Concurrent Hyperparathyroidism and Wilson’s Disease in a Patient With Methanol Toxicity: A Rare Case Report

Abstract

Background:

Wilson’s disease (WD) is a rare genetic disorder that impairs copper metabolism, leading to its deposition in various organs, including the liver, brain, and cornea. Endocrine disorders, particularly hyperparathyroidism, are uncommon in WD. Methanol toxicity, a medical emergency, is rarely associated with WD and hyperparathyroidism, making this case particularly unique. We report a rare instance of this complex triad.

Case Presentation:

A 53-year-old male with untreated WD presented with nausea, vomiting, dizziness, and blurred vision after ingesting methanol. Clinical examination revealed optic neuropathy, consistent with methanol toxicity, despite normal fundoscopy. Laboratory investigations revealed significant hypercalcemia and elevated parathyroid hormone (PTH) levels, confirming hyperparathyroidism. Imaging, including a prior technetium-99m sestamibi scan, indicated hyperfunctioning parathyroid tissue. Dialysis was initiated for methanol toxicity, and metabolic acidosis was corrected.

Conclusion:

This case emphasizes the rare coexistence of WD, hyperparathyroidism, and methanol toxicity, presenting significant diagnostic and therapeutic challenges. The pathophysiological interactions between these conditions are not well understood and warrant further research to improve management strategies and clinical outcomes.

Plain Language Summary

A Rare Case of Copper Metabolism Disorder, High Calcium Levels, and Methanol Poisoning in One Patient

Wilson’s Disease is a rare condition where the body cannot properly remove excess copper, leading to liver and brain problems. High calcium levels due to hyperparathyroidism can cause kidney stones and bone issues. Methanol poisoning, often from contaminated alcohol, is dangerous because it can lead to blindness and organ failure. This case report describes a 53-year-old man who was diagnosed with all three conditions at the same time. He had Wilson’s Disease but had never received treatment. After drinking methanol, he developed nausea, vomiting, and vision problems. While his eye exam appeared normal, doctors diagnosed optic nerve damage, a common complication of methanol poisoning. Blood tests showed high calcium and parathyroid hormone levels, leading to a diagnosis of hyperparathyroidism. We used a multidisciplinary approach to manage his condition, including dialysis to remove toxins and treatments for metabolic imbalances. This case is unique because these three conditions are rarely seen together. Understanding their interactions may help doctors better diagnose and treat patients with similar complex cases in the future.

Keywords

Wilson’s disease hyperparathyroidism methanol toxicity

Background

Wilson’s disease (WD), also known as hepatolenticular degeneration, is a rare autosomal recessive disorder that impairs copper metabolism by affecting the ATPase Copper Transporting Beta gene. Estimated prevalence is between 1:30 000 and 1:50 000 with a broad perspective of hepatic, and neuropsychiatric manifestations.^1,2

Copper ion secretion to the blood can lead to its deposition in the brain, kidney, cornea and other organs as well.³ The diagnosis requires a combination of clinical signs and symptoms, along with serum ceruloplasmin measurement, urinary copper excretion, liver biopsy, or molecular testing. WD is also characterized by low levels of blood copper and ceruloplasmin and increased urinary copper excretion and high levels of copper in the liver.^2,4

Endocrine disorders are rarely associated with WD. Hypoparathyroidism secondary to WD results from parathyroid gland atrophy due to copper deposition. In addition, Chronic copper deposition may lead to parathyroid dysfunction, with hypoparathyroidism due to glandular atrophy or, rarely, hyperplasia, potentially from compensatory mechanisms.^5
-8

Methanol toxicity, caused by ingestion or exposure to methanol-containing substances, is a well-known medical emergency that can lead to severe complications, including metabolic acidosis, visual disturbances, and central nervous system dysfunction. However, the association between methanol toxicity and the simultaneous occurrence of hyperparathyroidism and WD is extremely rare and has not been extensively reported in the medical literature.

In this study, we report a rare case of methanol toxicity in a 53-year-old male with untreated WD and concurrent hyperparathyroidism. The case underscores the unusual coexistence of these conditions, potentially linked to parathyroid hyperplasia from chronic copper deposition, posing significant diagnostic and management challenges. The 4-year treatment gap reflects real-world challenges in WD management. As in Tallis et al’s case,⁹ socioeconomic barriers, particularly chelation therapy costs and asymptomatic early-stage disease often delay intervention,¹⁰ increasing complication risks.

