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Delusional Disorder Wikipedia

. ^ https://www.webmd.com/schizophrenia/qa/how-can-you-recover-from-delusional-disorder ^ https://my.clevelandclinic.org/health/diseases/9599-delusional-disorder#:~:text=Environmental%2Fpsychological.,vulnerable%20to%20developing%20delusional%20disorder . ^ https://my.clevelandclinic.org/health/diseases/9599-delusional-disorder#:~:text=Environmental%2Fpsychological.

DPYSL2, DRD2, DRD4, ADRA1D, ELANE, HLA-A, NGF, SLC6A3, TH
Paget's Disease Of Bone Wikipedia

Calcified Tissue International . 91 (2): 97–113. doi : 10.1007/s00223-012-9599-0 . PMID 22543925 . ^ Charles, Julia F.; Siris, Ethel S.; Roodman, G.

TNFRSF11A, SQSTM1, OPTN, DCSTAMP, NUP205, PML, CSF1, ZNF687, RIN3, INPP5D, IL6, KHDRBS1, PIGN, NUP62, DCTN4, DPYS, GTF2H1, SLC25A43, VCP, TNFRSF11B, CFDP1, GEMIN4, PSMD2, EIF4G2, PDB1, VDR, DKK1, TNF, ERBB2, ESR1, KRT7, SOST, NFE2L2, IL1A, IL1B, HNRNPA2B1, HNRNPA1, TNFSF11, ATG5, AR, GABPA, CALCA, KEAP1, CEACAM5, PABPN1, SOCS1, LPAR2, GNE, WASHC5, TUBA1B, NEURL1, VAV3, CASP8AP2, ACP5, ATG7, SLCO6A1, AAA1, KRT8P3, STMP1, FSIP2, GSTK1, GOLGA6A, UCMA, C9orf72, ARID2, NFAM1, KMT2C, POSTN, BIRC6, SMURF1, ACKR3, ATG16L1, GDE1, QPCT, TARDBP, TUBA1A, ATF7, CXCR6, AAAS, SPP1, XRCC1, CTNNB1, MTOR, FOS, FKBP5, FKBP4, FGF2, EPHB2, EGF, EDNRA, DNAH8, DMD, CTSB, CSF2, BEST1, CEBPB, CASR, BTF3P11, BRS3, BRCA2, BGLAP, BCL2, APP, APEX1, ADRA2B, ADRA1A, GCG, GJA1, GPR42, GRP, NR1H2, TRIP6, TP53, TIA1, TAF12, TAF2, SSTR4, ACTA1, SOD1, PTH, MAPK1, PDPK1, NFKB2, NEU1, MUC1, KRT8, CXCL8, IL6ST, IL3, IL1R1, IGFALS, IAPP, FOXA1, ELDR
- Paget's Disease Of Bone Mayo Clinic
  
  Overview Paget's (PAJ-its) disease of bone interferes with your body's normal recycling process, in which new bone tissue gradually replaces old bone tissue. Over time, bones can become fragile and misshapen. The pelvis, skull, spine and legs are most commonly affected. The risk of Paget's disease of bone increases with age and if family members have the disorder. However, for reasons unknown to doctors, the disease has become less common over the past several years and is less severe when it does develop. Complications can include broken bones, hearing loss and pinched nerves in your spine.
Thyroid Dyshormonogenesis 3 OMIM

Inheritance Vono-Toniolo et al. (2005) stated that in most instances of TG-related goitrous hypothyroidism affected individuals have related parents and are homozygous for inactivating mutations in the TG gene. ... Mapping In 5 affected and 5 unaffected members of a family with goiter due to a qualitative and quantitative defect in TG, Baas et al. (1984) analyzed the presence of an RFLP in the TG gene (188450) and found mendelian segregation of the polymorphism and goiter, suggesting that the rare variant was linked to a normal TG allele providing strong evidence for autosomal dominant inheritance of the TG synthesis defect in this family. Molecular Genetics Ieiri et al. (1991) gave the first report of individuals with documented TG gene mutations. The index patient and 2 of her 5 sibs presented with hypothyroidism, congenital goiter, and a marked impairment of TG synthesis. ... Although serum T4 was low and serum TG undetectable, serum T3 was increased. ... Baas et al. (1984) suggested that since the tertiary and quaternary structure of TG is very important for hormone formation, a change in 1 of the 2 subunits (heterozygosity) may lead to severely impaired hormonogenesis of the heterodimeric TG and thus autosomal dominant inheritance of this disorder characterized by relatively high levels of abnormal TG.

TG
Autoimmune Thyroid Disease, Susceptibility To, 3 OMIM

Tomer et al. (2002) identified a microsatellite inside TG intron 27, designated Tgms2, that showed strong evidence for linkage to AITD (MLS, 2.9), further suggesting that the TG gene is linked to AITD. Tomer et al. (2002) stated that TG was the first thyroid-specific gene to be found linked and associated with AITD. ... Molecular Genetics Association with Variation in the TG Gene Ban et al. (2003) sequenced all 48 exons of the TG gene and identified 14 single-nucleotide polymorphisms (SNPs). ... The finding of a unique SNP haplotype at exons 10 and 12 of the mouse Tg gene led Ban et al. (2003) to conclude that TG is a susceptibility gene for AITD in both humans and mice. ... Shirasawa et al. (2004) noted that association of the TG gene with AITD was found in Caucasians.

TG
Congenital Toxoplasmosis Orphanet

Etiology CTX is caused by the mother's primo-infection by Tg, an intracellular protozoan parasite of the Apicomplexa phylum, and transmission to the fetus by trans-placental infection. Nearly 25% of exposed fetuses are infected. Mother is infected by Tg through ingestion of ooccysts present in cat faeces and soil, or of cysts present in uncooked meat. ... Given the poor specificity of clinical signs observed in Tg infection, serological findings and PCR amplification of Tg specific sequences are the main diagnostic clues. ... Differential diagnosis Differential diagnosis includes other congenital infections (rubella, CMV, HSV1 and HSV2, regrouped with Tg infection in the TORCH syndrome) and pseudo-TORCH and Aicardi-Goutières syndromes. ... Diagnosis is confirmed only with serological or PCR findings of Tg infection in the mother and the amniotic fluid.

