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Innovative Medicines & Omics Vitamin D deficiency and cherry angiomas

for lesions that are numerous, rapidly proliferating, or cherry angiomas. The patient reported the sudden onset
cosmetically concerning. Despite their benign nature, of multiple erythematous, dome-shaped lesions, 2 – 5 mm
sudden eruptions of cherry angiomas have been linked to in diameter, predominantly localized to the breast and
various systemic conditions, underscoring the need for a neck regions (Figure 1). These lesions were asymptomatic

deeper understanding of their pathogenesis and potential but raised concern due to their abrupt appearance and
triggers. 2 clustering, prompting clinical investigation.
Vitamin D, a fat-soluble secosteroid, plays a pivotal role Comprehensive laboratory evaluations were performed
in calcium homeostasis, bone metabolism, and immune to identify potential systemic conditions. A complete blood
regulation. Beyond these traditional roles, Vitamin D count revealed normal values: White blood cell count
exerts broad effects on cellular growth, differentiation, of 6,500/µL (normal: 4,000 – 11,000/µL), hemoglobin
and angiogenesis. Deficiency in Vitamin D, particularly level of 13.8 g/dL (normal: 12 – 15 g/dL), and platelet
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in its severe forms, has been implicated in a range of count of 265,000/µL (normal: 150,000 – 450,000/µL).
dermatological conditions, including psoriasis, eczema, Liver function tests showed aspartate aminotransferase
and delayed wound healing. At a molecular level, Vitamin and alanine aminotransferase levels of 25 U/L and
D regulates gene expression through its active form, 30 U/L, respectively (normal: 10 – 40 U/L and 7 – 56 U/L),
1,25-dihydroxyvitamin D (calcitriol), which binds to the excluding hepatic dysfunction. Renal function tests
Vitamin D receptor (VDR) expressed in various tissues, were within normal limits, with a serum creatinine level
including the skin. Through VDR signaling, Vitamin D of 0.9 mg/dL (normal: 0.6 – 1.2 mg/dL) and blood urea
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modulates pathways that regulate inflammation, immune nitrogen of 15 mg/dL (normal: 7 – 20 mg/dL), ruling out
responses, and endothelial function. Given the established renal impairment. A lipid profile was within normal ranges,
link between Vitamin D and vascular health, it is plausible with total cholesterol at 170 mg/dL (normal: <200 mg/dL),
to hypothesize that severe Vitamin D deficiency could triglycerides at 110 mg/dL (normal: <150 mg/dL), high-
contribute to the development of cherry angiomas. One density lipoprotein at 65 mg/dL (normal: ≥60 mg/dL),
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proposed mechanism involves endothelial dysfunction and and low-density lipoprotein at 90 mg/dL (normal:
increased oxidative stress resulting from impaired VDR <100 mg/dL). Thyroid function tests revealed a thyroid-
signaling. Vitamin D deficiency may disrupt angiogenesis, stimulating hormone level of 2.2 mIU/L (normal: 0.4 –
leading to excessive capillary proliferation and structural 4.0 mIU/L) and free thyroxine at 1.5 ng/dL (normal: 0.8
changes in dermal blood vessels. On a molecular level, – 2.8 ng/dL), excluding thyroid dysfunction. Inflammatory
Vitamin D is known to inhibit pro-angiogenic factors markers, including C-reactive protein at 6 mg/L (normal:
such as vascular endothelial growth factor (VEGF). In the <10 mg/L) and erythrocyte sedimentation rate at 12 mm/h
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context of Vitamin D deficiency, upregulation of VEGF (normal: 0 – 20 mm/h), were also within normal limits,
and other angiogenic mediators may promote capillary ruling out systemic inflammation.
dilation and proliferation, leading to the development of However, serum Vitamin D levels revealed a profound
cherry angiomas. 7
deficiency, measuring 3 ng/mL (normal range: 30
In this report, we present the case of a 27-year-old – 100 ng/mL). This was the only abnormal finding and
married female who experienced a sudden onset of cherry warranted further exploration as a potential contributing
angiomas localized to the breast and neck regions. Clinical factor to the pathogenesis of cherry angiomas. Given the
evaluation and laboratory investigations revealed severe absence of other systemic or local triggers, we hypothesize
Vitamin D deficiency, with serum levels significantly below that the patient’s severe Vitamin D deficiency may have
the normal range. In the absence of other systemic or local contributed to endothelial dysfunction and dysregulated
triggers, we propose that severe Vitamin D deficiency angiogenesis. These mechanisms align with emerging
contributed to their development. This case highlights evidence linking Vitamin D to vascular stability and capillary
a novel hypothesis linking severe Vitamin D deficiency proliferation. Vitamin D plays a crucial role in endothelial
to cherry angiomas through endothelial and angiogenic homeostasis by suppressing pro-angiogenic mediators such
dysregulation. Further studies are warranted to explore as VEGF. A deficiency in Vitamin D may disrupt these
this association on a larger scale and to elucidate the pathways, promoting capillary dilation and proliferation,
underlying molecular mechanisms. which could explain the sudden onset of cherry angiomas in
this patient. This case highlights a novel hypothesis linking
2. Case presentation severe Vitamin D deficiency to the development of cherry

We describe a 27-year-old Arab female with no significant angiomas and underscores the need for further research to
medical history and genetic or familial predisposition to investigate the underlying mechanisms. 8

Volume 2 Issue 2 (2025) 114 doi: 10.36922/imo.8087