Can I Overdose on Vitamin D?
Oral formulation of insulin shows promise in management of blood glucose in diabetic ratsNach aktuellen Studien dürfte eine unzureichende Versorgung mit Vitamin D nicht nur glucosr allgemeine und die kardiovaskuläre Mortalität vitamin d glucose levels, sondern auch ein wichtiger ätiologischer Faktor bei der Pathogenese zahlreicher chronischer Erkrankungen wie Diabetes mellitus Typ 1 und Typ 2 sein [1, 2]. Eine Normalisierung des Vitamin-D-Status könnte bei Diagnose eines TypDiabetes dazu beitragen, die noch vorhandenen Betazellen vor der weiteren Zerstörung zu schützen [1, 3, 6]. In einer vitamin d glucose levels Kohortenstudie mit Dabei zeigte sich, dass Neugeborene, denen im ersten Lebensjahr täglich 2. Kinder, bei denen libido steigern mann lebensmittel ersten Lebensjahr Rachitis auftrat, hatten im Vergleich zu nicht erkrankten Kindern ein 3-fach höheres Risiko für TypDiabetes .
Diabetes und Vitamin D
In stage 1 VDDR, urinary amino acid and phosphate excretion are normal with minimal or no findings of rickets on radiographs. VDDR occasionally resembles PHP type 2 in clinical presentation and biochemical features, creating difficulties in the differential diagnosis of these two entities.
Here we report an infant diagnosed with VDDR. In addition to inadequate vitamin D intake, usage of antiepileptic drugs AED may have led to the worsening of the vitamin D deficiency. The patient presented with a history of febrile convulsions, for which he received phenobarbital treatment. The initial findings of hypocalcemia, hyperphosphatemia and normal tubular reabsorption of phosphate, mimicking PHP 2, responded well to vitamin D and oral Ca treatment with normalization of serum Ca, phosphorus P , ALP and PTH levels.
In a recent study, it was shown that after the nationwide vitamin D supplementation campaign in , the prevalence of VDDR declined from 6. There are some studies reporting the resurgence of this disorder in developed countries 2 , 3.
Children with PHP present with hypocalcemia and normal or elevated serum phosphorus P concentrations despite elevated serum PTH levels. The disorder is subdivided into several distinct entities. Pediatricians in developed countries have limited experience in treating children with VDDR 4. He was born at term with a birth weight of g to nonconsanguineous parents. He had a convulsion for the first time at age 8 months and, antiepileptic phenobarbital treatment was started. The patient had had febrile convulsions on 7 different occasions since then.
He was breastfed only until 6 months of age and received complementary feedings thereafter. His neurodevelopment was appropriate for age. The patient had a history of frequent infections. He had been hospitalized due to pyelonephritis at the age of 16 months. Mild enlargement of the wrists was noted bilaterally. Interpopliteal distance was 5. Initial laboratory investigations showed the following levels: Tubular reabsorption of phosphate was 0. A diagnosis of vitamin D deficiency was made and, oral U vitamin D was started.
In addition, oral Ca was given for 15 days. Three weeks later, serum Ca level was 9. VDDR is a disorder biochemically characterized by elevated serum ALP activity, normal or decreased serum Ca and inorganic phosphate concentrations, secondary hyperparathyroidism and decreased serum 25 OH D levels. Fraser et al 5 described three stages of VDDR on the basis of clinical and laboratory data. Stage 1 is characterized by hypocalcemia, normal P, normal urinary amino acid and phosphate excretion with minimal or no findings of rickets on radiographs.
Stage 3 is similar to stage 2 but associated with hypocalcemia and advanced rickets. In this original study, which is based on the classical teaching of rickets staging, hypocalcemia was attributed to lack of PTH secretion in the first stage of VDDR. The earlier studies also showed normal PTH levels in this stage 6. Later on, it was shown that PTH levels were actually increased in stage 1 of VDDR at a time when the phosphaturia or aminoaciduria were still absent.
