Inherited or congenital disorders associated with macroglossia include Down syndrome , Beckwith-Wiedemann syndrome , primary amyloidosis , and congenital hypothyroidism .
It is commonly observed with type 2 glycogen storage disease (232300), neurofibromatosis (162200), congenital hypothyroidism, and the Beckwith-Wiedemann syndrome (130650). Inheritance Macroglossia was reported as an isolated hereditary trait, apparently for the first time, by Reynoso et al. (1986). ... In each of the 2 families, the proband was a baby born with big tongue, leading to the diagnosis of congenital hypothyroidism or atypical Down syndrome. Reynoso et al. (1994) described 2 additional families with isolated autosomal dominant macroglossia.
It has also been associated with individuals exposed to arsenic -containing insecticides and Thorotrast . [ citation needed ] In dogs, hemangiosarcoma is relatively common, with the golden retriever and Labrador retriever at higher risk of the disease than other breeds. [3] See also [ edit ] Glomangiosarcoma Kaposi's sarcoma , a different type of cancer that also involves endothelial-type cells List of cutaneous conditions Stewart–Treves syndrome References [ edit ] ^ Kumar, Vinay; Abbas, Abul K.; Aster, Jon C., eds. (2013). ... Classification D ICD - 10 : C49.9 ICD-O : M9120/3 External resources eMedicine : med/138 Orphanet : 263413 v t e Tumours of blood vessels Blood vessel Hemangiosarcoma Blue rubber bleb nevus syndrome Hemangioendothelioma Composite Endovascular papillary Epithelioid Kaposiform Infantile Retiform ) Spindle cell Proliferating angioendotheliomatosis Hemangiopericytoma Venous lake Kaposi's sarcoma African cutaneous African lymphadenopathic AIDS-associated Classic Immunosuppression-associated Hemangioblastoma Hemangioma Capillary Cavernous Glomeruloid Microvenular Targeted hemosiderotic Angioma Cherry Seriginosum Spider Tufted Universal angiomatosis Angiokeratoma of Mibelli Angiolipoma Pyogenic granuloma Lymphatic Lymphangioma / lymphangiosarcoma Lymphangioma circumscriptum Acquired progressive lymphangioma PEComa Lymphangioleiomyomatosis Cystic hygroma Multifocal lymphangioendotheliomatosis Lymphangiomatosis Either Angioma / angiosarcoma Angiofibroma
Examples of these chemicals include vinyl chloride and arsenic. Genetic syndromes. Certain gene changes that people can be born with can raise the risk of having angiosarcoma. Examples include the gene changes that cause neurofibromatosis, Maffucci syndrome, or Klippel-Trenaunay syndrome, and the BRCA1 and BRCA2 genes.
Classically, the pain occurs weeks after the injury and persists indefinitely. The syndrome is notoriously variable. Some authors prefer use of the term causalgia or complex regional pain syndrome.
This page does not serve as an official recognition of post-finasteride syndrome by the NIH. Please see our Disclaimer for more details. This page was created to provide a list of resources where you can find more information about reported adverse events of 5-alpha reductase inhibitors, which is sometimes referred to as post-finasteride syndrome. Some patients who have taken finasteride have referred to side effects such as sexual dysfunction and depression (sometimes severe).
No chromosomal or immunologic defects were detected, thus excluding Fanconi anemia, Bloom syndrome, xeroderma pigmentosum, and ataxia telangiectasia, as well as Nijmegen breakage syndrome.
However, people with specific genetic syndromes such as multiple endocrine neoplasia type I , Von Hippel-Lindau syndrome , Neurofibromatosis type 1 , and tuberous sclerosis are at risk of insulinomas and other endocrine tumors .