COL2A1, TLR9, ABCA4, ALOX12, CD9, DHFR, HLA-DQA1, TLR4, NLRP1, IRAK4, ERAP1, TBATA
Hyperlipidemia Due To Hepatic Triacylglycerol Lipase Deficiency Orphanet

Hyperlipidemia due to hepatic triacylglycerol lipase deficiency is a rare, genetic hyperalphalipoproteinemia disorder characterized by elevated plasma cholesterol and triglyceride (TG) levels with a marked TG enrichment of low- and high-density lipoproteins (HDL), presence of circulating beta-very low density lipoproteins and elevated HDL cholesterol levels, in the presence of a very low, or undetectable, postheparin plasma hepatic lipase activity.

LIPC, HMGCL, APOB, CETP, LDLR
- Hepatic Lipase Deficiency GARD
  
  Hepatic lipase deficiency is a rare condition that is characterized by increased levels of certain fats (known as triglycerides and cholesterol ) in the blood. Affected people may also have increased levels of high-density lipoproteins (HDLs) and decreased levels of low-density lipoproteins (LDLs), which are two molecules that help transport fats throughout the body. Hepatic lipase deficiency may be associated with an increased risk of developing atherosclerosis and/or heart disease ; however, additional research is needed on the long-term outlook of people with this condition. Hepatic lipase deficiency is caused by changes (mutations) in the LIPC gene and is inherited in an autosomal recessive manner. Treatment is based on the signs and symptoms present in each person.
- Hepatic Lipase Deficiency MedlinePlus
  
  Hepatic lipase deficiency is a disorder that affects the body's ability to break down fats (lipids). People with this disorder have increased amounts of certain fats, known as triglycerides and cholesterol, in the blood. These individuals also have increased amounts of molecules known as high-density lipoproteins (HDLs) and decreased amounts of molecules called low-density lipoproteins (LDL). These molecules transport triglycerides and cholesterol throughout the body. In people with hepatic lipase deficiency, the LDL molecules are often abnormally large.
- Hepatic Lipase Deficiency OMIM
  
  Description Hepatic lipase deficiency is characterized by premature atherosclerosis, elevated total cholesterol, triglycerides (TG), and very low density lipoprotein (VLDL), as well as TG-rich low density lipoprotein (LDL) and HDL subfractions (summary by Hegele et al., 1991).
Thiopurines, Poor Metabolism Of, 2 OMIM

Thiopurines are converted into cytotoxic thioguanine nucleotides (TG), which are incorporated into DNA and cause cell death. ... In vitro functional expression studies confirmed that wildtype NUDT15 inactivates thiopurine metabolites and decreases thiopurine cytotoxicity. Direct monitoring of DNA-TG levels in patient white blood cells showed that the ratio of DNA-TG levels to mercaptopurine dosage varied by NUDT15 genotype, such that those with low-activity diplotypes had higher DNA-TG content.

NUDT15
Hypobetalipoproteinemia, Familial, 2 OMIM

Romeo et al. (2009) sequenced the ANGPTL3, ANGPTL5 (607666), and ANGPTL6 (609336) genes in a large multiethnic population and identified multiple rare nonsynonymous sequence variations that were associated with low plasma triglyceride (TG) levels but not other metabolic phenotypes. Functional studies showed that all mutant alleles of ANGPTL3 that were associated with low plasma TG levels (see, e.g., 604774.0003 and 604774.0005) interfered either with synthesis or secretion of the protein, or with the ability of the ANGPTL protein to inhibit lipoprotein lipase (LPL; 609708). ... In the other 2 families, Pisciotta et al. (2012) identified compound heterozygosity for a 1-bp and a 4-bp deletion (604774.0004 and 604774.0005); the 4-bp deletion had previously been found to be associated with low plasma TG levels by Romeo et al. (2009) and designated as being an in/del at chr1:62,836,264. Homozygotes or compound heterozygotes showed absence of ANGPTL3 in plasma and reduced plasma levels of TG-containing lipoproteins and of HDL particles that contained only apolipoprotein A-I and pre-beta high density lipoprotein. ... Compared to ANGPTL3 mutation-negative individuals from the cohort, homozygotes and compound heterozygotes had significantly lower levels of total, LDL, and HDL cholesterol and TG, whereas ANGPTL3 heterozygotes had lower TG levels but similar levels of total, LDL, and HDL cholesterol, suggesting that gene dosage affects only the TG plasma levels.

ANGPTL3, APOB, DOCK7
Thyroid Cancer, Nonmedullary, 1 OMIM

The best positive predictive value is obtained by the slope of serum TG levels. Serum TG assays are sometimes unsatisfactory for monitoring thyroid cancer because interference caused by anti-TG antibodies may reduce the sensitivity of the tests during thyroid hormone therapy. Savagner et al. (2002) developed a complementary method using real-time quantitative RT-PCR based on the amplification of TG mRNA. Two different pairs of primers were used for the determination of the frequency of 1 of the variants of the alternative splicing of TG mRNA. ... The TG mRNA values allowed the definition of a positive cutoff point at 1 pg/microg total RNA. This cutoff point, tested on the group of patients treated for thyroid cancer, produced fewer false negative results than those obtained with serum TG assays. Wagner et al. (2005) tested the preoperative sensitivity of RT-PCR for TG and TSHR mRNA to detect thyroid cancer. TSHR and TG mRNA transcripts were detected by RT-PCR assays previously determined to be specific for cancer cells.