It was also shown that the regulation and action of PTH were disturbed in vitamin D deficiency, and restored after vitamin D treatment 7. In PHP patients, biochemical findings hypocalcemia and hyperphosphatemia are consistent with hypoparathyroidism. PHP type 1a is characterized by hormone resistance in addition to a peculiar constellation of developmental and somatic defects that are collectively termed as AHO.
The AHO phenotype consists of short stature, round face, obesity, brachydactyly, subcutaneous ssifications, and rarely dental defects and sensorineural abnormalities. Our patient had none of these findings. Serum PTH levels cannot be relied on to differentiate between these two disorders. A detailed history should be taken, including vitamin D intake, sun exposure and use of drugs that interfere with vitamin D metabolism. In our patient, vitamin D support was inadequate and phenobarbital treatment probably aggravated the deficiency.
Evidence of rickets on physical and radiological examination is also important in the differential diagnosis, although clinical signs may be minimal or absent in stage 1 VDDR. On the other hand, PHP may present with bony deformities resembling rickets Nevertheless, if the differential diagnosis cannot be made properly in marginal cases, showing the normalization of biochemical and physical abnormalities after vitamin D treatment may help in clarifying the diagnosis 4.
Febrile seizures, a common and usually benign complaint in infancy and early childhood, are not known to be associated with rickets. Hoecker et al 11 reported that recurrent febrile convulsions might be an unusual presentation of nutritional rickets. Since vitamin D is reported to have an important role in immune defense mechanisms 12 , it may be speculated that the febrile convulsions triggered by fever during frequent infections in this patient could be attributable to vitamin D deficiency.
There are several studies reporting that decreased serum 25 OH D and altered bone metabolism were associated with AED treatment in children Many AEDs are known to be inducers of hepatic cytochrome P metabolism, resulting in increased hepatic metabolism of vitamin D. Some authors recommend monitoring of the vitamin D status in children taking AEDs, especially those receiving polypharmacotherapy In our patient, we thought that in addition to inadequate vitamin D intake, usage of AED may have led to the worsening of the vitamin D deficiency.
The demonstration of normalization of phosphocalcic parameters i. Vitamin D deficiency should be kept in mind in the differential diagnosis of hypocalcemia in children, especially those being treated with AEDs. National Center for Biotechnology Information , U. J Clin Res Pediatr Endocrinol. Published online Nov 8. Received Jul 8; Accepted Oct 7. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
This article has been cited by other articles in PMC. The initial findings of hypocalcemia, hyperphosphatemia and normal tubular reabsorption of phosphate, mimicking PHP 2, responded well to vitamin D and oral Ca treatment with normalization of serum Ca, phosphorus P , ALP and PTH levels Conflict of interest: Vitamin D deficiency rickets, Pseudohypoparathyroidism, antiepileptic drugs.
Prevalence of vitamin D deficiency rickets in the eastern part of Turkey. Rickets resurgence in the United Kingdom: Srivastava T, Alon US. Clin Pediatr Phila ; Hyperparathyroidism as the cause of hyperaminoaciduria and phosphaturia in human vitamin D deficiency.
Functional hypoparathyroidism in infantile hypocalcaemic stage I vitamin D deficiency rickets. S Afr Med J. Hyperphosphataemic rickets in an Asian infant. Vitamin D deficiency masquerading as pseudohypoparathyroidism type 2. J Assoc Physicians India. Pseudohypoparathyroidism presenting with bony deformities resembling rickets.
Vitamine D against diabetes type 1 - Diabetes Type 1 is curable!
Vitamin D verbessert die Insulinsensitivität und -sekretion im peripheren Gewebe . Das konnte im Muskel, in der Leber und an den Betazellen des Pankreas. Mit einem gesunden Vitamin D-Spiegel reduzieren Sie Ihr Diabetes Risiko! L. u.a.: Vitamin D Deficiency in Obese Children and Its Relationship to Glucose. Vitamin D (Calciferol) ist in den letzten Jahren stark in den Mittelpunkt des gesundheitlichen Tai K, et al: Vitamin D, glucose, insulin, and insulin sensitivity .