Approximately 50% of affected children have abnormal findings at birth (such as club foot or twisted metatarsals, cleft palate, inward curving fingers due to underdeveloped bones and brachydactyly, or ear swelling caused by injury during birth). Height is in the normal range before puberty. As adults, people with recessive MED are only slightly more diminished in stature, but within the normal range. Lateral knee radiography can show multi-layered patellae. Genetics
Multiple epiphyseal dysplasia (MED) encompasses a spectrum of skeletal disorders, most of which are inherited in an autosomal dominant form. However, there is an autosomal recessive form.Associated genes include COL9A1, COL9A2, COL9A3, COMP, and MATN3.Types include:

In the dominant form, mutations in five genes are causative: COMP (chromosome 19), COL9A1 (chromosome 6), COL9A2 (chromosome 1), COL9A3 (chromosome 20), and MATN3 (chromosome 2). However, in approximately 10%–20% of samples analyzed, a mutation cannot be identified in any of the five genes above, suggesting that mutations in other as-yet unidentified genes are involved in the pathogenesis of dominant MED.The COMP gene is mutated in 70% of the molecularly confirmed MED patients. Mutations are in the exons encoding the type III repeats (exons 8–14) and C-terminal domain (exons 15–19). The most common mutations in COL9A1 are in exons 8-10, in COL9A2 in exons 2-4, and in COL9A3 in exons 2-4. Altogether, those mutations cover 10% of the patients. The other 20% of affected people have mutations in MATN3 gene, all found within exon 2.
Prevention
The need for medications to prevent stress ulcer among those in the intensive care unit is unclear. As of 2014, the quality of the evidence is poor. It is unclear which agent is best or if prevention is needed at all. Benefit may only occur in those who are not being fed. Possible agents include antacids, H2-receptor blockers, sucralfate, and proton pump inhibitors (PPIs). Tentative evidence supports that PPIs may be better than H2 blockers.Concerns with the use of stress ulcer prophylaxis agents include increased rates of pneumonia and Clostridium difficile colitis. Treatment
The principles of management are the same as for the chronic ulcer. The steps of management are similar as in erosive gastritis.Endoscopic means of treating stress ulceration may be ineffective and operation required. It is believed that shunting blood away from the mucosa makes the mucous membrane ischaemic and more susceptible to injury.Treatment of stress ulceration usually begins with prevention. Careful attention to respiratory status, acid-base balance, and treatment of other illnesses help prevent the conditions under which stress ulcers occur. Patients who develop stress ulcers typically do not secrete large quantities of gastric acid; however, acid does appear to be involved in the pathogenesis of the lesions. Thus it is reasonable either to neutralize acid or to inhibit its secretion in patients at high risk.In case of severe hemorrhagic or erosive gastritis and stress ulcers, a combination of antacids and H2-blockers may stop active bleeding and prevent bleeding from happening again.