Vitamin D Chest Pain
Vitamin D is integral for bone health, and severe deficiency can cause rickets in children and osteomalacia in adults. Although osteomalacia can cause severe generalized bone pain, there are only a few case reports of chest pain associated with vitamin D deficiency. We describe 2 patients with chest pain that were initially worked up for cardiac etiologies but were eventually diagnosed with costochondritis and vitamin D deficiency. Vitamin D deficiency is known to cause hypertrophic costochondral junctions in children ("rachitic rosaries") and sternal pain with adults diagnosed with osteomalacia. We propose that vitamin D deficiency may be related to the chest pain associated with costochondritis. In patients diagnosed with costochondritis, physicians should consider testing and treating for vitamin D deficiency.
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Case Reports in Medicine
Volume 2012, Article ID 375730, 3 pages
doi:10.1155/2012/375730
Case Report
Chest Pain and Costochondritis Associated with
Vitamin D Deficiency: A Report of Two Cases
Robert C. Oh and Jeremy D. Johnson
Department of Family Medicine, Tripler Army Medical Center, Honolulu, HI 96859, USA
Correspondence should be addressed to Robert C. Oh, roboh98@gmail.com
Received 5 February 2012; Accepted 4 March 2012
Academic Editor: Mohamud Daya
Copyright © 2012 R. C. Oh and J. D. Johnson. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
Vitamin D is integral for bone health, and severe deficiency can cause rickets in children and osteomalacia in adults. Although
osteomalacia can cause severe generalized bone pain, there are only a few case reports of chest pain associated with vitamin D
deficiency. We describe 2 patients with chest pain that were initially worked up for cardiac etiologies but were eventually diagnosed
with costochondritis and vitamin D deficiency. Vitamin D deficiency is known to cause hypertrophic costochondral junctions in
children ("rachitic rosaries") and sternal pain with adults diagnosed with osteomalacia. We propose that vitamin D deficiency may
be related to the chest pain associated with costochondritis. In patients diagnosed with costochondritis, physicians should consider
testing and treating for vitamin D deficiency.
1. Introduction
Chest pain is a leading cause of ambulatory visits and ac-
counts for over 6 million emergency room visits in the United
States [1 ]. After serious cardiopulmonary conditions are
considered, musculoskeletal causes of chest pain, including
costochondritis, are commonly attributed to the final diag-
nosis [2 ,3 ]. Costochondritis is not clearly understood, but
may be related to inflammation of the costochondral
junctions associated with illness, coughing, or trauma [3 ].
Although there are a few reports of osteomalacia and vitamin
D deficiency associated with chest pain [4– 6 ], we are not
aware of any literature reports of costochondritis associated
with vitamin D deficiency. This paper describes two cases
of patients with chest pain, eventually diagnosed with
costochondritis and vitamin D deficiency.
2. Cases
Case 1. A 35-year-old white female presented to the family
medicine clinic in Hawaii with complaints of chronic chest
pain for the last 3 years. She recently moved from North-
ern Virginia to Hawaii. Chart review was notable for a
negative cardiac workup, including a treadmill stress test,
and echocardiogram. Over the last 3 years, the diagnoses
of her chest pain included anxiety, esophageal reflux, and
costochondritis. In Hawaii, her exam was remarkable only
for tenderness to palpation over the left and right costo-
chondral junctions. Since she reported very little milk intake
or sun exposure, a serum 25-OH Vitamin D (25-OHD)
level was obtained and returned at 42 nmol/L (17 ng/mL),
consistent with deficiency. She was started on Vitamin D,
1000 international units (IU) daily. On 3-month followup,
her repeat serum 25-OHD was 72 nmol/L (29 ng/mL) and
she had complete resolution of her chest pain.
Case 2. A 42-year-old Asian female with historcarotid Dop-
pley of hypertension and hyperlipidemia presented to a
Hawaii emergency department with complaints of substernal
chest pain. She was admitted to the hospital for a rule-
out myocardial infarction protocol. In the hospital, she was
found to have marked tenderness along the left costochon-
dral junction. She did not routinely drink milk and despite
living in Hawaii, she reported little sun exposure due to
her work hours. After ruling out for myocardial infarction,
she was discharged with followup for a treadmill stress test,
which was normal. Prior to her discharge, a serum 25-
OHD level was drawn to rule out vitamin D deficiency.
