in well-differentiated pancreatic neuroendocrine tumors identified four important findings: [28] [6] as expected, the genes mutated in NETs, MEN1 , ATRX , DAXX , TSC2 , PTEN and PIK3CA , [28] are different from the mutated genes previously found in pancreatic adenocarcinoma . [29] [30] one in six well-differentiated pancreatic NETs have mutations in mTOR pathway genes, such as TSC2 , PTEN and PIK3CA . [28] The sequencing discovery might allow selection of which NETs would benefit from mTOR inhibition such as with everolimus , but this awaits validation in a clinical trial . mutations affecting a new cancer pathway involving ATRX and DAXX genes were found in about 40% of pancreatic NETs. [28] The proteins encoded by ATRX and DAXX participate in chromatin remodeling of telomeres ; [31] these mutations are associated with a telomerase -independent maintenance mechanism termed ALT (alternative lengthening of telomeres) that results in abnormally long telomeric ends of chromosomes . [31] ATRX / DAXX and MEN1 mutations were associated with a better prognosis . [28] References [ edit ] ^ Burns WR, Edil BH (March 2012).

MEN1, ATRX, DAXX, ELK3, TP53, EPHB1, SLC6A2, CEACAM5, CEACAM7, UQCRFS1, DHDDS, CHPT1, RALBP1, CIB1, SEMA4D, RIPK1, CXCR4, VEGFA, TTR, GNA12, TSC2, TFE3, CDKN1B, PSG2, POMC, MYCN, CEACAM3, GRN, MUC16
Dowling-Degos Disease GARD

Dowling-Degos disease is characterized by a lacy or net-like (reticulate) pattern of abnormally dark skin coloring (hyperpigmentation) in the body's folds and creases.

ADAM10, KRT5, POFUT1, POGLUT1, ADAR
- Reticulate Acropigmentation Of Kitamura OMIM
  
  A number sign (#) is used with this entry because of evidence that reticulate acropigmentation of Kitamura (RAK) is caused by heterozygous mutation in the ADAM10 gene (602192) on chromosome 15q21. Description Reticulate acropigmentation of Kitamura (RAK) is a rare pigmentary disorder that usually shows an autosomal dominant pattern of inheritance with high penetrance. Typical features include reticulate, slightly depressed, sharply demarcated brown macules without hypopigmentation, affecting the dorsa of the hands and feet in the first or second decade of life. The macules gradually darken and extend to the proximal regions of the extremities; progression of the eruptions stops in middle age. The increased pigmentation is found on the flexor aspects of the wrists, neck, patella, and olecranon.
- Reticulate Acropigmentation Of Kitamura Wikipedia
  
  Reticulate acropigmentation of Kitamura Other names RAK [1] Specialty Dermatology Reticulate acropigmentation of Kitamura consists of linear palmar pits and pigmented macules 1 to 4 mm in diameter on the volar and dorsal aspects of the hands and feet, usually inherited in an autosomal-dominant fashion. [2] : 856 [3] [4] Contents 1 Genetics 2 See also 3 References 4 External links Genetics [ edit ] This condition is associated with mutations in the a disintegrin and metalloproteinase domain-containing protein 10 ( ADAM10 ) gene. This association was first shown in 2013. See also [ edit ] Skin lesion List of cutaneous conditions References [ edit ] ^ RESERVED, INSERM US14-- ALL RIGHTS. "Orphanet: Reticulate acropigmentation of Kitamura" . www.orpha.net . Retrieved 23 April 2019 . ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders.
- Reticulate Acropigmentation Of Kitamura Orphanet
  
  A rare, genetic, hyperpigmentation of the skin disease characterized by childhood to adulthood-onset of reticulate, slightly depressed, sharply demarcated, brown, macular skin lesions without hypopigmentation, affecting the dorsa of the hands and feet, and, occasionally, progressing to involve limbs, neck, forehead and/or trunk. Interrupted dermatoglyphics and palmoplantar pits may be additionally observed. Histologically, hyperpigmented lesions show slightly elongated and thinned rete ridges, mild hyperkeratosis without parakeratosis and absence of incontinentia pigmenti.
Glucagonoma Orphanet

Serum glucagon levels are markedly elevated (>500 pg/mL) and levels of more than 1000 pg/mL are considered diagnostic if the patient also displays features of glucagonoma syndrome.