Insulinoma is the most common type of functioning pancreatic neuroendocrine tumor (see this term) characterized most commonly by a solitary, small pancreatic lesion that causes hyperinsulinemic hypoglycemia. Epidemiology The incidence in the general population is 1/1,000,000-1/250,000 (but higher in autopsy studies). There is a slight female predominance. It is the most common endogenous cause of hyperinsulinemic hypoglycemia. Malignant insulinoma has an incidence 0.01/100,000 in Europe. Clinical description Insulinoma can present at any age but the median age of diagnosis is in the 5th decade of life. It manifests with various autonomic and neuroglycopenic symptoms such as tremor, palpitations, weakness, diaphoresis, hyperphagia, visual disturbances, confusion, behavioral and personality changes, seizures and coma.
A number sign (#) is used with this entry because of evidence that polymicrogyria with or without vascular-type Ehlers-Danlos syndrome (PMGEDSV) is caused by homozygous or compound heterozygous mutation in the COL3A1 gene (120180) on chromosome 2q32. Heterozygous mutation in the COL3A1 gene causes the vascular type of Ehlers-Danlos syndrome (EDSVASC; 130050), which is an autosomal dominant disorder. Description Polymicrogyria with or without vascular-type Ehlers-Danlos syndrome is an autosomal recessive disorder with a highly variable phenotype. ... In 2 sibs with polymicrogyria without vascular-type Ehlers-Danlos syndrome, who were born of unrelated parents from the same mountain village in Chechnya, Vandervore et al. (2017) identified a homozygous missense mutation in the COL3A1 gene (P49A; 120180.0039). ... Horn et al. (2017) identified the same homozygous P49A mutation in 2 sibs, born of unrelated parents from Chechnya and Ingushetia, with polymicrogyria without vascular-type Ehlers-Danlos syndrome. Each unaffected parent was heterozygous for the mutation.
The mortality rate is approximately 1 in 10. [1] An equivalent clot in the vasculature that exits the liver carrying deoxygenated blood to the right atrium via the inferior vena cava , is known as hepatic vein thrombosis or Budd-Chiari syndrome . [2] Contents 1 Signs and symptoms 2 Causes 3 Mechanism 4 Diagnosis 5 Treatment 6 See also 7 References 8 External links Signs and symptoms [ edit ] See also: Portal hypertension § Signs and symptoms Portal vein thrombosis causes upper abdominal pain, possibly accompanied by nausea and an enlarged liver and/or spleen; the abdomen may be filled with fluid ( ascites ). [3] A persistent fever may result from the generalized inflammation. [1] While abdominal pain may come and go if the thrombus forms suddenly, long-standing clot build-up can also develop without causing symptoms, leading to portal hypertension before it is diagnosed. [4] [2] Other symptoms can develop based on the cause. ... The prevalence of PVT in patients with cirrhosis is unclear, with a wide variety of incidence claimed by various researchers (estimated to be 1 in 100 by some while others believe it affects nearly 1 in 4). [5] Thrombophilia (including inherited conditions such as factor V Leiden deficiency, protein C or S deficiency, or antiphospholipid antibody syndrome ) is another common cause. [3] Nearly one-third of patients have a myeloproliferative disorder (e.g. polycythemia vera [6] or primary thrombocytosis), most commonly due to a Janus kinase 2 (JAK2) gene mutation. [1] Oral contraceptive use or pregnancy are other non-inherited tendencies for thrombosis. ... If blood flow to the gastrointestinal tract has been compromised chronically, surgery may be