Case Presentation

In September 2022, a 53-year-old male was admitted to our medical department presenting with nausea, vomiting, lethargy, loss of appetite, dizziness, and blurred vision, which he described as black and white. These symptoms developed approximately 4 hours following the accidental ingestion of methanol-containing solvent. The patient reported vomiting 3 times but denied any episodes of diarrhea, abdominal tenderness, cough, or shortness of breath.

The patient’s medical history was notable for fatty liver disease, depression, and a diagnosis of WD 4 years prior. He was non-adherent to chelation therapy due to socioeconomic constraints, despite the confirmed diagnosis. His medication regimen included sertraline 150 mg, propranolol 10 mg, and clonazepam 1 mg daily. His family history was significant for Parkinson’s disease in his mother and diabetes mellitus in his siblings.

Physical examination revealed bilateral mid-sized pupils non-reactive to light, though visual acuity remained unimpaired and fundoscopy was normal. Despite normal fundoscopy, further ophthalmologic assessment revealed optic neuropathy, consistent with methanol toxicity, and a poor visual prognosis (Figure 1).

Figure 1.

Fundoscopic examination revealing optic neuropathy in a 53-year-old male with methanol toxicity and untreated WD.

During his hospital stay, the patient experienced multiple episodes of hematemesis. An esophagogastroduodenoscopy revealed a mucosal tear at the lower esophageal sphincter suggestive of a Mallory-Weiss tear, alongside antral gastritis (Figure 2).

Figure 2.

Esophagogastroduodenoscopy revealed a mucosal tear at the lower esophageal sphincter suggestive of a Mallory-Weiss tear in our patient.

Laboratory investigations at the time of admission showed significant hypercalcemia, prompting a suspicion of hyperparathyroidism. Table 1. Persistent hypercalcemia and elevated PTH levels (197.1 pg/mL) predating acute renal dysfunction by 4 years, alongside prior technetium-99 m sestamibi scan confirmation of parathyroid adenoma, supported primary hyperparathyroidism. A review of prior lab and imaging results from 5 years earlier revealed a total serum calcium of 11.8 mg/dL, elevated alkaline phosphatase (555 U/L), aspartate aminotransferase (127 IU/L), and alanine aminotransferase (145 IU/L), which had initially gone uninvestigated. Further endocrine evaluation identified a PTH level of 197.1 pg/mL 4 years prior, suggesting primary hyperparathyroidism. Also, a parathyroid technetium-99m sestamibi scan confirmed hyperfunctioning parathyroid tissue beneath the left thyroid lobe. Figure 3.

Table 1.

Laboratory Results at Admission.

Category	Test	Patient value	Normal range
ABG parameters	pH	7.23	7.35-7.45
	PCOc (mmHg)	25	35-45
	HCO3¯ (mmol/L)	12.1	23-29
	Base Excess (mmol/L)	−15.4	−3 to +3
	PO2 (mmHg)	26.3	75-100
	Anion Gap (mmol/L)	27.9	4-12
Hematology	WBC (×103/L)	10.7	4.5-11
	RBC (×10¹²/L)	5.06	4.35-5.65
	Neutrophils (%)	85	40-70
	Lymphocytes (×103/L)	10	1.0-4.0
	Hemoglobin (g/dL)	15	7.5-10
	Platelets (×103/L)	313	150-400
	INR	1.1	1.0-1.25
	RDW-CV (%)	15.7	11-14.5
Electrolytes	Sodium (mmol/L)	144	135-145
	Potassium (mmol/L)	5.5	3.5-4.5
	Calcium (mg/dL)	12.2	8.6-10.3
Liver/Kidney function	AST (U/L)	28	0-40
	ALT (U/L)	21	0-34
	LDH (U/L)	320	0-247
	Amylase (U/L)	103	<100
	Urea (mg/dL)	62	15-45
	Uric acid (mg/dL)	3.5	3.6-8.2
	Total protein (g/dL)	9.3	6.6-8.3
	Albumin (g/dL)	5.8	3.5-5
	Creatinine (mg/L)	2.4	0-5
	ALP (IU/L)	583	80-306
	Calcium (mg/dL)	12.2	8.6-10.3
	Glucose (mg/dL)	104	70-100
Thyroid function	Total T3 (μg/dL)	8.7	4.4-12.5
	Total T3 (ng/dL)	69.8	60-220
	TSH (μIU/mL)	0.89	0.4-4.0
Urinalysis	Ketones	Negative	Negative
	Glucose	Negative	Negative
	Protein	Negative	Negative
	Blood	Negative	Negative
	Bilirubin	Negative	Negative
	Nitrite	Negative	Negative
	pH	6	4.6-8