2 Case Reports in Medicine
On followup, her vitamin D level returned 27 nmol/L
(11 ng/mL) and she continued to report chest pains. She was
started on oral Vitamin D2 50,000 IU once a week for 8 weeks
and maintained on 1,000 IU a day thereafter. Repeat 25-OHD
level 2 months later was 82 nmol/L (33 ng/mL). Her chest
pain resolved with treatment.
3. Discussion
In this paper, both patients had extensive workups done
with concern for cardiac disorders but were eventually di-
agnosed with costochondritis and vitamin D deficiency. We
hypothesize that these patients' costochondritis may have
been related to vitamin D deficiency. Vitamin D is integral
for bone health, and serum 25-OH vitamin D (25-OHD) is
predictive for body stores of vitamin D [7– 9 ]. While there
is controversy over what defines deficient or optimal serum
levels of 25-OHD, levels less than 50nmol/L (20 ng/mL)
lead to increase in bone turnover markers and increase in
parathyroid hormone (PTH) [10 ]. Another study found that
defective bone mineralization was evident in patients with
serum 25-OHD less than 75 nmol/L (30 ng/mL) but none
above that threshold [11]. The recent Institute of Medicine
report found evidence that a serum 25-OHD level above
50 nmol/L (20 ng/mL) is generally suffi cient for bone health
for 97.5% of the population. Hence, a 25-OHD level less
than 50 nmol/L (20 ng/mL) is generally considered consistent
with vitamin D deficiency [7 ,8 ]. Severe vitamin D deficiency,
defined as a 25-OHD less than 25 nmol/L (10 ng/mL), can
cause rickets in children and osteomalacia in adults [12 ].
Rickets classically causes "bow legs" or "knock-knees" due
to disordered growth along weight-bearing bone. "Rachitic
rosaries" describes hypertrophied costochondral junctions in
relation to defective mineralization [13 ,14 ]. Osteomalacia,
the adult version of rickets, can cause diff use bone pain.
Tenderness to the anterior tibia, sternum, and costochondral
joints can indicate osteomalacia and vitamin D deficiency
[14 ,15 ]. Although bone biopsy is the gold standard for
osteomalacia, it is not generally practiced. Bone pain and
vitamin D levels less than 25 nmol/L (10 ng/mL) are often
suffi cient for the clinical diagnosis of osteomalacia.
Although both patients did not have had levels less than
25 nmol/L (10 ng/mL) to suggest osteomalacia, we theorize
that milder forms of vitamin D deficiency can cause a
spectrum of pain along the sternum and costochondral
junctions similar to patients with rickets and osteomala-
cia. Costochondritis continues to be a poorly defined entity
but may represent a milder, earlier form of osteomalacia
associated with higher serum 25-OHD levels. Importantly,
osteomalacia and vitamin D deficiency may not be consid-
ered when a patient presents with complaints consistent with
costochondritis, as testing for vitamin D deficiency in these
patients has not been reported, nor is it routine.
A review of the literature revealed no reported cases of
costochondritis associated with vitamin D deficiency, and
only a few case reports of chest pain associated with vitamin
D deficiency. One case described chronic chest and leg
pain of 2 years duration in a 34-year-old female [4 ]. After
two years of conservative treatment with anti-inflammatory
medications, she was eventually diagnosed with osteomalacia
associated with aluminum-containing antacid use. Alumi-
num containing antacids may cause osteomalacia by binding
to phosphate, causing a negative phosphate balance and
eventual disordered bone growth. However, there was no
serum 25-OH vitamin D (25-OHD) level measured to sup-
port the diagnosis of osteomalacia. She improved with vita-
min D supplementation and decreased antacid use. Another
case reported a 37-year-old Indian living in Germany who
was subsequently diagnosed with vitamin D deficiency and
osteomalacia. Chest pain was the only presenting symptom.
His 25-OHD level was undetectable. He was started on
high-dose vitamin D and then maintenance vitamin D with
resolution of his chest pain [5 ]. Lastly, a 21-year-old Turkish
female living in Germany presented with left-sided chest
pain with unremarkable electrocardiogram, troponin and
d-dimer [6 ]. Her 25-OHD level was 9 nmol/L (4 ng/mL),
and she was diagnosed with osteomalacia causing her chest
pain. Treatment with vitamin D, calcium, and calcitonin
resolved her symptoms in two months. These case reports are
suggestive of osteomalacia and severe vitamin D deficiency
as the cause of chest pains. It is possible that the spectrum of
bone pain, including costochondritis, may be correlated to
the degree of vitamin D deficiency.
