Cystic Fibrosis probably treated by Vitamin D (if use enough of the right type ) – Oct 2019

Vitamin D deficiency and its treatment in cystic fibrosis.

J Cyst Fibros. 2019 Oct;18 Suppl 2:S66-S73. doi: 10.1016/j.jcf.2019.08.022.

Daley T1, Hughan K2, Rayas M3, Kelly A4, Tangpricha V5.

• 1 Division of Pediatric Endocrinology and Metabolism, Emory + Children's Pediatric Institute, Department of Pediatrics, Emory University, School of Medicine, 1400 Tullie Road, Atlanta, GA 30329, USA. Electronic address: Tanicia.daley at emory.edu.
• 2 Division of Pediatric Endocrinology and Diabetes, UPMC Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, 4401 Penn Avenue, Pittsburgh, PA 15224, USA. Electronic address: kara.hughan at chp.edu.
• 3 Division of Pediatric Endocrinology and Diabetes, University of Texas Health San Antonio, 7703 Floyd Curl, San Antonio, TX 78229, USA. Electronic address: rayas at uthscsa.edu.
• 4 Division of Pediatric Endocrinology and Diabetes, Children's Hospital of Philadelphia, Perelman School of Medicine of University of Pennsylvania, 2716 South Street, Philadelphia, PA 19146, USA. Electronic address: kellya at email.chop.edu.
• 5 Atlanta VA Medical Center, 1670 Clairmont Road NE, Decatur, GA 30300, USA; Division of Endocrinology, Metabolism, and Lipids, Department of Medicine, Emory University, School of Medicine, 101 Woodruff Circle NE, Atlanta, GA 30322, USA. Electronic address: vin.tangpricha at emory.edu.

Vitamin D deficiency is a common finding in individuals with cystic fibrosis (CF), despite routine supplementation. Hypovitaminosis D is often the result of fat malabsorption, but other contributors include increased latitude, poor nutritional intake, decreased sun exposure, impaired hydroxylation of vitamin D, and non-adherence to the prescribed vitamin D regimen. Vitamin D is critical for calcium homeostasis and optimal skeletal health, and vitamin D deficiency in CF can lead to skeletal complications of osteopenia and osteoporosis.
Over time, our understanding of treatment regimens for vitamin D deficiency in CF has evolved, leading to recommendations for higher doses of vitamin D to achieve target levels of circulating 25-hydroxyvitamin D.
There is also some evidence that vitamin D deficiency may have non-skeletal consequences such as an increase in pulmonary exacerbations.
The exact mechanisms involved in the non-skeletal complications of vitamin D deficiency are not clearly understood, but may involve the innate immune system. Future clinical studies are needed to help address whether vitamin D has a role in CF beyond skeletal health.