BRAF, NKX2-1, CCDC6, RET, FOXE1, NCOA4, PPARG, KRAS, PAX8, NTRK1, NRAS, DIRC3, NTRK3, ETV6, ALK, GAS8-AS1, PTCSC3, HRAS, MIR485, EIF1AX, SNAI1, ERC1, TPR, TFG, DIO3, MIR431, MIR381, MIR409, MIR369, MIR376C, MIR758, PCM1, TRIM27, MIR299, MIR539, MIR136, TRIM33, LPAR4, MIR654, TRIM24, MIR379, MIR382, WARS1, WDR20, MIR380, BEGAIN, NDUFA13, MIR377, MIR376A1, MIR127, MIR370, MIR134, MIR337, MIR323A, MIR433, MIR154, DIO3OS, MIR329-1, MIR496, MIR323B, MIR376A2, MIR487B, MIR411, MIR655, MIR656, MIR770, MIR300, MIR543, DYNC1H1, MIR889, MIR1247, MIR1197, MIR1193, ZEB1, GOLGA5, MIR487A, MIR493, MIR410, PPP2R5C, MIR412, MIR432, MIR494, SNAI2, MIR376B, ZEB2, MIR495, APC, HABP2, PTEN, NRG1, DICER1, TAS2R38, PTCH1, MINPP1, MAPK1, PIK3CG, TPCN1, PIK3CD, PIK3CB, CTNNB1, PIK3CA, PCNX2, ESR1, EGFR, F9, VAV3, TP53, BRCA2, MIR146B, BCL2, CCND1, TGFB1, HT, AKT1, JAG1, TG, LINC02454, TERT, LOC110806263, LGALS3, MIR222, SEC23B, MMP9, CXCR4, LIG4, TPM3, TPO, TSHR, SLC5A5, MIR221, VEGFA, EPHB2, MIR146A, COX2, FN1, CD274, MET, KRT19, MIR21, PTGS2, TIMP1, GABPA, SPP1, NCAM1, MTCO2P12, ATM, MUC1, MAP2K7, IGF1, KIT, TNF, ESR2, CD44, HIF1A, RASSF1, SLC2A1, CXCL12, HGF, VEGFC, NFE2L2, MAPK3, TTF1, MIR204, PRPF31, VDR, DUSP6, CDKN1B, MIR451A, XIAP, TFF3, PDGFRA, CYP24A1, THBS1, KDR, RUNX2, PTH, LEP, CHEK2, STAT3, ERBB2, MMP2, MIR144, PCNA, RAF1, VIM, CDKN2A, PTCH2, MDK, IRAK1, MTOR, MT1G, ROCK1, SOX2, IGF1R, CITED1, S100A4, GDF1, MYC, NOTCH1, LEPR, MDM2, TACSTD2, H3P10, ICAM1, FOXP3, MIR30A, CRK, ACKR3, TGFA, NOB1, NEAT1, MIR141, SMUG1, MIR155, MIR15A, HTC2, AKT3, DPP4, SPHK1, CENPJ, UCA1, HMGA2, TIMP3, EDN1, MIR486-1, XRCC1, AR, SNHG12, MIR613, IL6, SLC5A8, PTCSC2, MT1A, MMP11, WNK1, ORI6, SPHK2, MALAT1, MIR34B, IL10, MIR150, MIR96, MLH1, MIR199A1, MIR199A2, MCL1, MIR200A, SYTL2, MIR497, MIR29A, MIR206, SP1, KRT20, AIMP2, AHSA1, GRAP2, RAP1A, TP63, TTF2, RNH1, RPE65, KLK7, S100A11, WNT5A, VHL, UVRAG, SLC2A3, TWIST1, PPP1R13L, PROX1, TERF2IP, SGSM3, SHC3, GDE1, SIRT6, IL22, STOML2, PDGFRB, RABGEF1, CKAP4, PDCD4, POLDIP2, RNF19A, DKK1, ZHX2, MAP2K1, YAP1, ABL1, MS4A1, COL1A1, VEGFD, CCR7, HLA-G, MAPK14, DIO2, CDH1, HLA-DRB1, DIO1, EZH2, HOXD13, EDNRA, FOXO1, FAS, EGF, HMGB1, GSTM1, GPI, HSP90AA1, MIR122, MIR139, DCTN6, EBP, SOX11, GLI1, NNMT, TNFSF10, MIR202, MIR137, MIRLET7E, CDKN1A, NRP1, HOPX, TENM1, ITCH, PLAU, AKAP9, PLG, EIF4E, SLPI, DNMT1, SERPINA1, PGR, DDR2, NRCAM, P2RX7, MIR126, PAK1, ZNRD2, FGF2, PDPN, NT5E, CIB1, PCBP4, POSTN, FGFR1, CRNDE, FASLG, POLR2E, ZNRF3, KIDINS220, NOTCH3, MIR10A, PDPK1, ARNTL, MIR509-1, MIR149, MIR145, DUSP5, RAC1, CAV1, MIR7-2, RARA, MIR34A, RARG, NAPSA, MIR195, OPN1LW, RELA, CCK, ABCG2, SLIT2, MIR363, FOS, FLT3, CCL21, FLT1, RPL36A, CLDN10, MIR199B, CLDN1, S100A6, FOXO3, TMSB10, LPAR2, MIAT, MIR183, CXCL14, PTN, CDK4, PAG1, PRKAA1, PRKAA2, PRKAB1, DNMT3A, CA12, GAS5, FOXM1, MIR375, GAS1, CDH6, KEAP1, CASP3, EIF4A3, RAPGEF5, GORASP1, MIR335, PSMD9, E2F1, SFTPB, GABRB2, NECTIN4, SELL, FRTS1, NCL, C3, SYT1, TOP2A, TRAF6, JAK1, JUN, CXXC5, IL27, CASC2, HOXA@, LAMB3, LAMC2, IL17D, CREBBP, ITGA3, LINC00313, HAGLR, LGALS1, CPSF2, LMNA, MIR2861, TLR4, ERRFI1, LRP4, CRABP1, ITGA5, ITGA2, SIRT1, IL1B, H3P23, YY1, CLIP2, KLB, IFI27, DEUP1, IGFBP5, CTSC, IHH, IL1A, ZCCHC12, FALEC, HSPA5, CXCL8, CXCR2, ABHD11-AS1, LIPH, IL13RA2, IL17A, TMED7, CXCL10, INSR, EPCAM, LPAR3, ANGPT1, MTDH, PTK2B, TMED10, MT1X, MIR933, AHR, AKT2, CISH, TMED7-TICAM2, TMED10P1, GSTT1, TICAM2, TEK, ALDH1A1, MST1, DCN, MSH2, FOXD2-AS1, UNC5B-AS1, HOTAIR, HLA-C, HOXA-AS2, MCM5, CYP27B1, ETV5, MDM4, HLA-DQB1, CYTOR, THRB, RASAL1, KDM1A, KLLN, PDCD1LG2, NT5C1A, STON2, DCSTAMP, SLCO6A1, PROK1, GPR151, ADAT2, E2F7, PROSER3, CLPTM1L, AFAP1L2, LIMD2, SPZ1, RTN4IP1, LMLN, CHEK1, TMEM139, FSD1L, ECRG4, XKR4, AHNAK2, FOXQ1, FAM83F, HTRA3, ABHD11, TMPRSS13, PKHD1L1, MCM3AP-AS1, SH3BGRL3, HSDL2, MAL2, ARL11, RBM45, MRGPRX3, TLR10, MRGPRX4, PRAP1, LINC01278, CYP2R1, ACBD5, CPT1C, TRIM8, HOOK3, KLF17, CHI3L1, HSPD1, WNT10A, IL17RB, LARP7, CRKL, RAB23, CREM, FXYD5, DUOX1, TLR9, CREB1, DLL4, CROT, SLC35F2, XAF1, TRIM44, GATAD2A, CPOX, PGPEP1, ELOVL2, PINX1, TUG1, PIWIL2, THAP1, RMDN3, ZNF654, LAPTM4B, IMPACT, CRY2, MBIP, IL23A, DUOX2, SETD2, DROSHA, PYCARD, CTLA4, UHRF1, TFCP2L1, CERS2, PSAT1, EHD2, CSNK1G2, CD207, NOX4, SIRT7, CSF2, TAS2R3, F11R, CSF1R, CSF1, RMDN1, HSPA14, TCEAL9, MZB1, TNFRSF12A, REV1, LGR4, SYBU, NAA15, IWS1, CXCL16, IL22RA1, ACE2, LGR6, SCOC, PROK2, MYO1G, ERAP2, SOX17, HHIP, MRPL41, CDK15, MRPL44, CCR3, TRAK2, OTUB2, MAPKAP1, FSD1, MUL1, TNFAIP8L2, LIN28A, E2F8, CKS2, TRPM3, ZNF703, C6orf47, ANKRD36B, NCOA5, TCIM, RUFY2, WDR11, ATF7IP, CHFR, AGK, COX8A, PBK, MYDGF, PDGFC, TMPRSS4, KLF6, EMSY, TNRC6C, SMYD2, CTNNBIP1, TWSG1, CEMIP, DANCR, SRGAP1, MIB1, SEMA6A, MRTFA, CNGB1, RELCH, TEKT4, MIR130A, RMDN2, GGTLC4P, MIR622, MIR625, MIR630, AMPD1, AMFR, MIR663A, LINC00460, GGTLC3, GGT2, CCR2, ALOX5, ALDH1A3, MIR