IGF-1 is necessary for bone formation, and decreased levels in anorexia nervosa contribute to a loss of bone density and potentially contribute to osteopenia or osteoporosis. Anorexia nervosa can also result in reduction of peak bone mass. Buildup of bone is greatest during adolescence, and if onset of anorexia nervosa occurs during this time and stalls puberty, low bone mass may be permanent.Hepatic steatosis, or fatty infiltration of the liver, can also occur, and is an indicator of malnutrition in children. Neurological disorders that may occur as complications include seizures and tremors. Wernicke encephalopathy, which results from vitamin B1 deficiency, has been reported in patients who are extremely malnourished; symptoms include confusion, problems with the muscles responsible for eye movements and abnormalities in walking gait. The most common gastrointestinal complications of anorexia nervosa are delayed stomach emptying and constipation, but also include elevated liver function tests, diarrhea, acute pancreatitis, heartburn, difficulty swallowing, and, rarely, superior mesenteric artery syndrome. Delayed stomach emptying, or gastroparesis, often develops following food restriction and weight loss; the most common symptom is bloating with gas and abdominal distension, and often occurs after eating. Other symptoms of gastroparesis include early satiety, fullness, nausea, and vomiting. The symptoms may inhibit efforts at eating and recovery, but can be managed by limiting high-fiber foods, using liquid nutritional supplements, or using metoclopramide to increase emptying of food from the stomach. Gastroparesis generally resolves when weight is regained. Cardiac complications
Anorexia nervosa increases the risk of sudden cardiac death, though the precise cause is unknown.
As a result, further research is necessary to study the long term effective outcomes of FMT. Prognosis
After a first treatment with metronidazole or vancomycin, C. difficile recurs in about 20% of people. This increases to 40% and 60% with subsequent recurrences. Epidemiology
C. difficile diarrhea is estimated to occur in eight of 100,000 people each year. Among those who are admitted to hospital, it occurs in between four and eight people per 1,000. In 2011, it resulted in about half a million infections and 29,000 deaths in the United States.Due in part to the emergence of a fluoroquinolone-resistant strain, C. difficile-related deaths increased 400% between 2000 and 2007 in the United States. According to the CDC, "C. difficile has become the most common microbial cause of healthcare-associated infections in U.S. hospitals and costs up to $4.8 billion each year in excess health care costs for acute care facilities alone." History
Ivan C. Hall and Elizabeth OToole first named the bacterium Bacillus difficilis in 1935, choosing its specific epithet because it was resistant to early attempts at isolation and grew very slowly in culture. André Romain Prévot subsequently transferred it to the genus Clostridium, which made its binomen Clostridium difficile. Its combination was later changed to Clostridiodes difficile after being transferred to the new genus Clostridioides.Pseudomembranous colitis first was described as a complication of C. difficile infection in 1978, when a toxin was isolated from people with pseudomembranous colitis and Kochs postulates were met.