Abbreviations: ALP, alkaline phosphatase; ALT, alanine amino transferase; AST, aspartate amino transferase; CRP, C reactive protein; INR, International Normalized Ratio; LDH, lactate dehydrogenase; PCO₂, partial pressure of carbon dioxide; pH, potential of hydrogen; PO₂, partial pressure of oxygen; RDW-CV, red cell distribution width - coefficient of variation; TSH, thyroid stimulating hormone.

Figure 3.

Technetium-99m sestamibi scan showing persistent radiotracer uptake beneath the left thyroid lobe, suggestive of hyperfunctioning parathyroid tissue from 5 years prior. (A) 15 minutes. (B) 180 minutes.

Pathology results from 5 years earlier further indicated elevated serum glutamic-oxaloacetic transaminase and serum glutamic-pyruvic transaminase levels, measuring 53 and 81 U/L, respectively. The patient also exhibited decreased ceruloplasmin, increased urinary copper excretion, and the presence of a Kayser-Fleischer ring, consistent with WD. A liver needle biopsy at that time revealed mild portal and lobular inflammation, graded as 3 with a stage of 1.

Additionally, investigations for WD revealed a 24-hour urinary copper excretion of 350 µg (reference range: 15-70 µg), a ceruloplasmin level of 38 mg/dL (reference range: 15-60 mg/dL), and a blood copper level of 122 µg/dL (reference range: 70-150 µg/dL). These findings were consistent with untreated WD.

A non-contrast brain MRI showed intra-axial high signal intensity foci in the right frontal lobe (20 × 12 mm) and bilateral occipital lobes (right: 16 and 9 mm; left: 18 mm) on T2 fluid-attenuated inversion recovery, with corresponding signal voids on Apparent Diffusion Coefficient maps, suggestive of acute ischemic infarctions. The MRI also noted a 23 mm retention cyst in the right maxillary sinus. An orbital MRI was unremarkable.

Given the patient’s acute renal dysfunction and hypercalcemia, dialysis was initiated. Despite these interventions, the patient developed leukocytosis and was empirically started on vancomycin (1 g IV every 4 hours).

The concurrence of methanol toxicity, WD, and primary hyperparathyroidism in this patient presents a highly complex and rare clinical scenario, demanding careful consideration in management and treatment strategies.

Following discharge, the patient was scheduled for regular multidisciplinary follow-up. Despite initial non-adherence, he resumed chelation therapy with D-penicillamine and underwent partial parathyroidectomy. At 6-month follow-up, serum calcium had normalized to 9.1 mg/dL, though optic neuropathy remained irreversible. Liver function tests showed improvement (ALT 68 U/L), and 24-hour urinary copper excretion decreased to 150 µg/day. The diagnostic and therapeutic timeline, including key clinical events and findings, is summarized in Table 2.

Table 2.

Diagnostic and Therapeutic Timeline of the Patient.

Year of occurrence	Events	Clinical findings
2017	Initial WD symptoms	Elevated liver enzymes, Kayser-Fleischer ring noted
2018	Hyperparathyroidism diagnosis	Ca²+: 11.8 mg/dL, PTH: 197.1 pg/mL, sestamibi scan confirmed parathyroid adenoma
2022	Methanol toxicity admission	pH: 7.23, AG: 27.9, visual disturbances
2022	Post-discharge	Partial parathyroidectomy, resumed D-penicillamine

Discussion

This case report highlights the exceptionally rare and complex clinical presentation of concurrent hyperparathyroidism and WD in a patient with methanol toxicity. To our knowledge, this combination has been scarcely reported in the literature, with only one similar case documented by Tallis et al in 1990.⁹ The interplay between these conditions presents significant diagnostic and therapeutic challenges, which are worth exploring in depth.