required to remove dead intestine. [1] Different considerations are made in the management of PVT in pediatric patients or those who have already received a liver transplant. [1] See also [ edit ] Pylephlebitis Budd–Chiari syndrome References [ edit ] ^ a b c d e f g h i DeLeve LD, Valla DC, Garcia-Tsao G (2009). ... Merck Classification D ICD - 10 : I81 ICD - 9-CM : 452 External resources eMedicine : radio/571 v t e Cardiovascular disease (vessels) Arteries , arterioles and capillaries Inflammation Arteritis Aortitis Buerger's disease Peripheral artery disease Arteriosclerosis Atherosclerosis Foam cell Fatty streak Atheroma Intermittent claudication Critical limb ischemia Monckeberg's arteriosclerosis Arteriolosclerosis Hyaline Hyperplastic Cholesterol LDL Oxycholesterol Trans fat Stenosis Carotid artery stenosis Renal artery stenosis Other Aortoiliac occlusive disease Degos disease Erythromelalgia Fibromuscular dysplasia Raynaud's phenomenon Aneurysm / dissection / pseudoaneurysm torso : Aortic aneurysm Abdominal aortic aneurysm Thoracic aortic aneurysm Aneurysm of sinus of Valsalva Aortic dissection Aortic rupture Coronary artery aneurysm head / neck Intracranial aneurysm Intracranial berry aneurysm Carotid artery dissection Vertebral artery dissection Familial aortic dissection Vascular malformation Arteriovenous fistula Arteriovenous malformation Telangiectasia Hereditary hemorrhagic telangiectasia Vascular nevus Cherry hemangioma Halo nevus Spider angioma Veins Inflammation Phlebitis Venous thrombosis / Thrombophlebitis primarily lower limb Deep vein thrombosis abdomen Hepatic veno-occlusive disease Budd–Chiari syndrome May–Thurner syndrome Portal vein thrombosis Renal vein thrombosis upper limb / torso Mondor's disease Paget–Schroetter disease head Cerebral venous sinus thrombosis Post-thrombotic syndrome Varicose veins Gastric varices Portacaval anastomosis Caput medusae Esophageal varices Hemorrhoid Varicocele Other Chronic venous insufficiency Chronic cerebrospinal venous insufficiency Superior vena cava syndrome Inferior vena cava syndrome Venous ulcer Arteries or veins Angiopathy Macroangiopathy Microangiopathy Embolism Pulmonary embolism Cholesterol embolism Paradoxical embolism Thrombosis Vasculitis Blood pressure Hypertension Hypertensive heart disease Hypertensive emergency Hypertensive nephropathy Essential hypertension Secondary hypertension Renovascular hypertension Benign hypertension Pulmonary hypertension Systolic hypertension White coat hypertension Hypotension Orthostatic hypotension
In the absence of a tumour or advanced cirrhosis, PVT may be caused by localised intra-abdominal inflammation or be associated with a general prothrombotic state caused by a myeloproliferative syndrome (25% of cases), G20210A mutations in the factor II (prothrombin) gene (10% of cases), antiphospholipid syndrome, or by deficiencies of antithrombin, protein C, protein S or factor V Leiden.
Fibrochondrogenesis is a very severe disorder of bone growth. Affected infants have a very narrow chest, which prevents the lungs from developing normally. Most infants with this condition are stillborn or die shortly after birth from respiratory failure. However, some affected individuals have lived into childhood. Fibrochondrogenesis is characterized by short stature (dwarfism) and other skeletal abnormalities. Affected individuals have shortened long bones in the arms and legs that are unusually wide at the ends (described as dumbbell-shaped). People with this condition also have a narrow chest with short, wide ribs and a round and prominent abdomen.
