Hypophosphatemia
| Classification according to ICD-10 | |
|---|---|
| E83.3 | Disorders of phosphorus metabolism and phosphatase |
| ICD-10 online (WHO version 2019) | |
A hypophosphatemia is a decrease in the phosphate level in the blood is below 0.8 mmol / l. The main causes are alcoholism , artificial nutrition without added phosphate and the use of agents to neutralize stomach acid ( antacids ). The consequences of hypophosphataemia are disorders of mineral metabolism and the supply of energy and oxygen to the cells. The treatment is carried out by giving vitamin D and phosphate.
Epidemiology
Hypophosphataemia is rare in the general population. In hospital patients the incidence of hypophosphataemia is approx. 3%, in patients in intensive care units approx. 30%. In patients with blood poisoning ( sepsis ) the incidence can be up to 80%, in alcoholics up to 30%, in severe injuries up to 75% and in chronic obstructive pulmonary diseases up to 20%.
etiology
The causes are a reduced intake of phosphate due to an unbalanced diet or as part of intravenous nutrition (intensive care medicine). In the case of a pre-existing phosphate deficiency and malnutrition (e.g. anorexia nervosa ), inadequate phosphate intake as part of nutritional therapy can lead to severe phosphate deficiency symptoms . The administration of insulin also leads to a drop in the phosphate level. Ingestion of large amounts of antacids causes phosphate to bind to the drug in the stomach and thus to a reduced absorption of phosphate. Chronic diarrhea can lead to hypophosphataemia through increased phosphate loss. Several congenital disorders of the phosphate transport system in the kidney lead to phosphate loss in the urine. Other causes of hypophosphataemia are vitamin D deficiency, respiratory alkalosis , overactive parathyroid glands (primary hyperparathyroidism ) and the syndrome of hungry bone after surgical removal of the parathyroid glands . Another cause of the development of hypophosphatemia is hemodialysis in patients with renal insufficiency , in which, among other things, phosphate is withdrawn from the blood .
Vitamin D 3 is also formed from 7-dehydrocholesterol in the skin with the help of UV-B radiation ( Dorno radiation) , so a lack of light can also be a cause.
The decrease in the phosphate level leads to a decrease in the energy-rich phosphate compound adenosine triphosphate in all cells . The level of 2,3-bisphosphoglycerate in the erythrocytes falls ; this makes the delivery of oxygen from the blood to the tissue more difficult.
Severe hypophosphataemia (serum phosphate level <0.3 mmol / l) can lead to hemolytic anemia due to the destruction of red blood cells and rhabdomyolysis due to the destruction of muscle cells . Pronounced, chronic hypophosphataemia can lead to mineralization disorders of the bone. In hospital patients, moderate hypophosphatemia is associated with increased complication rates in the course of the disease, but the low phosphate level may not be the cause of the complications, but the consequence of the more severe course of the disease (see also surrogate markers ).
Familial hypophosphatemic rickets
This congenital disease is also called phosphate diabetes , in English "x-linked hypophosphatemia". In familial hypophosphatemic rickets , the reabsorption of phosphate in the renal tubules is disturbed. As a result, more phosphate is excreted and hypophosphataemia occurs in the blood. The synthesis of active vitamin D (1,25-dihydroxy vitamin D) is reduced. This creates rickets. The cause is a mutation on the X chromosome, which leads to the loss of function of the phosphate-regulating neutral endopeptidase (PHEX). A loss of function of PHEX leads to an excessive increase in FGF-23 (fibroblast growth factor 23) in the blood. In addition to the originally discovered function of stimulating fibroblasts to grow, FGF-23 has an important function as the primary regulator of phosphate by controlling the phosphate reabsorption of the kidneys. An excess of FGF-23 worsens the renal phosphate reabsorption. FGF-23 can be blocked with the monoclonal antibody burosumab. In a phase II study with 52 children, after treatment with burosumab, the phosphate reabsorption of the kidney tubules was improved, the serum phosphate increased, the body growth improved, the pain and the severity of rickets decreased.
therapy
In the case of moderate phosphate deficiency, increased phosphate intake can be achieved by consuming more milk and dairy products. If this is not enough, sodium or potassium phosphate can be taken. For intensive care patients, phosphate supplements can also be administered intravenously. A phosphate overdose should be avoided; this manifests itself in kidney failure , a drop in the calcium level ( hypocalcemia ), a drop in blood pressure ( hypotension ) and changes in the ECG .
See also
Individual evidence
- ↑ Alphabetical index for the ICD-10-WHO version 2019, volume 3. German Institute for Medical Documentation and Information (DIMDI), Cologne, 2019, p. 395
- ↑ Steven M. Brunelli, Stanley Goldfarb: Hypophosphatemia: clinical consequences and management . In: Journal of the American Society of Nephrology . tape 18 , no. 7 , July 2007, ISSN 1046-6673 , p. 1999-2003 , doi : 10.1681 / ASN.2007020143 , PMID 17568018 .
- ↑ Subconjunctival auto-hemotherapy of eye burns in our cases . March 17, 2012, doi: 10.4016 / 46352.01 , PMID 1405409
- ↑ Munro Peacock, Karl L. Insogna, Jeffrey Humphrey, Xiaoping Zhang, Takahiro Ito: Randomized trial of the anti-FGF23 antibody KRN23 in X-linked hypophosphatemia . In: The Journal of Clinical Investigation . tape 124 , no. 4 , April 1, 2014, ISSN 0021-9738 , p. 1587–1597 , doi : 10.1172 / JCI72829 , PMID 24569459 , PMC 3973088 (free full text) - ( jci.org [accessed December 13, 2018]).
- ↑ Thomas O. Carpenter, Michael P. Whyte, Erik A. Imel, Annemieke M. Boot, Wolfgang Högler: Burosumab Therapy in Children with X-Linked Hypophosphatemia . In: New England Journal of Medicine . May 23, 2018, doi : 10.1056 / NEJMoa1714641 ( nejm.org [accessed December 13, 2018]).
