Consequently, less intensive (de-intensification) use of radiotherapy or chemotherapy, as well as specific therapy, is under investigation, enrolling HPV+OPC in clinical trials to preserve disease control and minimise morbidity in selected groups based on modified TNM staging and smoking status. HPV+ cancer of the oropharynx are staged as (AJCC 8th ed. 2016): Tumour stage T0 no primary identified T1 2 cm or less in greatest dimension T2 2–4 cm T3 >4 cm, or extension to lingual surface of epiglottis T4 moderately advanced local disease, invading larynx, extrinsic muscle of tongue, medial pterygoid, hard palate, or mandible or beyond Nodal stage Nx regional lymph nodes cannot be assessed N0 no regional lymph nodes involved N1 one or more ipsilateral nodes involved, less than 6 cm N2 contralateral or bilateral lymph nodes, less than 6 cm N3 lymph node(s) larger than 6 cm Clinical stage Stage I: T0N1, T1–2N0–1 Stage II: T0N2, T1–3N2, T3N0–2 Stage III: T0–3N3, T4N0-3 Stage IV: any metastases (M1) However, the published literature and ongoing clinical trials use the older seventh edition that does not distinguish between HPV+OPC and HPV-OPC - see Oropharyngeal Cancer - Stages. The T stages are essentially similar between AJCC 7 and AJCC 8. with two exceptions.
Osteogenesis imperfecta (OI) is a group of genetic disorders that mainly affect the bones. The term "osteogenesis imperfecta" means imperfect bone formation. People with this condition have bones that break easily, often from mild trauma or with no apparent cause. Multiple fractures are common, and in severe cases, can occur even before birth. Milder cases may involve only a few fractures over a person's lifetime. There are at least eight recognized forms of osteogenesis imperfecta, designated type I through type VIII.
Osteogenesis imperfecta (OI) is a group of genetic disorders that mainly affect the bones. Osteogenesis imperfecta type 1 is the mildest form of OI and is characterized by bone fractures during childhood and adolescence that often result from minor trauma. Fractures occur less frequently in adulthood. People with mild forms of the condition typically have a blue or grey tint to the part of the eye that is usually white (the sclera), and may develop hearing loss in adulthood. Affected individuals are usually of normal or near normal height. Most of the mutations that cause osteogenesis imperfecta type 1 occur in the COL1A1 gene. These genetic changes reduce the amount of type I collagen produced in the body, which causes bones to be brittle and to fracture easily.
Osteogenesis imperfecta (OI) comprises a heterogeneous group of genetic disorders characterized by increased bone fragility, low bone mass, and susceptibility to bone fractures with variable severity. Epidemiology Prevalence is estimated at between 1/10,000 and 1/20,000. Clinical description Age at diagnosis depends on the severity of the disease. Five clinically distinct types of OI have been identified. The most clinically relevant characteristic of all types of OI is bone fragility, which manifests as multiple spontaneous fractures. Osteogenesis imperfecta type II is lethal, type III is severe, types IV and V are moderate, and type I is mild (see these terms).
A number sign (#) is used with this entry because OI type I (OI1) is caused by heterozygous mutation in the COL1A1 gene (120150) or the COL1A2 gene (120160). Description Osteogenesis imperfecta type I is a dominantly inherited, generalized connective tissue disorder characterized mainly by bone fragility and blue sclerae. In most cases, 'functional null' alleles of COL1A1 on chromosome 17 or COL1A2 on chromosome 7 lead to reduced amounts of normal collagen I. Clinical Features Osteogenesis imperfecta (see Byers, 1993) is characterized chiefly by multiple bone fractures, usually resulting from minimal trauma. Affected individuals have blue sclerae, normal teeth, and normal or near-normal stature (for growth curves, see Vetter et al., 1992).
Osteogenesis imperfecta type I is a mild type of osteogenesis imperfecta (OI; see this term), a genetic disorder characterized by increased bone fragility, low bone mass and susceptibility to bone fractures. Epidemiology The overall prevalence of OI is estimated at between 1/10,000 and 1/20,000 but the prevalence of type I is unknown. Clinical description OI type I is nondeforming with normal height or mild short stature, blue sclera, and no dentinogenesis imperfecta (DI; see this term). Etiology OI type I is caused by mutations in the COL1A1 and COL1A2 genes (17q21.31-q22 and 7q22.1 respectively). Genetic counseling Transmission is autosomal dominant.
Beighton (1981) reported a kindred in which 20 members in at least 3 generations had opalescent teeth, blue sclerae, wormian bones, and normal height. In the 6 affected individuals who had skeletal surveys, moderate generalized osteoporosis was noted; the older individuals had mild flattening and biconcavity of the vertebral bodies. Only 1 affected individual, an adolescent male, had pronounced platybasia and had sustained 10 femoral fractures on mild trauma. Only the proband had hearing loss. No individuals had joint hyperextensibility. It is not known whether the syndrome is the same as OI type I (166200).