WD and Endocrine Manifestations

Although WD is mainly known for its hepatic and neuropsychiatric manifestations due to abnormal copper deposition, its association with endocrine disorders like hyperparathyroidism is rare, though reported in some case studies.⁷ Hypoparathyroidism is more commonly described in WD due to copper deposition causing glandular atrophy and dysfunction, but cases of hyperparathyroidism in WD have also been documented, suggesting that both conditions can coexist in some cases.¹¹

As demonstrated in our case and Tallis et al’s⁹ report, WD’s endocrine manifestations extend beyond classical hepatic/neurological features. The mechanisms behind this relationship are not fully understood, but chronic copper accumulation in the parathyroid glands could contribute to their dysfunction.^12,13

In our patient, hyperparathyroidism was diagnosed years before Wilson’s disease (WD), with elevated PTH and hypercalcemia observed 4 years prior to the WD diagnosis, suggesting that copper-induced parathyroid dysfunction may precede the classic WD symptoms. In contrast, hypoparathyroidism typically develops later due to copper accumulation in the parathyroid glands, leading to glandular atrophy. This comparison highlights the complex and evolving nature of endocrine dysfunction in WD.

Recent studies suggest that copper accumulation in the parathyroid glands may not only lead to atrophy but could also trigger parathyroid hyperplasia. Copper’s role in this process may involve its effects on oxidative stress, calcium-sensing receptor (CaSR) signaling, or mitogenic pathways that promote parathyroid cell proliferation. Animal models of Wilson’s disease have shown that copper deposition can disrupt normal calcium homeostasis and alter parathyroid function, potentially contributing to hyperparathyroidism.^12,14
-16 These studies highlight the complexity of copper’s effects on endocrine tissues and support the hypothesis that long-term copper exposure could lead to parathyroid hyperplasia.

Tallis et al⁹ documented the only other known case of WD with hyperparathyroidism. In their patient, hyperparathyroidism manifested as a parathyroid adenoma after 8 years of penicillamine therapy for established WD. In contrast, our patient’s hypercalcemia and elevated PTH were documented 4 years prior to WD diagnosis, suggesting either independent development or that copper-mediated parathyroid dysfunction (possibly via hyperplasia) may precede classical WD manifestations. Both cases implicate copper in parathyroid pathology, but highlight different temporal relationships and potential mechanisms. While copper deposition in WD classically causes parathyroid atrophy and hypoparathyroidism, our case and Tallis et al’s report suggest that chronic copper overload may also trigger parathyroid hyperplasia or adenoma formation.⁹ Proposed mechanisms include copper-mediated oxidative stress disrupting calcium-sensing receptor (CaSR) signaling or direct stimulation of parathyroid cell proliferation via mitogenic pathways.^9,17
-19

In our patient, WD was confirmed by characteristic biochemical findings, including elevated urinary copper excretion and decreased serum ceruloplasmin levels. Concurrent hyperparathyroidism, diagnosed years before the current presentation, was suggested by persistent hypercalcemia and elevated PTH levels. This case highlights the importance of endocrine evaluations in patients with WD, as both hypoparathyroidism and hyperparathyroidism may be overlooked, leading to delayed diagnosis and management of associated complications.^5,20

Methanol Toxicity and Its Exacerbating Factors

Methanol toxicity is a well-known medical emergency characterized by metabolic acidosis, optic neuropathy, and central nervous system depression.^21,22 Our patient presented with classic symptoms of methanol toxicity, including nausea, vomiting, and visual disturbances, which rapidly progressed to optic neuropathy. The severity of the patient’s metabolic acidosis and optic neuropathy might have been exacerbated by his underlying conditions, including WD and untreated hyperparathyroidism, which may have contributed to an altered metabolic response to methanol.^23,24

The concurrence of these conditions reflects clinically significant interactions. While hyperparathyroidism-induced hypercalcemia primarily affects renal calcium handling, potentially leading to nephrolithiasis and renal dysfunction, its potential interaction with WD remains theoretically important but not well-documented. More established is the dual mitochondrial toxicity. Copper accumulation impairs cytochrome c oxidase²⁵ while methanol’s formate metabolites disrupt oxidative phosphorylation²⁶ likely compounding metabolic disturbances. Tallis et al’s⁹ case similarly demonstrated that WD can involve unexpected endocrine manifestations, though through different mechanisms.