Favored sites are breasts, thighs, buttocks and penis, [1] all areas with subcutaneous fat. [3] : 122 In rare cases, the fascia and muscle are involved. [4] Development of the syndrome is associated with the use of large loading doses at the start of treatment. [5] Contents 1 Mechanism 2 Diagnosis 2.1 Differential diagnosis 3 Prevention 4 Treatment 5 History 6 See also 7 References Mechanism [ edit ] The coagulation cascade. ... Warfarin necrosis is also different from another drug eruption associated with warfarin, purple toe syndrome , which usually occurs three to eight weeks after the start of anticoagulation therapy. ... PMID 8236128 . v t e Adverse drug reactions Antibiotics Penicillin drug reaction Sulfonamide hypersensitivity syndrome Urticarial erythema multiforme Adverse effects of fluoroquinolones Red man syndrome Jarisch–Herxheimer reaction Hormones Steroid acne Steroid folliculitis Chemotherapy Chemotherapy-induced acral erythema Chemotherapy-induced hyperpigmentation Scleroderma-like reaction to taxanes Hydroxyurea dermopathy Exudative hyponychial dermatitis Anticoagulants Anticoagulant-induced skin necrosis Warfarin necrosis Vitamin K reaction Texier's disease Immunologics Adverse reaction to biologic agents Leukotriene receptor antagonist-associated Churg–Strauss syndrome Methotrexate-induced papular eruption Adverse reaction to cytokines Other drugs Anticonvulsant hypersensitivity syndrome Allopurinol hypersensitivity syndrome Vaccine adverse event Eczema vaccinatum Bromoderma Halogenoderma Iododerma General Skin and body membranes Acute generalized exanthematous pustulosis Bullous drug reaction Drug-induced acne Drug-induced angioedema Drug-related gingival hyperplasia Drug-induced lichenoid reaction Drug-induced lupus erythematosus Drug-induced nail changes Drug-induced pigmentation Drug-induced urticaria Stevens–Johnson syndrome Injection site reaction Linear IgA bullous dermatosis Toxic epidermal necrolysis HIV disease-related drug reaction Photosensitive drug reaction Other Drug-induced pseudolymphoma Fixed drug reaction Serum sickness-like reaction
Specialty Gastroenterology Fundic gland polyposis is a medical syndrome where the fundus and the body of the stomach develop many fundic gland polyps . ... Infrequently, the two lesions may coexist. [3] Foci of dysplasia can sometimes be seen. [4] Disease associations [ edit ] FGPs can be found in association with the following genetic conditions: [4] familial adenomatous polyposis attenuated familial adenomatous polyposis syndromes Zollinger-Ellison syndrome [6] [7] gastric adenocarcinoma associated with proxymal polyposis of the stomach (GAPPS): this condition, described in three families [8] is characterized by development of antral adenomas and FGPs, with early development of severe dysplasia and gastric cancer, in absence of overt intestinal polyposis. ... "Fundic gland polyps: do they arise as a by-product of hypergastrinemia in patients with Zollinger-Ellison syndrome?". Human Pathology . 31 (7): 889–90. doi : 10.1053/hupa.2000.8908 . ... "Intramucosal cysts in the gastric body of patients with Zollinger-Ellison syndrome". Human Pathology . 31 (2): 140–8. doi : 10.1016/S0046-8177(00)80213-0 . ... "Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS): a new autosomal dominant syndrome". Gut . 61 (5): 774–9. doi : 10.1136/gutjnl-2011-300348 .
Acute erythroid leukemia Other names Di Guglielmo syndrome Bone marrow smear from a case of erythroleukemia Specialty Hematology , oncology Acute erythroid leukemia is a rare form of acute myeloid leukemia (less than 5% of AML cases [1] ) where the myeloproliferation is of erythroblastic precursors. ... Contents 1 Signs and symptoms 2 Causes 3 Diagnosis 3.1 M6a (Erythroleukemia) 3.2 M6b (Pure erythroid leukemia) 3.3 M6c (Erythroleukemia and Pure erythroid leukemia) 4 Treatment 5 Prognosis 6 Epidemiology 7 History 8 References 9 External links Signs and symptoms [ edit ] The most common symptoms of AEL are related to pancytopenia (a shortage of all types of blood cells), including fatigue , infections , and mucocutaneous bleeding . [2] Almost half of people with AEL exhibit weight loss , fever and night sweats at the time of diagnosis. [2] Almost all people with AEL are anemic , and 77% have a hemoglobin level under 10.0 g/dl. [2] Signs of thrombocytopenia are found in about half of people with AEL. [2] Causes [ edit ] The causes of AEL are unknown. [3] Prior to a 2008 