In our paper, both patients were at significant risk for
vitamin D deficiency despite living in an area with abundant
sunshine. Vitamin D can only be obtained through ultravi-
olet light exposure, vitamin-D-rich foods, and supplementa-
tion. Both patients reported little to no milk intake, no other
vitamin supplementation, and little sun exposure, putting
them at high risk for deficiency. The IOM recently increased
the recommended daily allowance (RDA) of vitamin D
for adults from 400 IU to a minimum of 600 IU in order
to maintain 25-OHD levels above 50nmol/L (20 ng/mL)
for 97.5% of the population [7 ]. However, other expert
recommendations have suggested much higher levels of
vitamin D, ranging from 400 to 2000 IU daily to maintain
adequate serum 25-OHD; depending on risk factors present
[8 ,9 ]. Sun exposure can provide the most e ffi cient means
of maintaining vitamin D stores; however, dark-skinned
individuals absorb less ultraviolet radiation from sunlight
and thus convert less 7-dehydrocholesterol into vitamin D.
People living at higher latitudes are at increased risk for
deficiency, but studies show that even in areas with adequate
sunshine, vitamin D deficiency can be highly prevalent [16 ,
17].
Our paper has clear limitations. With prevalence of
vitamin D deficiency reported to be up to 36% in young
adults [12 ], costochondritis may be merely an unrelated
association. However, with treatment of deficiency and
normalization of their serum vitamin D, both patients' cos-
tochondritis improved, further supporting vitamin D defi-
ciency as a potential cause of their costochondritis. The
improvement of symptoms may also be attributed to self-
limited costochondritis rather than the vitamin D sup-
plementation. However, it is notable that once adequate
treatment was initiated, no further cases of chest pains have
been reported—including the patient who had 3 years of
chronic chest pain. This further strengthens our hypothesis
Case Reports in Medicine 3
that vitamin D deficiency may be a cause of costochondritis.
We recommend further prospective studies, specifically in
primary care, to help elucidate the association of vitamin D
deficiency and costochondritis.
4. Conclusion
In patients with costochondritis, or bony sternal pain, physi-
cians should consider vitamin D deficiency and osteomalacia
and elicit any risk factors for deficiency. Patients with
costochondritis who are at risk for vitamin D deficiency
shouldbetestedwithaserum25-OHDlevelandtreatedif
found to be vitamin D deficient. Studies looking further at
the association of costochondritis and vitamin D deficiency
are warranted.
Conflict of Interests
The authors declare no conflict of interests.
Disclaimer
The views expressed in this manuscript are those of the
authors and do not reflect the offi cial policy or position of
the Department of the Army, Department of Defense, or the
U.S. Government.
Disclosure
This paper was presented as an oral case presentation at the
Uniformed Services Academy of Family Physicians Annual
Conference, New Orleans, LA, February 2010.
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... Etyopatogenezi tam olarak bilinmemekle birlikte minör travmalar, tekrarlayan öksürük ve postviral enfeksiyonların rol aldığı düşünülmektedir (4). Literatürde D vitamini eksikliğine bağlı mineralizasyonun bozulması da etkili olabilir (6). Acil servislere göğüs ağrısı ile başvuran hastaların yaklaşık %30' unu oluşturmaktadır (7). ...