608, MIR766, MIR675, ALCAM, VTRNA2-1, MIR744, MIR922, MIR940, MIR885, TNRC6C-AS1, LINC00271, CD24, ANGPT2, MIR599, MIR1915, ARAF, BMI1, BGN, BGLAP, BAX, B2M, ATP5F1E, ATF1, ARR3, MIR520A, MIR524, MIR506, RASSF10, MIR584, NORAD, CXADRP1, GGTLC5P, PAX8-AS1, APRT, APOA4, ANXA5, ANXA1, MIR564, MIR574, MIR577, MIR1183, NR0B1, CCDC80, LOC102723407, MIR4516, MIR4429, MIR5189, BANCR, ADRA2B, COMETT, NAMA, BLACAT1, SAMMSON, LINC01186, ADRA1A, LOC102724971, MIR4728, CCND2-AS1, BISPR, PARP1, CERNA3, LOC105379528, RNU1-55P, ADCYAP1R1, ADCYAP1, ADCY1, LNCRNA-ATB, H3P17, MIR4500, COMMD3-BMI1, MIR1270, MIR320E, MIR1266, MIR1271, MIR1261, MIR1179, MIR1304, AFM, MIR718, MIR761, HOTTIP, AP2A1, MIR4316, MIR3144, SNHG16, MIR3151, LINC00673, MIR3619, MIR3663, PROX1-AS1, APTR, LINC01672, LUCAT1, HOTAIRM1, TTN-AS1, DLG1-AS1, BMP4, BMPR1A, BRCA1, LINC01061, SCAI, UBAC2, RSPO2, ZNF677, GSTK1, AGRN, CDX2, KMT5A, CCL4L1, IYD, LOC390714, MIRLET7B, SNHG15, MIR106A, MIR106B, MIR125A, CDKN3, HIPK2, MIR130B, CDKN1C, CDK8, MIR143, CDK7, MIR148A, SLC26A4-AS1, RPL34-AS1, BRS3, USF3, PAQR3, C8orf37, CBLL2, OXER1, DACT2, GLIS3, NLRP6, EMX2OS, TIGIT, PRSS55, ANO5, SKA1, RSPO1, HOXA11-AS, JAZF1, GPRC6A, ZNRF2, TTTY10, FNDC5, MRGPRX1, MAGEA2B, CEBPB, B4GALNT3, LINC00514, CDK2, CDH2, MIR18A, MIR361, ZFAS1, GPR166P, MIR148B, CASR, MIR324, CASP9, MIR339, MIR346, CASP8, CASP6, MIR196B, CASP2, MIR181A2, CAMP, CALCA, CAD, CA9, MIR384, MIR422A, RGMB-AS1, MIR20B, TMEM50B, MPPED2, BUB1B, VN1R17P, NRARP, NR2F1-AS1, PRDM16-DT, MIR182, MIR190A, CD74, CD68, MIR20A, CD63, MIR203A, CD38, CD34, MIR211, MIR212, MIR214, MIR215, MIR219A1, MIR22, CD247, CD1A, MIR23A, CCNG1, MIR296, CBL, MIR31, RUNX3, ATAD2, AKAP13, CTNNA1, PTGDS, MAPK8, LRRC32, PRL, PRLR, GAPDH, GAP43, HTRA1, KLK10, PSG1, PSMD8, GAGE5, GAGE4, PTGIS, FLVCR1, GAGE1, G6PD, PTPRJ, NECTIN1, PVT1, RAD52, FUT4, FUCA1, RAP1GAP, RARB, RARRES2, RBP2, GCGR, GGT1, PRKCE, PRKAR1A, SLC26A4, PECAM1, PGM1, PHB, SERPINB5, SERPINE2, GCLC, GPC3, GLA, PIN1, PITX2, PKM, PLA2G1B, PLA2G2A, PLD2, PLK1, PMP22, PMS2, POMC, POU5F1B, PPARA, GJB2, GH1, PRKACA, PRKACG, FPR2, FOSB, RGS4, FKBP5, SLC6A9, SLC16A2, FKBP4, SOD2, SOD3, FGFR4, SOX9, SOX12, SPARC, SPG7, SPINT1, SRC, SRF, SRY, SST, SSTR4, STAT1, FGF1, STK11, STRN, SYPL1, MAP3K7, TBX1, TCF4, TBX3, SLC6A2, FOXF1, RNASE2, SLC1A5, BRD2, ROS1, RRAS, RXRG, S100A1, FLI1, S100A13, S100B, SERPINB3, SCD, SCN4B, CCL2, CCL3, CCL4, CCL5, CCL20, CXCL11, CXCL5, SDC4, SDHB, SELE, SFRP1, SHH, SHMT1, SKP2, ENPP2, GLI2, GLP1R, JUNB, CD82, KCNJ2, HOXD10, KIF5B, HOXA9, HOXA3, LAIR1, LASP1, LBR, LCN2, LDHA, HNF4A, FOXA2, HMGB2, LMO7, LOX, LOXL1, BCAM, HMBS, SMAD3, SMAD4, MAGEA2, MARK1, MC1R, MCM3, JUND, ITGB4, MAP3K5, ITGB2, TNC, HSP90AB1, ID1, ID3, IDH1, IFNG, HSPA9, IGFBP1, IGFBP7, IL1R1, IL2, IL2RA, IL4, HPRT1, IL11, IL11RA, IL13, IL18, IDO1, INS, INPPL1, IRS1, ISG20, ITGAV, ITGB1, MCM7, MEN1, PDCD1, GSN, GPX3, GRK6, NFKB1, NGF, NGFR, NNAT, NME1, NOS2, NOS3, GPR42, UTS2R, CXCR3, ROR2, NUCB2, PEBP1, PRDX1, SERPINE1, PRKN, PAX6, PC, SERPINA5, GNAS, GLS, CDK16, PCYT1A, MYH9, MMUT, MFAP1, MUC4, MGMT, CXCL9, MKI67, HLA-B, MME, MMP1, HLA-A, HK2, HIC1, MMP13, MOG, MPZ, MRC1, ABCC1, HBB, MSH3, MSMB, GUSB, MT1E, MT1F, MT1M, MT2A, MTF1, MTHFR, GSR, TCF7L2, FCGR3B, TERC, TAB1, CFD, ATG7, ARFGEF1, NPC2, TXNRD2, DECR1, PDLIM5, CXCR6, CLDN16, CERS1, POLQ, PTGES3, CHL1, FRS2, AKR1C2, HPSE, HCP5, EHD1, RAB40B, DCT, COPS6, OGFR, WDR5, ACE, HUS1, GPNMB, NQO1, ANKRD26, RAPGEF3, WSCD2, NUP93, RAB11FIP3, SART3, HDAC9, HDAC4, TRIM14, DPT, PJA2, TLK1, WDR1, FGF19, NR1I3, RBX1, SCO2, NAALADL1, PLXNC1, PSME3, TRIM13, SPRY2, STUB1, PAK4, TLR6, NDRG1, RACK1, TUSC2, CILK1, DUSP2, CYP1A1, LRIG1, DNM3, CYLD, CXADR, DGCR5, PHGDH, FGF21, EHF, BEX3, LAT, TSPAN13, DKK3, SNX5, SERP1, CUX1, HPGDS, RBMX, CTSL, CTSB, EML4, IGHV3OR16-7, IGHV3-69-1, TRBV2, TRBJ1-2, TRBJ1-1, WWTR1, BRMS1, DCK, QPCT, MMRN1, ATF6, RPIA, DAPK1, USP33, SMG1, RRS1, KAZN, CUX2, USP22, CYP19A1, ANGPTL2, HEY1, BRD4, PES1, SRRM2, PSD4, CYP2D6, AMACR, LDOC1, SNHG1, TRIM29, SLC7A11, IL17RA, RASGRP3, PRDX6, CCL4L2, FCGR3A, EPHB4, SUMO1, UGCG, USF1, EPHB1, VAV2, EPAS1, ENG, EMX2, ELK3, ELF3, TRPV1, ELAVL2, WIPF1, WNT1, EIF4EBP1, WNT7A, XRCC3, ZIC1, CNBP, TRIM26, EPHA2, EGR2, NTT, EDNRB, LPAR1, EPHB3, EPS15, ACP3, TSG101, TFAP2A, TFE3, FCER2, FBN1, FASN, TGFBR1, TGFBR2, EZH1, EWSR1, TK1, TLR1, TLR2, TLR3, TM7SF2, ETV4, ETS1, TP53BP1, TPI1, ERCC5, ERBB4, ERBB3, TPT1, CRISP2, HSP90B1, CCT3, SLC7A5, CND, TP53I3, TNFRSF10B, TNFRSF10A, E2F4, IQGAP1, SOCS2, PROM1, KSR1, CDK5R1, PER2, CCNA1, BTRC, MAP3K14, SOCS3, USP6, OSMR, BUB3, AURKB, PTTG1, CRLF1, DHRS3, STK17B, KLF4, COX5A, ATG5, ADAMTS1, PTGES, SCEL, CDC23, NAA10, BECN1, TKTL1, BAP1, CDC45, FZD1, FZD4, PLA2G6, TAGLN2, RECK, CAVIN2, CUL3, TYMP, MAP4K3, PARG, APOL1, LMO4, LGR5, CDC14B, KHSRP, PSMG1, ECE1, EIF4EBP3, E2F6, SOCS1, PDE5A, IRS2, CDR3
- Papillary Thyroid Cancer Wikipedia
  