MEN1, GCGR, CDKN1A, CDKN2B, CDKN2C, CDKN1B, GCG, SST, FFAR1, SSTR5, SSTR2, SMS, GPR119, EHMT1, PARP14, FOXA2, IL1B, IAPP, HMGN2, GRN, GLP1R, DAXX, ZGLP1
- Glucagonoma Wikipedia
  
  Glucagonoma Specialty Oncology Glucagonoma is a very rare tumor of the pancreatic alpha cells that results in the overproduction of the hormone , glucagon . Typically associated with a rash called necrolytic migratory erythema , weight loss, and mild diabetes mellitus, most people with glucagonoma contract it spontaneously. [1] However, about 10% of cases are associated with multiple endocrine neoplasia type 1 (MEN-1) syndrome. [1] Contents 1 Causes 2 Mechanism 3 Diagnosis 4 Treatment 5 History 6 References 7 External links Causes [ edit ] Although the cause of glucagonoma is unknown, some genetic factors may lead to the condition. A family history of multiple endocrine neoplasia type 1 (MEN1) is a risk factor. [1] Additionally, those with Mahvash disease have an increased risk for glucagonoma, as glucagon receptor gene (GCGR) is mutated. [2] Mechanism [ edit ] Glucagonoma results from the overproduction of glucagon , a peptide hormone located in the pancreatic alpha cells . [3] Classic symptoms include, but are not limited to, necrolytic migratory erythema (NME), diabetes mellitus, and weight loss. [3] NME presents in about 70% of cases of glucagonoma, [4] and is characterized by erythematous lesions over the distal extremities and the groin area. [3] NME has occasionally been observed in people who do not have glucagonoma. [2] People who develop glucagonoma from Mahvash disease also do not develop NME, implying that working glucagon receptors are needed in order for NME to be present in a person. [3] Weight loss, the most commonly associated effect with glucagonoma, results from the glucagon hormone, which prevents the uptake of glucose by somatic cells. [3] Diabetes is not present in all cases of glucagonoma, [3] but does frequently result from the insulin and glucagon imbalance. [5] Diagnosis [ edit ] The presence of glucagonoma syndrome, the symptoms that accompany the pancreatic tumor, as well as elevated levels of glucagon in the blood, are what is used to diagnose glucagonoma. [6] When a person presents with a blood glucagon concentration greater than 500 mg/mL along with the glucagonoma syndrome, a diagnosis can be established. [3] It is important to note that not all cases of hyperglucagonemia will lead to a diagnosis of glucagonoma. [3] Elevated blood levels of glucagon are associated with other disorders like pancreatitis and kidney failure . [3] About 60% of people diagnosed with glucagonoma are women. [7] Most of those that are diagnosed are between 45–60 years of age. [7] Treatment [ edit ] People who are diagnosed with sporadic glucagonoma often have an increased mortality rate compared to those with MEN1, as the latter group will go to the doctor for periodic visits. [4] People whose tumor have metastasized cannot easily be treated as the tumor is resistant to chemotherapy. [4] The only curative therapy for glucagonoma is surgery, and even this is not always successful. [6] [4] Heightened glucagon secretion can be treated with the administration of octreotide , a somatostatin analog, which inhibits the release of glucagon. [8] Doxorubicin and streptozotocin have also been used successfully to selectively damage alpha cells of the pancreatic islets. These do not destroy the tumor, but help to minimize progression of symptoms. [ citation needed ] History [ edit ] Fewer than 251 cases of glucagonoma have been described in the literature since their first description by Becker in 1942. Because of its rarity (fewer than one in 20 million worldwide), long-term survival rates remain unknown.
Azotemia, Familial OMIM

Furthermore, urea is reabsorbed actively by the tubule; this process is apparently brought into play particularly in states of low protein intake. Net reabsorption might be due to exaggerated active reabsorption or to deficient secretion.