-
![Fatih Bağcıer]()
GİRİŞ Göğüs ağrısı, dünya çapında en yaygın tıbbi yardım alma nedenlerinden birisi olarak bilinmektedir (1). Birinci basamak sağlık kuruluşlarına gelen hastaların %1 ile %3'ünü bu şikayet ile gelen hastalar oluşturur. Bu başvuruların hemen hemen yarısı kas iskelet sistemi ile ilişkili hastalıklardan kaynaklanan göğüs ağrısıdır (2). Kardiyovasküler, pulmoner, gastroenterolojik nedenli ve psikojenik faktörler de göğüs ağrısına neden olabilirler. Ayrıca omuz eklem ku-şağındaki patolojiler, servikal, torakal omurga ve diyafram alt bölgesi anatomik yapılarındaki olası patolojiler göğüs bölgesine yansıyan ağrıya neden olabilir (3). Göğüs ağrısının nedenleri arasında kalp, akciger ve ozefagus gibi intratorasik yapilar olabilir. Kalp gibi torakal bölge lokalizasyonlu yapilardaki agriyi ileten serbest sinir uc-lari, ayni seviyede spinal kord dorsal boynuzda cilt, kas ve eklemlerden afferent uyariyi alan internöronlarla sinaps yapar. Visseral ve somatik ağrı yollarinin aynı internoronda birleşmesi nedeniyle viseral ağrı visseral bölgeden uzak somatik alanlarda yansıyan agrıya neden olur (3). Bu nedenle, göğüs ağrısının nedeninin kas-iskelet sistemi kaynaklı mı ya da visseral bir organ kökenli mi olduğunu kesin olarak tanımlamak zor olabilir. Bu nedenle göğüs ağrısı tanısı ile başvuran olgularda kas iskelet sistemi kaynaklı ol-duğu düşünülmeden önce olası diğer nedenlerin ekarte edilmesi gereklidir (3,4). Örneğin anjinal ağrı, lokalizasyon olarak bu ağrının yayılım paternini etkileyebi-lecek olan kostokondrit veya subakromiyal bursit ile birlikte ortaya çıkabilir. Bu nedenle orta ve ileri yaşlı hastalarda eğer kalp hastalıkları ile ilişkili güçlü risk fak-törleri varsa öncelikle elektrokardiyogram, ekokardiyografi gibi tetkiklerle değer-22 Uzman Doktor, Kars Harakani Devlet Hastanesi,
... Seasonal variations correspond with varying pain levels as well [6]. Vitamin D deficiency has been associated with headache, abdominal, knee, and back pain, persistent musculoskeletal pain, costochondritic chest pain, and failed back syndrome and with fibromyalgia [6,45,[53][54][55][56][57][58][59]. ...
The emergence of new data suggests that the benefits of Vitamin D extend beyond healthy bones. This paper looks at Vitamin D and its role in the aetiology and maintenance of chronic pain states and associated comorbidities. The interfaces between pain and Vitamin D and the mechanisms of action of Vitamin D on pain processes are explored. Finally the association between Vitamin D and pain comorbidities such as sleep and depression is investigated. The paper shows that Vitamin D exerts anatomic, hormonal, neurological, and immunological influences on pain manifestation, thereby playing a role in the aetiology and maintenance of chronic pain states and associated comorbidities. More research is necessary to determine whether Vitamin D is useful in the treatment of various pain conditions and whether or not the effect is limited to patients who are deficient in Vitamin D.
Background: In children, vitamin D deficiency can result in the hypertrophy of costochondral junctions and sternal pain. Objectives: In this study, we aimed at determining the correlation between children's vitamin D status and costochondritis. Methods: This cross-sectional study included a control group (100 healthy children) and a study group (100 children with costochondritis). Examination of patients included chest radiography, physical examination, history-taking, electrocardiography, echocardiography, and serum measurement of 25-hydroxyvitamin D, phosphorus, calcium, and alkaline phosphatase. The Chi-square test, Spearman's correlation test, and independent samples t-test were also performed for analyzing the data. Results: The groups showed no significant difference regarding age, gender, or body mass index (P = 0.315, P = 0.671, and P = 0.097, respectively). The history of patients experiencing idiopathic chest pain showed cardiac disease in 13% of their families, without report of death in the family. The pain was mainly located in the left precordium (64%), followed by the right precordium and the midsternal region (32% and 18%, respectively). A significantly lower level of 25-OHD was found in the study group than in the control group (P < 0.0001). Based on the findings, the groups were not significantly different regarding the evaluated biochemical parameters, except for alkaline phosphatase (P = 0.007). The results showed that pain duration and episodes were significantly associated with vitamin D insufficiency (r = -0.621, P = 0.002; r = -0.213, P = 0.021, respectively). Conclusions: Vitamin D insufficiency should be considered in costochondritis. Also, pain duration and episodes have associations with vitamin D insufficiency. This finding emphasizes the necessity of evaluating nutritional parameters in children with non-cardiac chest pain.