  Additional lateral neck nodes can be removed at the same time if an ultrasound guided FNA and thyroglobulin TG cancer washing was positive on the pre-operative neck node ultrasound evaluation. ... Thyroid total body scans are less reliable at finding recurrence than TG and ultrasound. Papillary tumors tend to be more aggressive in patients over age 45.
- Thyroid Carcinoma, Hurthle Cell OMIM
  
  A number sign (#) is used with this entry because Hurthle cell tumors are associated with chromosomal abnormalities or mutations in the RAS gene (190020), the PAX8/PPARG fusion gene (see 167415), or the NDUFA13 gene (609435). Description Hurthle cell carcinoma of the thyroid accounts for approximately 3% of all thyroid cancers. Although they are classified as variants of follicular neoplasms, they are more often multifocal and somewhat more aggressive and are less likely to take up iodine than are other follicular neoplasms (Sanders and Silverman, 1998). Hurthle cell tumors, also known as oxyphil cell tumors, are composed of cells with increased numbers of mitochondria, which corresponds morphologically to their voluminous, granular, eosinophilic cytoplasm (Maximo et al., 2005). Cytogenetics Chromosomal aberrations by comparative genomic hybridization (CGH) are common in Hurthle cell neoplasms.
- Differentiated Thyroid Carcinoma Orphanet
  
  A rare, slow-growing, epithelial thyroid carcinoma typically presenting as an asymptomatic thyroid mass and is classed as either papillary thyroid cancer (PTC), follicular thyroid cancer (FTC) or Hurthle cell thyroid cancer (HCTC). Epidemiology The annual incidence of differentiated thyroid cancer (DTC) is about 1/10,000, and the incidence appears to be increasing. The female to male ratio is about 3:1. Clinical description PTC, FTC, and HCTC have similar presentations, and constitute about 75, 20, and 5 percent of cases, respectively. About 10 percent of PTC are classified as tall cell variant, the most aggressive from of PTC. HCTC is generally considered slightly more aggressive than PTC and FTC.
Hypertriglyceridemia, Familial OMIM

