It is vital to screen patients and their caretakers for psychiatric conditions such as depression or anxiety, as well as screen children for signs and symptoms of child abuse, neglect, or emotional deprivation.Children who have FTT caused by a genetic or medical problem may have differences in growth patterns compared to children with FTT due to inadequate food intake. A decrease in length with a proportional drop in weight can be related to long-standing nutritional factors as well as genetic or endocrine causes. Head circumference, as well, can be an indicator for the etiology of FTT. If head circumference is affected initially in addition to weight or length, other factors are more likely causes than inadequate intake. Some of these include intrauterine infection, teratogens, and some congenital syndromes.Children who have a medical condition causing FTT may have additional signs and symptoms specific to their condition. Fetal alcohol syndrome (FAS) has been associated with FTT, and can present with characteristic findings including microcephaly, short palpebral fissures, a smooth philtrum and a thin vermillion border. Disorders that cause difficulties absorbing or digesting nutrients, such as Crohns disease, cystic fibrosis, or celiac disease, can present with abdominal symptoms. Symptoms can include abdominal pain, abdominal distention, hyperactive bowel sounds, bloody stools, or diarrhea. Cause
Traditionally, causes of FTT have been divided into endogenous and exogenous causes. These causes can also be largely grouped into three categories: inadequate caloric intake, malabsorption/caloric retention defect, and increased metabolic demands. Endogenous (or "organic")
Endogenous causes are due to physical or mental issues affecting the child.
This weakening is ascribed to KSHV/HHV8 infection that is commonly further promoted by concurrent human immunodeficiency virus (i.e. HIV) infection, prior organ transplantation, the decline in immunity that develops with aging, and/or cirrhosis of the liver due to hepatitis B or C virus. The plasmacytoid cells in PEL are also commonly infected with the Epstein-Barr virus (i.e. EBV). EBV is a known cause of various Epstein-Barr virus-associated lymphoproliferative diseases including various B-cell lymphomas. However, the role of this virus in the development of PEL is not clear, although some studies suggest that EBV infection cooperates with KSHV/HHV8 infection to promote the development and/or progression of this disease.Formally, PEL is defined by the World Health Organization, 2016 as a KSHV/HHV8-positive and KSHV/HHV8-driven large B-cell lymphoma. This lymphoma also belongs to a group of lymphoid neoplasms with plasmablastic differentiation that involve malignant plasmablasts but differ from PEL in the types of tissues where they accumulate, the gene abnormalities they carry, and/or the predisposing conditions involved in their development. More than 50, 30, and 60% of all PEL cases, respectively, develop in individuals who already have KSHV/HHV8-positive Kaposis sarcoma, human herpesvirus 8-associated multicentric Castleman disease, and/or (especially in HIV-positive individuals) evidence of bearing EBV-infected plasmablasts.Primary effussion lymphoma is an extremely aggressive cancer that is highly resistant to various chemotherapy treatments. It has carried a median survival time of ~5 months, with overall survival rates at 1, 3, and 5 year of only 30, 18, and 17%, respectively.