- Bin Zhang
- Ying Jiang
- Chun-Song Cheng
- You-ping Guo
Costochondritis (ChC), especially chronic ChC, typically manifests as spontaneous vague pain in anterior chest area and often occurs in adolescents for unknown reasons; it has prevented many collegiate athletes from participating in physical training and competitions. A 21-year-old female collegiate taekwondo athlete suffering from chronic chest pain was sent by her coaches for diagnosis and treatment. Seated motion palpation was used to identify spontaneous and motion-involved pain areas. Palpation in the supine position was used to initially rule out breast diseases. X-ray, electrocardiogram, and cardiac Doppler ultrasound were used in conjunction with myocardial enzyme testing to rule out lung and cardiovascular diseases. The patient was treated using herbal medicines applied via an external patch. The medicine was comprised of Rhizoma Corydalis and borneol, and the treatment lasted for seven weeks. For five weeks patches were applied at a frequency of two or three times per day, followed by a two-week period of once per day. The patient reported that the pain was relieved after two weeks of external herb use, and the autonomic chest pain had resolved. Re-examination after one month showed that her upper limb range of motion was close to normal, and her psychological burden had almost disappeared. It is possible to seek more active medicinal treatment and more practical external products for young athletes who is suffering chronic ChC that affects the sport training and competitive performances. Please cite this article as: Zhang B, Jiang Y, Cheng CS, Lin H, Guo YP. External application of two unrestricted herbal medicines to treat costochondritis in a young collegiate athlete: A case report. J Integr Med. 2020; Epub ahead of print.
Osteomalacia is a bone disease, characterized by the inability of newly formed bone matrix to undergo mineralization. The most common symptoms are generalized bone pain and widespread body pain, while some patients are asymptomatic. Restless leg syndrome (RLS) is a sensory-motor neurological disease. The main symptoms are abnormal sensations in the legs and dysesthesia. Symptoms worsen at night and affect sleep quality. We present a case of a woman with a progressive hip and feet pain. Many biochemical, clinical, and radiological tests were performed for diagnosis. All were found to be normal. The patient was diagnosed as having RLS. 0.25 mg pramipexole was given for treatment. Patient symptoms patient escalated over six months. The patient was reassessed after six months. Vitamin D levels had not been previously examined. We found low vitamin D and calcium levels, as well as pseudofractures in radiography. The diagnosis was changed to osteomalacia. Vitamin D and calcium treatment were started. Symptoms began to regress from the first week of treatment.
- Amba Ayloo
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![Teresa Cvengros]()
- Srimannarayana Marella
This article summarizes the evaluation and treatment of musculoskeletal causes of chest pain. Conditions such as costochondritis, rib pain caused by stress fractures, slipping rib syndrome, chest wall muscle injuries, fibromyalgia, and herpes zoster are discussed, with emphasis on evaluation and treatment of these and other disorders. Many of these conditions can be diagnosed by the primary care clinician in the office by history and physical examination. Treatment is also discussed, including description of manual therapy and exercises as needed for some of the conditions.
- Th. Mosimann
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![Christian Meier]()
Wir stellen eine 21-jährige aus der Türkei stammende muslimische Patientin mit atypischen links-thorakalen Schmerzen vor. Klinisch und laborchemisch konnte die Diagnose einer Osteomalazie aufgrund mangelnder Sonnenexposition u.a. wegen traditioneller Kleidung gestellt werden. Unter Vitamin-D- und Kalziumsubstitution normalisierten sich sowohl Klinik als auch das Labor. Bei muslimisch gekleideten Frauen mit Knochenschmerzen sollte an eine Osteomalazie gedacht werden. Ob prophylaktisch eine Vitamin-D- und Kalziumsubstitution durchgeführt werden sollte, wird in der Literatur kontrovers diskutiert und kann u.a. von der anamnestisch erhobenen täglichen Kalziumaufnahme der Patientin abhängig gemacht werden.
