Severe Hypocalcemia as an Unexpected Trigger for Psoriasis Exacerbation in Chronic Hypoparathyroidism: A Case Report

Abstract

Hypoparathyroidism-induced hypocalcemia represents a rare cause for psoriasis exacerbation through various mechanisms including disruption of calcium-dependent keratinocyte differentiation and proliferation pathways. Epidermal barrier function and normal keratinization processes are normally maintained by normal calcium levels, where its deficiency can end in abnormal inflammatory processes and impaired skin homeostasis. We present a 52-year-old Egyptian male with chronic post-surgical hypoparathyroidism who developed severe psoriatic plaques during periods of profound hypocalcemia (7.2 mg/dL). Marked improvement of skin lesions as well as normalization of calcium levels were achieved through psoriasis therapy along with aggressive calcium, demonstrating the therapeutic importance of addressing underlying metabolic abnormalities in dermatological conditions, especially psoriasis.

Introduction

Psoriasis is a chronic autoimmune dermatosis that affects genetically susceptible people and is triggered by environmental factors and immune disorders. Such triggers might include drugs, infections, and electrolyte disorders. It is characterized by the formation of inflammatory plaques on the skin, histologically described as cutaneous inflammation, increased epidermal proliferation, hyperkeratosis, angiogenesis, abnormal keratinization, shortened maturation time, and parakeratosis.

Calcium and vitamin D play important roles in the pathogenesis of psoriasis. Calcium regulates keratinocyte differentiation, proliferation, and barrier function, while vitamin D deficiency is associated with increased inflammation and severity of psoriasis.^1,2

Adult hypoparathyroidism is caused mainly by surgical complications, especially following thyroidectomy, with the risk of severe hypocalcemia. Its presentation may be asymptomatic or associated with several types of clinical features that appear abruptly or chronically.^3,4 Acute hypocalcemia is marked by tetany resulting from heightened neuromuscular irritability. However, many other manifestations have been attributed to hypocalcemia, including psoriasis by further disrupting calcium homeostasis and depleting active vitamin D.^5,6

Here, we present a case of psoriasis triggered by severe hypocalcemia secondary to hypoparathyroidism successfully treated with aggressive calcium reposition.

Case Presentation

A 52-year-old Egyptian male with a 10-year history of hypoparathyroidism secondary to thyroidectomy for papillary thyroid carcinoma was admitted due to multiple, itchy, dry, erythematous plaques involving his scalp, elbows and knees. He also complained of increased muscle cramps, tingling sensations in his hands and feet. For the past 2 months his hypoparathyroidism was managed with calcium and Vitamin D supplementations. There was no significant family history of autoimmune diseases.

His vitals were stable. On examination, the patient had multiple erythematous plaques with silvery scales on the scalp, elbows, and knees with some areas exhibiting fissuring. He exhibited positive Chvostek’s sign, hyperreflexia, and mild tenderness in proximal muscles.

Laboratory investigations of CBC, liver, and renal function tests were normal. His total calcium, ionized calcium levels were found to be low with undetectable parathyroid hormone (PTH) levels, while high phosphate levels confirm hypoparathyroidism. He was also Vitamin D deficient. Total calcium was 7.2 mg/dL (normal range 8.5-10.5 mg/dL), ionized calcium was 3.5 mg/dL (normal range 4.6-5.3 mg/dL), PTH < 10 pg/mL (normal range 10-60 pg/mL), phosphate was 4.8 mg/dL (normal range 2.5-4.5 mg/dL), and 25-hydroxyvitamin D was 15 ng/mL (normal range > 30 ng/mL). Laboratory results are shown in Table 1.

Table 1.

Laboratory Results Upon Admission.