reclassification by the World Health Organization , cases that evolved from myelodysplastic syndromes , myeloproliferative neoplasms , chemotherapy for other cancers or exposure to toxins were defined as secondary AEL . [1] These cases are now likely to instead be classified as acute myeloid leukemia with myelodysplasia-related changes or therapy-related AML . [1] Diagnosis [ edit ] Acute erythroid leukemias can be classified as follows: M6a (Erythroleukemia) [ edit ] 50% or more of all nucleated bone marrow cells are erythroblasts , dyserythropoiesis is prominent and 20% or more of the remaining cells (non- erythroid) are myeloblasts . [4] [5] M6b (Pure erythroid leukemia) [ edit ] In rare cases the erythroid lineage is the only obvious component of an acute leukemia ; a myeloblast component is not apparent. ... That is, AEL is often associated with other risk factors, like monosomal karyotypes and a history of myelodysplastic syndrome . [9] Prognosis is worse in elderly patients, those with a history of myelodysplastic syndrome, and in patients who had previously received chemotherapy for the treatment of a different neoplasm. [1] [11] Epidemiology [ edit ] Acute erythroid leukemia is rare, accounting for only 3–5% of all acute myeloid leukemia cases. [2] One study estimated an occurrence rate of 0.077 cases per 100,000 people each year. [12] 64–70% of people with this condition are male, and most are elderly, with a median age of 65. [2] History [ edit ] The first known case of acute erythroid leukemia was described in 1912 by M. Copelli under the name erythromatosis . [2] [13] In 1917, Italian hematologist Giovanni Di Guglielmo (1886–1962), expanded on the description, coining the name "eritroleucemia" (Italian for erythroleukemia ). [2] [14] Di Guglielmo was the first to recognize the leukemic nature of the condition, and it is sometimes referred to as Di Guglielmo's syndrome in recognition of his work. [2] Ernst Neumark was widely credited for introducing Di Guglielmo's syndrome to English pathology. [15] Chris Squire , bassist from the progressive rock group Yes , died from complications related to acute erythroid leukemia on June 27, 2015. [16] References [ edit ] ^ a b c d e f Zuo Z, Polski JM, Kasyan A, Medeiros LJ (2010). ... Histology at University of Virginia Overview at Marist College Images at Nagoya University v t e Myeloid -related hematological malignancy CFU-GM / and other granulocytes CFU-GM Myelocyte AML : Acute myeloblastic leukemia M0 M1 M2 APL/M3 MP Chronic neutrophilic leukemia Monocyte AML AMoL/M5 Myeloid dendritic cell leukemia CML Philadelphia chromosome Accelerated phase chronic myelogenous leukemia Myelomonocyte AML M4 MD-MP Juvenile myelomonocytic leukemia Chronic myelomonocytic leukemia Other Histiocytosis CFU-Baso AML Acute basophilic CFU-Eos AML Acute eosinophilic MP Chronic eosinophilic leukemia / Hypereosinophilic syndrome MEP CFU-Meg MP Essential thrombocytosis Acute megakaryoblastic leukemia CFU-E AML Erythroleukemia/M6 MP Polycythemia vera MD Refractory anemia Refractory anemia with excess of blasts Chromosome 5q deletion syndrome Sideroblastic anemia Paroxysmal nocturnal hemoglobinuria Refractory cytopenia with multilineage dysplasia CFU-Mast Mastocytoma Mast cell leukemia Mast cell sarcoma Systemic mastocytosis Mastocytosis : Diffuse cutaneous mastocytosis Erythrodermic mastocytosis Adult type of generalized eruption of cutaneous mastocytosis Urticaria pigmentosa Mast cell sarcoma Solitary mastocytoma Systemic mastocytosis Xanthelasmoidal mastocytosis Multiple/unknown AML Acute panmyelosis with myelofibrosis Myeloid sarcoma MP Myelofibrosis Acute biphenotypic leukaemia
The authors suggested that the natural history of the disorder in this sibship was initial reactive changes in the marrow with subsequent progression to myelodysplasia with sideroblastosis, and finally to Di Guglielmo syndrome. The proband, aged 55 years, was investigated because 'most of my family have leukemia' and was found to have marrow hypocellularity.
A rare unclassified acute myeloid leukemia characterized by a proliferation of immature cells exclusively of the erythroid lineage without a significant myeloblastic component. Microscopically, the cells may be undifferentiated or proerythroblastic in appearance. Patients may present with pancytopenia with fatigue, infections, and mucocutaneous bleedings, as well as weight loss, fever, and night sweats. Prognosis is poor.