Lack of sun exposure is widely accepted as the primary cause of epidemic low vitamin D status worldwide. However, some individuals with seemingly adequate UV exposure have been reported to have low serum 25-hydroxyvitamin D [25(OH)D] concentration, results that might have been confounded by imprecision of the assays used. The aim was to document the 25(OH)D status of healthy individuals with habitually high sun exposure. This study was conducted in a convenience sample of adults in Honolulu, Hawaii (latitude 21 degrees ). The study population consisted of 93 adults (30 women and 63 men) with a mean (sem) age and body mass index of 24.0 yr (0.7) and 23.6 kg/m(2) (0.4), respectively. Their self-reported sun exposure was 28.9 (1.5) h/wk, yielding a calculated sun exposure index of 11.1 (0.7). Serum 25(OH)D concentration was measured using a precise HPLC assay. Low vitamin D status was defined as a circulating 25(OH)D concentration less than 30 ng/ml. Mean serum 25(OH)D concentration was 31.6 ng/ml. Using a cutpoint of 30 ng/ml, 51% of this population had low vitamin D status. The highest 25(OH)D concentration was 62 ng/ml. These data suggest that variable responsiveness to UVB radiation is evident among individuals, causing some to have low vitamin D status despite abundant sun exposure. In addition, because the maximal 25(OH)D concentration produced by natural UV exposure appears to be approximately 60 ng/ml, it seems prudent to use this value as an upper limit when prescribing vitamin D supplementation.
The objective was to provide guidelines to clinicians for the evaluation, treatment, and prevention of vitamin D deficiency with an emphasis on the care of patients who are at risk for deficiency. The Task Force was composed of a Chair, six additional experts, and a methodologist. The Task Force received no corporate funding or remuneration. Consensus was guided by systematic reviews of evidence and discussions during several conference calls and e-mail communications. The draft prepared by the Task Force was reviewed successively by The Endocrine Society's Clinical Guidelines Subcommittee, Clinical Affairs Core Committee, and cosponsoring associations, and it was posted on The Endocrine Society web site for member review. At each stage of review, the Task Force received written comments and incorporated needed changes. Considering that vitamin D deficiency is very common in all age groups and that few foods contain vitamin D, the Task Force recommended supplementation at suggested daily intake and tolerable upper limit levels, depending on age and clinical circumstances. The Task Force also suggested the measurement of serum 25-hydroxyvitamin D level by a reliable assay as the initial diagnostic test in patients at risk for deficiency. Treatment with either vitamin D(2) or vitamin D(3) was recommended for deficient patients. At the present time, there is not sufficient evidence to recommend screening individuals who are not at risk for deficiency or to prescribe vitamin D to attain the noncalcemic benefit for cardiovascular protection.
This article summarizes the new 2011 report on dietary requirements for calcium and vitamin D from the Institute of Medicine (IOM). An IOM Committee charged with determining the population needs for these nutrients in North America conducted a comprehensive review of the evidence for both skeletal and extraskeletal outcomes. The Committee concluded that available scientific evidence supports a key role of calcium and vitamin D in skeletal health, consistent with a cause-and-effect relationship and providing a sound basis for determination of intake requirements. For extraskeletal outcomes, including cancer, cardiovascular disease, diabetes, and autoimmune disorders, the evidence was inconsistent, inconclusive as to causality, and insufficient to inform nutritional requirements. Randomized clinical trial evidence for extraskeletal outcomes was limited and generally uninformative. Based on bone health, Recommended Dietary Allowances (RDAs; covering requirements of ≥97.5% of the population) for calcium range from 700 to 1300 mg/d for life-stage groups at least 1 yr of age. For vitamin D, RDAs of 600 IU/d for ages 1-70 yr and 800 IU/d for ages 71 yr and older, corresponding to a serum 25-hydroxyvitamin D level of at least 20 ng/ml (50 nmol/liter), meet the requirements of at least 97.5% of the population. RDAs for vitamin D were derived based on conditions of minimal sun exposure due to wide variability in vitamin D synthesis from ultraviolet light and the risks of skin cancer. Higher values were not consistently associated with greater benefit, and for some outcomes U-shaped associations were observed, with risks at both low and high levels. The Committee concluded that the prevalence of vitamin D inadequacy in North America has been overestimated. Urgent research and clinical priorities were identified, including reassessment of laboratory ranges for 25-hydroxyvitamin D, to avoid problems of both undertreatment and overtreatment.