Lab test	Result	Normal range	Comments
Calcium (total)	7.2 mg/dL	8.5-10.5 mg/dL	Hypocalcemia indicative of hypoparathyroidism.
Ionized calcium	3.5 mg/dL	4.6-5.3 mg/dL	Low ionized calcium supports diagnosis.
Phosphate	4.8 mg/dL	2.5-4.5 mg/dL	Hyperphosphatemia due to low PTH levels.
Parathyroid hormone (PTH)	<10 pg/mL	10-65 pg/mL	Undetectable PTH confirms hypoparathyroidism.
25-hydroxyvitamin D	15 ng/mL	>30 ng/mL	Vitamin D deficiency noted; contributes to symptoms.
Complete blood count (CBC)	Normal	Normal ranges for all parameters	No evidence of anemia or infection.
Liver function tests	Normal	Normal ranges	No hepatic dysfunction indicated.
Renal function tests	Normal	Normal (eg, Creatinine: 0.7-1.2 mg/dL)	Adequate renal function.

The skin biopsy confirmed the diagnosis of psoriasis and neck ultrasound revealed no residual thyroid or parathyroid tissue.

In view of hypoparathyroidism, the patient was placed on 2000 mg/day Calcium Carbonate, 1 mcg/day Calcitriol, and 400 mg/day Magnesium supplementation along with psoriasis treatment regimen which included clobetasol propionate twice daily, 15 mg/week of methotrexate with folic acid supplementation and narrowband UBV therapy twice weekly.

Four weeks later, his serum calcium increased from 7.2 to 8.5 mg/dL, phosphate levels normalized, and psoriatic lesions showed significant improvement with reduced scaling and erythema. Eight weeks later, serum calcium stabilized at 9.0 mg/dL, and psoriasis lesions had improved dramatically. The patient reported decreased muscle cramps and improved quality of life.

Discussion

Relationship Between Hypoparathyroidism and Psoriasis

This 52-year-old male patient had moderate to severe plaque psoriasis on the scalp and extensor surfaces concurrently with chronic hypoparathyroidism. Although only 2% to 4% of the population are affected by psoriasis, this specific association with hypoparathyroidism has been reported to be extremely rare. Hypoparathyroidism causes both hypocalcemia and low 1,25-dihydroxyvitamin D levels as parathyroid hormone (PTH) is needed for both renal production of 1,25-dihydroxyvitamin D and for the stimulation of calcium reabsorption in kidneys and bones. ⁷ Calcium homeostasis is essential for keratinocyte differentiation and epidermal barrier integrity. In normal epidermis, a steep calcium gradient should be present; this is achieved by the presence low calcium levels in the basal layer promote proliferation, and high levels in suprabasal layers that in turn trigger the activation of the calcium-sensing receptor (CaSR) and transient receptor potential canonical (TRPC) channels to increase intracellular calcium and drive terminal differentiation. However, in psoriasis, this gradient is disrupted and psoriatic keratinocytes exhibit reduced capacitive calcium influx and down-regulation of the TRPC channels. ⁸ CaSR has been identified as a psoriasis susceptibility gene and its deletion in keratinocytes may lead to decreased epidermal proliferation and impaired differentiation. ⁹

On the other hand, the binding of 1,25-dihydroxyvitamin D to the vitamin D receptor (VDR) in keratinocytes and immune cells results in differentiation promotion, IL-2, IL-6 suppression, interferon-γ production and the induction of regulatory T cells. ¹⁰ Formisano et al in a recent Meta-analyzes, showed that patients with psoriasis have significantly lower circulating 25-hydroxyvitamin D levels than controls with a mean difference ≈ 6.3 ng mL⁻¹. ¹¹ Moreover, hypoparathyroidism results in decreased renal 1α-hydroxylase activity, exacerbating vitamin D deficiency and depriving keratinocytes of this differentiation signal. Despite a lack of consistent clinical benefit of oral vitamin D supplementation in psoriasis as mentioned by Jenssen et al the severe deficiency in our patient likely contributed to psoriatic exacerbation. ¹²