Mapping Duggirala et al. (2000) conducted a genomewide scan for susceptibility genes influencing plasma triglyceride (TG) levels in a Mexican American population. They used both phenotypic and genotypic data from 418 individuals distributed across 27 low-income, extended Mexican American families. For the analyses, TG values were log transformed (ln TG). After accounting for the effects of sex and sex-specific age terms, they found significant evidence for linkage (lod = 3.88) of ln TG levels to a genetic location between the markers GABRB3 (137192) located at 15q11.2 and D15S165 located at 15q12-q13.1. This putative locus explains 39.7 +/- 7% (p = 0.000012) of total phenotypic variation in ln TG levels. Some evidence for linkage to 2 different locations on chromosome 7 was found.
Adiponectin, Serum Level Of, Quantitative Trait Locus 1 OMIM

The authors then genotyped rs17846866 in 2,000 Asian Indian patients with type 2 diabetes and 2,000 normal glucose-tolerant controls and found that individuals with the TG genotype had a significantly higher risk for diabetes compared to TT (odds ratio, 1.28; p = 0.008); however, no association with diabetes was observed with the GG genotype. Stratification of all study individuals by BMI showed that the odds ratio for obesity with the TG genotype was 1.53 (p less than 10(-7)) and for the GG genotype, 2.10 (p = 0.002). Among the normal glucose-tolerant controls, mean serum adiponectin levels were significantly lower among the GG and TG genotypes compared to TT (p = 0.007 and p = 0.001, respectively).

ADIPOQ, IL17A, LDLR, LEP, ADIPOR1
Diarrhea 7, Protein-Losing Enteropathy Type OMIM

The child had hyperlipidemia, with a fasting serum TG level of 325 at 1 month of age; her mother and father also had elevated fasting TG levels.

PLVAP, DGAT1
- Diarrhea 10, Protein-Losing Enteropathy Type OMIM
  
  A number sign (#) is used with this entry because of evidence that diarrhea-10 (DIAR10) is caused by homozygous mutation in the PLVAP gene (607647) on chromosome 19p13. Description Diarrhea-10 is a protein-losing enteropathy characterized by intractable secretory diarrhea and massive protein loss due to leaky fenestrated capillaries. Features include early-onset anasarca, severe hypoalbuminemia, hypogammaglobulinemia, and hypertriglyceridemia, as well as electrolyte abnormalities. Some patients exhibit facial dysmorphism and cardiac and renal anomalies. Intrafamilial variability has been observed, and the disease can be severe, with death occurring in infancy in some patients (Broekaert et al., 2018; Kurolap et al., 2018).
Glenolabral Articular Disruption Wikipedia

It is difficult to diagnose clinically, and requires surgical repair to correct the damage to the shoulder. [1] References [ edit ] ^ Sanders TG, Tirman PF, Linares R, Feller JF, Richardson R (January 1999).
Thyroid Dyshormonogenesis Wikipedia

Contents 1 Cause 2 Diagnosis 2.1 Types 3 Treatment 4 References 5 External links Cause [ edit ] This is due to inability to produce thyroid hormones due to congenital absence of peroxidase or dehalogenase enzymes [ citation needed ] Diagnosis [ edit ] Types [ edit ] One particular familial form is associated with sensorineural deafness ( Pendred's syndrome ). [ citation needed ] OMIM includes the following: Type OMIM Gene Type 1 274400 SLC5A5 Type 2A 274500 TPO Type 2B 274600 (Pendred) SLC26A4 Type 3 274700 TG Type 4 274800 IYD Type 5 274900 DUOXA2 Type 6 607200 DUOX2 Treatment [ edit ] These patients respond well to levothyroxine (synthetic T4) and the goiter may decrease in size if any.

SLC5A5, TPO, TG, DUOX2, IYD, DUOXA2
- Familial Thyroid Dyshormonogenesis Orphanet
  
  Familial thyroid dyshormonogenesis is a type of primary congenital hypothyroidism (see this term), a permanent thyroid hormone deficiency that is present from birth, which results from inborn errors of thyroid hormone synthesis. Epidemiology Thyroid dyshormonogenesis accounts for 10-15% of permanent congenital hypothyroidism (see this term). Clinical description Clinical manifestations are those of other forms of congenital hypothyroidism (see this term). In addition to features of hypothyroidism, patients with dyshormonogenesis can present with goiter. Etiology Dyshormonogenesis is caused by hereditary defects in the steps of thyroid hormone synthesis and secretion, the majority of which are transmitted in an autosomal recessive manner but at least one condition has autosomal dominant inheritance.
- Thyroid Dyshormonogenesis 1 OMIM
  
  Genetic Heterogeneity of Thyroid Dyshormonogenesis Other forms of thyroid hormone dysgenesis include TDH2A (274500), caused by mutation in the thyroid peroxidase gene (TPO; 606765) on 2p25; Pendred syndrome, a form of thyroid hormone dysgenesis associated with deafness (TDH2B; 274600) and caused by mutation in the SLC26A4 gene (605646) on 7q31; TDH3 (274700), caused by mutation in the thyroglobulin gene (TG; 188450) on 8q24; TDH4 (274800), caused by mutation in the iodotyrosine deiodinase gene (IYD; 612025) on 6q25; TDH5 (274900), caused by mutation in the DUOXA2 gene (612772) on 15q21; and TDH6 (607200), caused by mutation in the DUOX2 gene (606759) on 15q21.
Hashimoto Thyroiditis MedlinePlus

Learn more about the genes associated with Hashimoto thyroiditis FOXP3 HLA-DRB1 PTPN22 SLC26A4 TG Additional Information from NCBI Gene: CTLA4 Inheritance Pattern The inheritance pattern of Hashimoto thyroiditis is unclear because many genetic and environmental factors appear to be involved.