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![David A Hanley]()
- Ann Cranney
- Glenville Jones
- William D Leslie
The 2002 guidelines for the management of osteoporosis published by Osteoporosis Canada1 identified adequate vitamin D status, in addition to calcium from diet or supplements, as essential for the prevention of osteoporosis. Recent large clinical trials and meta-analyses have expanded our knowledge of the role of vitamin D in fractures, falls and other health outcomes, as well as its effect on disorders such as diabetes mellitus, autoimmune and infectious diseases, malignancies and cardiovascular disease. Current Canadian recommendations for "adequate intake" and "tolerable upper level" of vitamin D, which are more than 10 years old, were derived mainly from early nutritional science estimates of the minimal intake necessary to prevent florid deficiency states (rickets or osteomalacia). However, these levels have never been supported by adequately conducted dose-finding studies.2 This review is an update to the 2002 recommendations on vitamin D and is specific for adults, excluding times of pregnancy and lactation.
- M. Schiltknecht
- J. Furrer
Ce travail presente le tableau clinique d'une osteomalacie illustree par l'anamnese, le status et les examens paracliniques d'un patient âge de 37 ans avec des douleurs thoraciques. Cette maladie s'est developpee en raison d'un manque d'exposition au soleil pour des raisons ethniques (port d'une longue barbe et d'un turban en tant que sikh croyant) avec deficit en vitamine D.
- Anne M Proulx
- Teresa W Zryd
Costochondritis, an inflammation of costochondral junctions of ribs or chondrosternal joints of the anterior chest wall, is a common condition seen in patients presenting to the physician's office and emergency department. Palpation of the affected chondrosternal joints of the chest wall elicits tenderness. Although costochondritis is usually self-limited and benign, it should be distinguished from other, more serious causes of chest pain. Coronary artery disease is present in 3 to 6 percent of adult patients with chest pain and chest wall tenderness to palpation. History and physical examination of the chest that document reproducible pain by palpation over the costal cartilages are usually all that is needed to make the diagnosis in children, adolescents, and young adults. Patients older than 35 years, those with a history or risk of coronary artery disease, and any patient with cardiopulmonary symptoms should have an electrocardiograph and possibly a chest radiograph. Consider further testing to rule out cardiac causes if clinically indicated by age or cardiac risk status. Clinical trials of treatment are lacking. Traditional practice is to treat with acetaminophen or anti-inflammatory medications where safe and appropriate, advise patients to avoid activities that produce chest muscle overuse, and provide reassurance.
Parathyroid hormone (PTH) is only one measurable index of skeletal health, and we reasoned that a histomorphometric analysis of iliac crest biopsies would be another and even more direct approach to assess bone health and address the required minimum 25-Hydroxyvitamin D [25(OH)D] level. A cohort from the northern European population with its known high prevalence of vitamin D deficiency therefore would be ideal to answer the latter question. We examined 675 iliac crest biopsies from male and female individuals, excluding all patients who showed any signs of secondary bone diseases at autopsy. Structural histomorphometric parameters, including osteoid indices, were quantified using the Osteomeasure System according to ASBMR standards, and serum 25(OH)D levels were measured for all patients. Statistical analysis was performed by Student's t test. The histologic results demonstrate an unexpected high prevalence of mineralization defects, that is, a pathologic increase in osteoid. Indeed, 36.15% of the analyzed patients presented with an osteoid surface per bone surface (OS/BS) of more than 20%. Based on the most conservative threshold that defines osteomalacia at the histomorphometric level with a pathologic increase in osteoid volume per bone volume (OV/BV) greater than 2% manifest mineralization defects were present in 25.63% of the patients. The latter were found independent of bone volume per trabecular volume (BV/TV) throughout all ages and affected both sexes equally. While we could not establish a minimum 25(OH)D level that was inevitably associated with mineralization defects, we did not find pathologic accumulation of osteoid in any patient with circulating 25(OH)D above 75 nmol/L. Our data demonstrate that pathologic mineralization defects of bone occur in patients with a serum 25(OH)D below 75 nmol/L and strongly argue that in conjunction with a sufficient calcium intake, the dose of vitamin D supplementation should ensure that circulating levels of 25(OH)D reach this minimum threshold (75 nmol/L or 30 ng/mL) to maintain skeletal health.
Source: https://www.researchgate.net/publication/228116366_Chest_Pain_and_Costochondritis_Associated_with_Vitamin_D_Deficiency_A_Report_of_Two_Cases
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