Role of Parathyroid Hormone and Calcium in Immune Regulation

Most studies on psoriasis have documented increased PTH levels in psoriatic patients relative to healthy controls; PTH levels correlate with psoriasis area and severity index (PASI) scores and decline after treatment. ⁹ Elevated PTH levels may stimulate key drivers of psoriatic inflammation like Th17 cell differentiation and IL-17 production. Severe hypocalcemia can itself activate immune responses through several pathways; low extracellular calcium and vitamin D deficiency increase keratinocyte secretion of antimicrobial peptides and cytokines, thus amplifying recruitment of neutrophils and dendritic cells as well as promoting the IL-23/IL-17 axis. ¹³ The positive feedback loop between keratinocytes and immune cells leads to angiogenesis and persistent plaques. Correction of hypocalcemia may therefore reduce keratinocyte-derived cytokines and bring an end to this inflammatory loop. In the Sri Lankan case series of primary hypoparathyroidism with psoriasis, serum calcium was normalized with intravenous calcium and vitamin D within days and psoriatic lesions improved within 2 weeks. ¹⁴

Treatment Considerations

Our patient received phototherapy and systemic methotrexate because topical corticosteroids alone were insufficient. According to recent guidelines, systemic therapy is indicated when psoriasis affects more than 10% of the body surface area or significantly impairs quality of life. ¹⁵ Narrow-band ultraviolet B (NB-UVB) phototherapy 3 times weekly was reported to be effective in clearing thin plaques and also increasing cutaneous vitamin D synthesis, but the fact that it requires frequent clinic visits and makes it carry a theoretical risk of skin cancer. ¹⁵

Oral methotrexate (10-20 mg/week with folic acid) is a conventional systemic agent that inhibits dihydrofolate reductase, reduces keratinocyte proliferation and suppresses T-cell activation; roughly 60% of patients achieve significant improvement. ¹⁵ Biologic therapies targeting tumor necrosis factor-α or IL-17/IL-23 pathways offer higher efficacy but were not pursued in this case because the patient responded to methotrexate and phototherapy. Importantly, all psoriatic treatments must be used alongside the normalization of serum calcium, magnesium and 25-hydroxyvitamin D levels. In our case, raising serum calcium to 9.0 mg dL⁻¹ with calcium carbonate, calcitriol and magnesium supplementation coincided with marked regression of plaques and reduced muscle cramps, supporting the hypothesis that hypocalcemia exacerbated the disease.

Review of Similar Reported Cases

Several case reports have documented the co-occurrence of psoriasis flares and hypocalcemia due to hypoparathyroidism; underscoring the pivotal role of calcium homeostasis in both immune and epidermal regulation. Early reports from the 1960s through to the most recent in 2025 have shown that the normalization of calcium alone has led to substantial improvement in psoriatic or pustular psoriasis, regardless of whether the underlying cause of hypoparathyroidism was primary or postoperative.^{16 -20} In contrast to many of the previously published cases, where substantial improvement of psoriatic lesions was noted following the normalization of calcium alone, our patient required concurrent systemic therapy (methotrexate) and NB-UVB phototherapy along with correction of hypocalcemia. This suggests that when psoriasis is long-standing or more deeply established, hypocalcemia could act as an exacerbating factor rather than the primary driver of the disease activity. That being the case, metabolic correction with psoriasis-specific therapy should be considered essential, but not necessarily sufficient in the management of chronic plaque psoriasis associated with hypoparathyroidism.

Limitations

This case has many limitations. The lack of pre- and post- treatment photographs limits the ability to observe and quantify improvement. Furthermore, the short follow-up period prohibits the interpretation of long-term outcomes and recurrence. The patient received both concurrent systemic and phototherapy treatments along with calcium normalization, making it difficult to isolate the individual effect of each intervention. Despite these limitations, this case highlights a plausible link between calcium homeostasis and psoriatic activity, thereby contributing to the growing body of literature.

Conclusion

This case demonstrates how persistent hypocalcemia, as in cases of chronic hypoparathyroidism and active vitamin D deficiency, can eventually lead to psoriasis and complicate its management. The simultaneous correction of mineral imbalances and the initiation of systemic psoriasis therapy has led to a marked improvement in our patient underscoring the need to recognize and address endocrine comorbidities in psoriasis. Further studies are warranted to clarify whether the optimization calcium and vitamin D status can serve as a therapeutic adjunct in psoriasis.