TG, CTLA4, C1S, IL2RA, PTPN22, FOXD3, VAV3, PTEN, TRIM60, DCLRE1C, BACH2, HT, TTC7A, CA10, HLA-DRB1, TPO, POLG, PLCG2, CLCNKB, TBX2, IFNG, TSHR, RET, TIMM23, BRAF, SLC12A3, IL6, SEC23B, IL17A, SLC25A27, LPP, MIR3681HG, TNF, CXCL10, VDR, FOXP3, SLC6A4, IL10, IL1B, FAS, ISG20, TGFB1, RBM45, CD274, ATN1, HLA-DQA1, ICAM1, PTCH1, TP53, IL37, FASLG, LINC01193, KRT19, HLA-C, IL4, IL23R, CCDC6, SELENOS, SLC5A5, IL23A, CD40, F9, BCL2, IL18, MIR125A, TAS2R38, HLA-DQB1, STAT3, LGALS3, TSHB, IFNA13, MIR155, CAV1, IFNA1, MIR146A, CALCA, CASP8, HLA-G, IL5, TLR2, NCAM1, SIRT1, MBL2, SPP1, AQP3, IL1RL1, SLC26A4, PIK3CA, CD24, ICOS, INS, HLA-DRB4, IL12B, MIR451A, CLDN1, IL15, TRBV20OR9-2, S100A9, IFIH1, DPP4, CD68, EDN1, IL33, PTPRC, EPHB2, PTGS2, ESR1, ESR2, HLA-DPB1, CYP27B1, FCGRT, FLNB, FCRL3, IL17F, S100A8, AITD1, H2AC14, PPARG, HLA-B, HLA-A, HIF1A, MAPK1, TNFSF4, WDR11, TERT, AIM2, PDLIM7, MAGI2, GNA14, VIP, VEGFA, CD83, UBE2B, TK1, NCOA4, THRB, CDR3, EOMES, RASGRP1, TNFSF18, TLR4, IL18R1, IL18RAP, TNFRSF25, TNFSF10, UBE2L3, ABCA1, TNFSF13B, SCGB3A2, TPH2, EARS2, DOCK11, CEP128, IL34, SLC5A8, TIGIT, IFNL3, IFNL1, MIRLET7E, MIR142, MIR210, MIR22, MIR223, MIR27A, MIR29A, XRCC6P5, MIR326, SNORA21, KIR2DS2, LINC01672, PSC, IFNG-AS1, CERNA3, MTCO2P12, IP6K3, FCRL1, BTG3, ABCC11, PTGDR2, ECD, IKZF3, IKZF2, IL17RA, AGO2, IGHV3-23, SETD2, TBX21, IL21R, IL22, F11R, GHRL, SDK2, BANK1, CHDH, ZFAT, HAMP, C6orf47, IL21, FCRL2, UNC93B1, TLR10, FBN3, FCRLA, MBIP, PSMB9, TBX1, CCR5, CLDN7, CSF1R, CTSB, CTSS, CYBB, CYP19A1, DAP, DCK, DIO2, DNASE1, EDNRA, EPAS1, ERBB2, ETS1, F3, FCGR2B, FOXO3, MTOR, GAST, GAD1, GAD2, GAS6, GATA3, GEM, GHRH, GJA1, GLUL, GPX3, GZMB, COL1A1, CDX2, ABCC8, CD81, ADA, AFP, AGER, JAG1, AMH, AIRE, APOA1, AQP4, AVP, CCND1, BCL6, BDNF, BGLAP, BLK, C3, CASP3, CD1A, CD1C, CD3G, CD14, CD19, CD27, CD28, CD80, CD86, TNFRSF8, TNFSF8, SCARB1, CD38, HLA-DOA, HMGB1, IRF8, IFNA2, PIK3CB, PIK3CD, PIK3CG, PLAT, PRKAR1A, PRKCE, ACP1, PTGDS, PTH, RAB4A, MOK, RARA, RARG, RASGRF1, RENBP, S100A1, S100B, ATXN2, CCL5, CXCL11, SELENOP, SLAMF1, SLC22A4, SMN1, SMN2, SOAT1, SOS1, STAT1, STAT4, PCYT1A, PCNA, NT5E, SH2D1A, IGF1, IGH, IL1A, IL1RN, IL6R, IL7, IRAK2, ITGAL, ITGB2, KIR2DL2, KIR3DL1, KIT, LTA, MAOB, NRAS, MIF, CXCL9, NR3C2, MMP3, MMP9, COX2, NUDT1, MTTP, MTRR, MYC, NDUFB2, NFKB1, NFKBIA, LINC02605
- Hashimoto's Thyroiditis Wikipedia
  
  Testing for thyroid-stimulating hormone (TSH), free T3, free T4 , and the antithyroglobulin antibodies (anti-Tg), antithyroid peroxidase antibodies (anti-TPO, or TPOAb) and antimicrosomal antibodies can help obtain an accurate diagnosis. [26] Earlier assessment of the person may present with elevated levels of thyroglobulin owing to transient thyrotoxicosis , as inflammation within the thyroid causes damage to the integrity of thyroid follicle storage of thyroglobulin; TSH secretion from the anterior pituitary increases in response to a decrease in negative feedback inhibition secondary to decreased serum thyroid hormones.
- Hashimoto Thyroiditis OMIM
  
  In a family with several cases of Hashimoto struma, DeGroot et al. (1962) demonstrated an abnormal, small, iodinated protein in the serum and suggested that a defect in thyroid basement membrane may account for the appearance of this protein in the blood. Three sibs, their father, and their paternal aunt were affected. The paternal grandparents were dead. Hall et al. (1962) presented data that they felt supported autosomal dominant inheritance of the tendency to thyroid autoimmunity. Hall et al. (1964) studied 6 families in which the father had thyroid autoantibody and the mother did not. In each case female children had thyroid autoantibodies. Transplacental transmission was thus ruled out and genetic transmission was suggested.
- Hashimoto's Disease Mayo Clinic
  
  Overview Hashimoto's disease is an autoimmune disorder affecting the thyroid gland. The thyroid is a butterfly-shaped gland located at the base of the neck just below the Adam's apple. The thyroid produces hormones that help regulate many functions in the body. An autoimmune disorder is an illness caused by the immune system attacking healthy tissues. In Hashimoto's disease, immune-system cells lead to the death of the thyroid's hormone-producing cells.
Transplant Glomerulopathy Wikipedia

Specialty Pathology Transplant glomerulopathy ( TG ) is a disease of the glomeruli in transplanted kidneys .

AGTR1, PTCH1, PDGFC, KRT20, FOXP3, GPR182, VIM, PTPRO, PTPRC, PECAM1, MS4A1, IL17A, IL6R, IGHG3, IFNG, GZMB, FN1, CRP, HELT
Congenital Hypothyroidism GARD

Congenital hypothyroidism is a condition that affects infants from birth and results from a partial or complete loss of thyroid function ( hypothyroidism ). The thyroid gland makes hormones that play an important role in regulating growth, brain development, and metabolism in the body. Congenital hypothyroidism occurs when the thyroid gland fails to develop or function properly. In the United States and many other countries, all newborns are tested for congenital hypothyroidism as part of newborn screening. If untreated, congenital hypothyroidism can lead to intellectual disability and abnormal growth.

