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Ancestor membership does not transfer phenotype values between groups.","importantHtml":""},"sections":[{"bodyHtml":"<p>A mutation in the COL1A1 gene causes Caffey disease. The COL1A1 gene provides instructions for making part of a large molecule called type I collagen. Collagens are a family of proteins that strengthen and support many tissues in the body, including cartilage, bone, tendon, and skin. In these tissues, type I collagen is found in the spaces around cells. The collagen molecules are cross-linked in long, thin, fibrils that are very strong and flexible. Type I collagen is the most abundant form of collagen in the human body.</p><p>The COL1A1 gene mutation that causes Caffey disease replaces the protein building block (amino acid) arginine with the amino acid cysteine at protein position 836 (written as Arg836Cys or R836C). This mutation results in the production of type I collagen fibrils that are variable in size and shape, but it is unknown how these changes lead to the signs and symptoms of Caffey disease.</p><p class=\"section-source\"><a href=\"https://medlineplus.gov/genetics/condition/caffey-disease/#causes\">MedlinePlus Genetics: Causes</a></p>","key":"forms","title":"What causes Caffey disease?"},{"bodyHtml":"<p>The signs and symptoms of Caffey disease are usually apparent by the time an infant is 5 months old. In rare cases, skeletal abnormalities can be detected by ultrasound imaging during the last few weeks of development before birth. Lethal prenatal cortical hyperostosis, a more severe disorder that appears earlier in development and is often fatal before or shortly after birth, is sometimes called lethal prenatal Caffey disease; however, it is generally considered to be a separate disorder.</p><p>For unknown reasons, the swelling and pain associated with Caffey disease typically go away within a few months. Through a normal process called bone remodeling, which replaces old bone tissue with new bone, the excess bone is usually reabsorbed by the body and undetectable on x-ray images by the age of 2. However, if two adjacent bones have fused, they may remain that way, possibly resulting in complications. For example, fused rib bones can lead to curvature of the spine (scoliosis) or limit expansion of the chest, resulting in breathing problems.</p><p>Most people with Caffey disease have no further problems related to the disorder after early childhood. Occasionally, another episode of hyperostosis occurs years later. In addition, some adults who had Caffey disease in infancy have other abnormalities of the bones and connective tissues, which provide strength and flexibility to structures throughout the body. Affected adults may have loose joints (joint laxity), stretchy (hyperextensible) skin, or be prone to protrusion of organs through gaps in muscles (hernias).</p><p class=\"section-source\">Source: <a href=\"https://medlineplus.gov/genetics/condition/caffey-disease\">MedlinePlus Genetics</a></p>","key":"overview","title":"Condition overview"}],"sharedSources":[],"slug":"caffey-disease","sourceDocuments":[{"name":"Caffey disease","reviewed":"2013-04","sections":{"causes":{"fetchedAt":"2026-10-20T20:20:00.201534+00:00","label":"Causes","pageSha256":"9d64e3c6ebf5a216f7b7508aab0f8ce49f1f3752415497817ef7cbe474bfe9b5","sourceUrl":"https://medlineplus.gov/genetics/condition/caffey-disease/#causes","status":"available"}},"source_release":"2026-10-01","url":"https://medlineplus.gov/genetics/condition/caffey-disease"}],"sourceNote":"MedlinePlus descriptions and Causes; original HPO annotations.","takeawayHtml":"Cause explanations are from MedlinePlus Genetics. Feature values below retain their original sources and patient groups.","title":"Caffey disease"},"schemaVersion":1}