Clinical Interpretation

Untreated hyperparathyroidism, particularly with hypercalcemia, can worsen renal function by impairing calcium handling in the kidneys, increasing the risk of nephrolithiasis and reducing renal clearance. In this case, the patient’s elevated PTH and hypercalcemia likely compounded renal dysfunction, making him more susceptible to the nephrotoxic effects of methanol.^27,28 Methanol’s metabolites exacerbate renal and metabolic disturbances, suggesting that hyperparathyroidism may not only impair baseline renal function but also increase vulnerability to methanol toxicity, emphasizing the need for early management of hyperparathyroidism to prevent such complications.^29,30

Diagnostic Challenges and Management Strategies

The diagnostic complexity of this case cannot be overstated. Each of the conditions including WD, hyperparathyroidism, and methanol toxicity, presents with overlapping metabolic disturbances, which complicates the clinical assessment. The patient’s persistent hypercalcemia and elevated PTH levels were key indicators of hyperparathyroidism, yet these findings were only uncovered retrospectively. This case highlights the need for thorough and early biochemical screening in patients with complex clinical presentations, particularly those with a history of chronic metabolic disorders.

Management of such a rare triad of conditions requires a coordinated approach, involving multiple specialties, including hepatology, endocrinology, nephrology, and toxicology. The decision to initiate dialysis in this patient was critical in managing the acute renal dysfunction and severe hypercalcemia, and it underscores the importance of rapid intervention in such complex cases.

Implications for Clinical Practice and Future Research

The rarity of this case makes it a valuable contribution to the existing literature, emphasizing the need for clinicians to consider rare but possible coexisting conditions in patients with atypical presentations. While the exact pathophysiological interactions between WD, hyperparathyroidism, and methanol toxicity remain to be fully elucidated, this case suggests that the presence of one condition may exacerbate the others, leading to a more severe clinical presentation. Further research is warranted to explore the underlying mechanisms linking these conditions and to develop evidence-based guidelines for managing such complex cases. In particular, studies focusing on the long-term outcomes of patients with similar presentations could provide valuable insights into the best practices for diagnosis, management, and prognosis.

Conclusion

The simultaneous occurrence of hyperparathyroidism and WD in a patient with methanol toxicity is an exceptionally rare phenomenon. This case report serves to increase awareness among clinicians about this unique triad and emphasizes the importance of considering these conditions in the differential diagnosis of patients presenting with methanol toxicity. Further research and case studies are needed to elucidate the underlying mechanisms and explore optimal management.

Footnotes

Acknowledgements

Special thanks to all the fellow authors who contributed to this article.

Abbreviations

WD: Wilson’s Disease

PTH: Parathyroid Hormone

MRI: Magnetic Resonance Imaging

CaSR: Calcium-sensing receptor

ORCID iD

Alireza Fatemi

Ethical Considerations

The study and all experimental protocols were approved by the Professional Ethics Committee of the Golestan University of Medical Sciences. All methods were carried out in accordance with relevant guidelines and regulations.

Consent to Participate

An informed written consent was also obtained from the patient for the implementation of this project.

Consent for Publication

The patient provided written informed consent for publication of anonymized case details and accompanying images, including fundoscopy and endoscopy findings.

Author Contributions

Fatemeh Mohammadzadeh: Conceptualization, Investigation, Methodology, Project administration, Resources, Validation, Writing—review & editing. Alireza Fatemi: Conceptualization, Data curation, Formal analysis, Methodology, Supervision, Visualization, Writing—original draft, Writing—review & editing. Yasmin Yazdooei: Conceptualization, Data curation, Methodology, Resources, Validation, Writing—original draft. Alireza Norouzi: Conceptualization, Data curation, Visualization, Writing—review & editing.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Declaration of Conflicting Interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Guarantor Author

Alireza Fatemi accepts full responsibility for the study, including the conduct of the research, having access to the data, and controlling the decision to publish.

Preprint Disclosure

A previous version of this manuscript was submitted as a preprint to SSRN (SSRN 4983830). The current manuscript has been revised and expanded with additional clinical details.

References

Lynch

Campani

Innocenti

Dragoni

Forte

Galli

Practical insights into chronic management of hepatic Wilson’s disease. World J Clin Cases. 2022;10(14):4334-4347.

Tazin

Kumar

Orlang

Wilson’s disease manifestation in late adulthood: a case report and literature review. Cureus. 2022;14(9):e29797.