TSHR, DUOX2, TPO, PAX8, FOXE1, TG, GLIS3, NKX2-1, IGSF1, TSHB, IYD, POU1F1, CDCA8, TRHR, INHBB, ATP5PD, ARPC5, IGF1, NGFR, NEFL, PPARGC1A, G6PD, GHR, GH1, NEFH, EGR1, RUNX2, BGLAP, NEFM, NKX2-5, KDM6A, ADNP, KMT2D, TXNRD2, STAR, NNT, MRAP, TBC1D24, TUBB1, TRAPPC9, ADAMTSL1, B3GLCT, THRA, DUOXA2, GNB1, SLC5A5, GATA6, MC2R, PRKAR1A, PDE4D, DUOX1, GNAS, SLC26A4, TTF2, SOX3, SLC20A1, EPHA5, PHPT1, TTF1, SLC26A7, ASAH1, DECR1, SEMA6A, ENO2, DUOXA1, CSF1R, NLRP2, CHD7, DNAJC17, CNR2, NLGN3, DNAJB1P1, ALB, EFNA5, HLA-A, ZBTB20, NRGN, SERPINA7, JAG1, THRB, PRL, TNF, TRH, PAX2, VDR, HHEX, NOS2, NBN, KSR1, NCOR1, PDCD6, LEP, DNAJB1, ACHE
- Congenital Hypothyroidism Wikipedia
  
  Congenital hypothyroidism 6 week old female with jaundice due to hypothyroidism. Specialty Endocrinology Congenital hypothyroidism ( CH ) is thyroid hormone deficiency present at birth. If untreated for several months after birth, severe congenital hypothyroidism can lead to growth failure and permanent intellectual disability . Infants born with congenital hypothyroidism may show no effects, or may display mild effects that often go unrecognized as a problem. Significant deficiency may cause excessive sleeping , reduced interest in nursing , poor muscle tone , low or hoarse cry, infrequent bowel movements, significant jaundice , and low body temperature .
- Congenital Hypothyroidism Orphanet
  
  Congenital hypothyroidism (CH) is defined as a thyroid hormone deficiency present from birth. Epidemiology It occurs in approximately 1/2,000 to 1/4,000 newborns and is more common in Asian, Native American, and Hispanic infants. Clinical description The clinical manifestations are often subtle or not present at birth, probably as a result of trans-placental passage of some maternal thyroid hormone and the fact that many infants have some thyroid production of their own. More specific symptoms often do not develop until several months of age. Common clinical features include decreased activity and increased sleep, feeding difficulty and constipation, prolonged jaundice, myxedematous facies, large fontanels (especially posterior), macroglossia, a distended abdomen with umbilical hernia, and hypotonia.
Congenital Hypothyroidism MedlinePlus

These genes include DUOX2 , SLC5A5 , TG , and TPO . Mutations in each of these genes disrupt a step in thyroid hormone synthesis, leading to abnormally low levels of these hormones. ... Learn more about the genes associated with Congenital hypothyroidism DUOX2 PAX8 SLC26A4 SLC5A5 TG TPO TSHB TSHR Additional Information from NCBI Gene: DUOXA2 IYD NKX2-5 THRA TRHR Inheritance Pattern Most cases of congenital hypothyroidism are sporadic, which means they occur in people with no history of the disorder in their family.

TSHR, IFIH1, CEP128, PTH, GNAS, SLC5A5, TG, DUOX2, CHNG3
- Hypothyroidism Due To Tsh Receptor Mutations Orphanet
  
  A type of primary congenital hypothyroidism, a permanent thyroid hormone deficiency that is present from birth due to thyroid resistance to TSH. Epidemiology Resistance to TSH occurs in about 5% of cases of permanent congenital hypothyroidism. Clinical description Clinical manifestations are those of other forms of congenital hypothyroidism (CH; see this term). Goiter is always absent. Etiology Mutations in the TSH receptor gene ( TSHR ; 14q31) result in resistance to TSH, which causes a reduction in thyroid hormone production. Mutations in TSHR may also cause thyroid hypoplasia (see this term).
- Hypothyroidism, Congenital, Nongoitrous, 1 OMIM
  
  A number sign (#) is used with this entry because of evidence that congenital nongoitrous hypothyroidism-1 (CHNG1) is caused by homozygous or compound heterozygous mutation in the gene encoding the thyroid-stimulating hormone receptor (TSHR; 603372) on chromosome 14q31. Description Resistance to thyroid-stimulating hormone (TSH; see 188540), a hallmark of congenital nongoitrous hypothyroidism, causes increased levels of plasma TSH and low levels of thyroid hormone. Only a subset of patients develop frank hypothyroidism; the remainder are euthyroid and asymptomatic (so-called compensated hypothyroidism) and are usually detected by neonatal screening programs (Paschke and Ludgate, 1997). Genetic Heterogeneity of Congenital Nongoitrous Hypothyroidism Also see CHNG2 (218700), caused by mutation in the PAX8 gene (167415) on chromosome 2q14; CHNG3 (609893), mapped to chromosome 15q25.3; CHNG4 (275100), caused by mutation in the TSHB gene (188540) on chromosome 1p13; CHNG5 (225250), caused by mutation in the NKX2-5 gene (600584) on chromosome 5q35; CHNG6 (614450), caused by mutation in the THRA gene (190120) on chromosome 17q21; and CHNG7 (618573), caused by mutation in the TRHR gene (188545) on chromosome 8q24. Clinical Features Stanbury et al. (1968) described an 8-year-old boy with congenital hypothyroidism who was the offspring of parents related as first cousins once removed.
Onychomadesis Wikipedia

See also [ edit ] Patterned acquired hypertrichosis List of cutaneous conditions References [ edit ] ^ James WD, Berger TG, Elston DM (2006). Andrew's diseases of the skin: clinical dermatology (10th ed.).

HLA-C
Follicular Thyroid Cancer Wikipedia

Specialty ENT surgery , oncology Follicular thyroid cancer accounts for 15% of thyroid cancer and occurs more commonly in women over 50 years of age. Thyroglobulin (Tg) can be used as a tumor marker for well-differentiated follicular thyroid cancer. ... Minimally invasive thyroidectomy has been used in recent years in cases where the nodules are small. [6] Finding disease recurrence [ edit ] Some studies have shown that thyroglobulin (Tg) testing combined with neck ultrasound is more productive in finding disease recurrence than full- or whole-body scans (WBS) using radioactive iodine. However, current protocol (in the USA) suggests a small number of clean annual WBS are required before relying on Tg testing plus neck ultrasound. When needed, whole body scans consist of withdrawal from thyroxine medication and/or injection of recombinant human Thyroid stimulating hormone (TSH).

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