Ocular toxoplasmosis is an infection in the eye caused by the parasite, Toxoplasm a gondii. Toxoplasmosis is the most common cause of eye inflammation in the world. Toxoplamosis can be acquired or present at birth (congenital), having crossed the placenta from a newly infected mother to her fetus. Most humans acquire toxoplasmosis by eating raw or undercooked meat, vegetables or milk products, or by coming into contact with infected cat litterbox or sandboxes. In humans, the infection usually causes no symptoms, and resolves without treatment in a few months.
The term "Bilirubin-induced neurologic dysfunction (BIND)" is used for the signs and symptoms of kernicterus. In most cases, the syndrome develops by 3 to 4 years of age.
Functional protein S is lacking, which normally turns off clotting proteins, this increases risk of blood clots . [5] Diagnosis [ edit ] PTT blood tests Vacutainer tube The diagnosis for deficiency of protein S can be done via reviewing family history of condition and genetic testing, as well as the following: [1] [10] [11] Protein S antigen test Coagulation test (prothrombin time test) Thrombotic disease investigation Factor V Leiden test Differential diagnosis [ edit ] Among the possibilities for differential diagnosis of protein S deficiency are- Antiphospholipid syndrome , disseminated intravascular coagulation and antithrombin deficiency (though this list is not exhaustive) [2] Types [ edit ] There are three types of hereditary protein S deficiency: [2] [5] Type I – decreased protein S activity: decreased total protein S levels, as well as decreased free protein S levels Type II – decreased in regards to the cofactor activity of the protein Type III – decreased protein S activity: decreased free protein S levels (normal total protein S levels) Treatment [ edit ] Dabigatran In terms of treatment for protein S deficiency the following are consistent with the management (and administration of) individuals with this condition (the prognosis for inherited homozygotes is usually in line with a higher incidence of thrombosis for the affected individual [1] ): [2] [9] Unfractionated heparin (w/ warfarin) LMWH/Low molecular weight heparin Dabigatran Direct Factor Xa Inhibitors Graduated compressed stocking High degree of prophylaxis References [ edit ] ^ a b c d e f g h "Protein S Deficiency. ... 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Protein S deficiency is a disorder that causes abnormal blood clotting. When someone bleeds, the blood begins a complicated series of rapid chemical reactions to stop the bleeding. These chemical reactions involve proteins called blood coagulation factors . Other proteins in the blood, such as protein S, usually regulate these chemical reactions to prevent excessive clotting. When protein S is missing (deficient), clotting may not be regulated normally and affected individuals have an increased risk of forming a blood clot called a thrombosis .
Piblokto may be linked to repression of the personality of Inuit women . [1] The condition appears most commonly in winter. [2] It is considered to be a form of a culture-bound syndrome , although more recent studies (see Skepticism section) question whether it exists at all. Piblokto is also part of the glossary of cultural bound syndromes found in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). [3] Contents 1 History 2 Origin 3 Symptoms 4 Causes 5 Skepticism 6 See also 7 Notes 8 References 9 Further reading History [ edit ] Piblokto was first documented in 1892 and reports by European explorers describe the phenomenon as common to all Arctic regions. ... For example, transcultural psychiatry scholar Laurence Kirmayer writes: Most comprehensive psychiatric texts mention pibloktoq as a culture-bound syndrome characterized by sudden wild and erratic behaviour. ... C.; Hughes, C. C. (1985). The culture-bound syndromes: folk illnesses of psychiatric and anthropological interest . ... Higgs, Rachel D. (2011) " Pibloktoq - A study of a culture-bound syndrome in the circumpolar region ," The Macalester Review: Vol. 1: Iss. 1, Article 3.
Conditions affecting perceptions and/or cognition, such as agnosia , aphasia , etc. Tourette syndrome or Tic disorder. Epilepsy or Seizure disorder. Parkinsonian syndrome features such as tremors, stiff movements, etc. ... 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