Food and Drug Administration approved tadalafil to treat the signs and symptoms of benign prostatic hyperplasia, and for the treatment of BPH and erectile dysfunction (ED), when the conditions occur simultaneously. Self-catheterization Intermittent urinary catheterization is used to relieve the bladder in people with urinary retention. ... Wilt, Timothy J (ed.). "Beta-sitosterols for benign prostatic hyperplasia". ... Wilt, Timothy J (ed.). "Pygeum africanum for benign prostatic hyperplasia".
Description Benign prostatic hyperplasia (BPH) refers to the nonmalignant growth of the prostate gland, and is histologically defined as hyperplasia of the prostate gland. BPH is an age-related phenomenon in men beginning at about age 40 years. BPH may result in prostatic enlargement and clinical symptoms most commonly affecting the lower urinary tract. These symptoms may be obstructive, including hesitancy, weak flow, and urinary retention, or irritative, including increased frequency and urgency. However, not all men with histologic BPH will develop prostatic enlargement or urinary symptoms (review by Roehrborn, 2005).
Silicosis is a respiratory disease caused by breathing in (inhaling) silica dust. There are three types of silicosis: Simple chronic silicosis, the most common type of silicosis, results from long-term exposure (usually more than 20 years) to low amounts of silica dust. Simple chronic silicosis may cause people to have difficulty breathing. Accelerated silicosis occurs after 5 to 15 years of exposure of higher levels of silica. Swelling of the lungs and other symptoms occur faster in this type of silicosis than in the simple chronic form.
The effects on the immune system include an increase in CD4+ cell production attributable to nicotine, which has tentatively been linked to increased HIV susceptibility. Smoking increases the risk of Kaposi's sarcoma in people without HIV infection. One study found this only with the male population and could not draw any conclusions for the female participants in the study. Impotence The incidence of impotence (difficulty achieving and maintaining penile erection) is approximately 85 percent higher in male smokers compared to non-smokers. Smoking is a key cause of erectile dysfunction (ED). It causes impotence because it promotes arterial narrowing and damages cells lining the inside of the arteries thus leading to reduce penile blood flow. Female infertility See also: Female infertility § Tobacco smoking Smoking is harmful to the ovaries, potentially causing female infertility, and the degree of damage is dependent upon the amount and length of time a woman smokes. ... Research by NCAR radiochemist Ed Martell suggested that radioactive compounds in cigarette smoke are deposited in "hot spots" where bronchial tubes branch, that tar from cigarette smoke is resistant to dissolving in lung fluid and that radioactive compounds have a great deal of time to undergo radioactive decay before being cleared by natural processes.
Nelson Essentials of Pediatrics (7 ed.). Elsevier Health Sciences. p. 150. ... (eds.). Pediatric Endocrinology and Inborn Errors of Metabolism. New York: McGraw Hill Medical. p. 26. ^ Institute of Medicine (2002).
Phenylketonuria (commonly known as PKU) is an inherited disorder that increases the levels of a substance called phenylalanine in the blood. Phenylalanine is a building block of proteins (an amino acid) that is obtained through the diet. It is found in all proteins and in some artificial sweeteners. If PKU is not treated, phenylalanine can build up to harmful levels in the body, causing intellectual disability and other serious health problems. The signs and symptoms of PKU vary from mild to severe. The most severe form of this disorder is known as classic PKU. Infants with classic PKU appear normal until they are a few months old.
Phenylketonuria (PKU) is a genetic metabolic disorder that increases the body's levels of phenylalanine. Phenylalanine is one of the building blocks (amino acids) of proteins. Humans cannot make phenyalanine, but it is a natural part of the foods we eat. However, people do not need all the phenyalanine they eat, so the body converts extra phenylalanine to another harmless amino acid, tyrosine. People with PKU cannot properly break down the extra phenylalanine to convert it to tyrosine.
Phenylketonuria (PKU) is the most common inborn error of amino acid metabolism and is characterized by mild to severe mental disability in untreated patients. Epidemiology The prevalence of PKU shows considerable geographic variation. It is estimated to be 1/10,000 live births in Europe with a higher rate in some countries (Ireland, Italy). Prevalence is particularly high in Turkey: 1/4,000 live births. PKU is far rarer in the Finnish, African and Japanese populations. Clinical description In the absence of neonatal diagnosis, symptoms develop within a few months of birth, may be very mild to severe and include gradual developmental delay, stunted growth, microcephaly, seizures, tremors, eczema, vomiting, and musty odor.