Chen

Wang

Yao

Wang

XP.

Wilson’s disease: food therapy out of trace elements. Front Cell Dev Biol. 2022;10:1091580.

Lucena-Valera

Ruz-Zafra

Ampuero

Wilson’s disease: overview. Med Clin. 2023;160(6):261-267.

Zhang

Zhao

Han

Huai

MS.

Liver transplantation for hypoparathyroidism secondary to Wilson’s disease. Chin Med J. 2019;132(16):2008-2010.

Bilezikian

Khan

Potts

, et al. Hypoparathyroidism in the adult: epidemiology, diagnosis, pathophysiology, target-organ involvement, treatment, and challenges for future research. J Bone Miner Res. 2011;26(10):2317-2337.

Alkhouri

Gonzalez-Peralta

Medici

Wilson disease: a summary of the updated AASLD practice guidance. Hepatol Commun. 2023;7(6):2.

Kapoor

Shetty

Thomas

Paul

TV.

Wilson’s disease: an endocrine revelation. Indian J Endocrinol Metab. 2014;18(6):855-857.

Tallis

Kitchener

Thomas

AC.

Hyperparathyroidism in a patient with Wilson’s disease. Clin Chem. 1990;36(3):568-570.

10.

Jopowicz

Tarnacka

Neurological Wilson’s disease signs-hepatic encephalopathy or copper toxicosis?

Diagnostics. 2023;13(5):3.

11.

Pasieka

Wentworth

Yeo

Cremers

Dempster

Fukumoto

, et al. Etiology and pathophysiology of hypoparathyroidism: a narrative review. J Bone Miner Res. 2022;37(12):2586-2601.

12.

Rafati Rahimzadeh

Kazemi

Moghadamnia

. Copper poisoning with emphasis on its clinical manifestations and treatment of intoxication. Adv Public Health. 2024;2024(1):1-12.

13.

Dong

Xiang

Xia

, et al. Aberrant copper metabolism and hepatic inflammation cause neurological manifestations in a mouse model of Wilson’s disease. J Neuroinflammation. 2024;21(1):235.

14.

Fatima

Karoli

Jain

Hypoparathyroidism in a case of Wilson’s disease: rare association of a rare disorder. Indian J Endocrinol Metab. 2013;17(2):361-362.

15.

Durdana

Hypoparathyroidism- an unusual presentation of Wilson’s disease. Indian J Endocrinol Metab. 2021;25(6):576-578.

16.

Reed

Lutsenko

Bandmann

Animal models of Wilson disease. J Neurochem. 2018;146(4):356-373.

17.

Sawant

Chaudhari

Hamdulay

Kumar

Acharya

Beyond the norm: unusual coexistence of Wilson’s disease and hypoparathyroidism. Cureus. 2024;16(2):e54516.

18.

Chu

Qin

, et al. Calcium-sensing receptor (CaSR)-Mediated intracellular communication in cardiovascular diseases. Cells. 2022;11(19):9.

19.

Tian

Andrews

Yan

Yang

JJ.

Molecular regulation of calcium-sensing receptor (CaSR)-mediated signaling. Chronic Dis Transl Med. 2024;10(3):167-194.

20.

Mageed

Rawla

Mahmoud

Shahba

Systemic lupus erythematosus, hypoparathyroidism, and hemolytic anemia in a patient with Wilson’s disease. Rheumatology. 2019;57(4):239-242.

21.

Liberski

Kaluzny

Kocięcki

Methanol-induced optic neuropathy: a still-present problem. Arch Toxicol. 2022;96(2):431-451.

22.

Hassanpoor

Niyousha

Severe optic disc cupping following the methanol toxicity in a 20-year-old man: a case report. Iran J Med Sci. 2021;46(5):395-398.

23.

Gadodia

Singhal

Sharma

Methanol intoxication causing putaminal necrosis. J Emerg Trauma Shock. 2011;4(2):300-301.

24.

Alrougi

Saqah

Khojah

Amer

SA.

Occupational methanol toxicity: a case report study. Front Med. 2025;12:1545428. 2025.

25.

Ruiz

Libedinsky

Elorza

AA.

Role of copper on mitochondrial function and metabolism. Front Mol Biosci. 2021;8:711227.

26.

Liberski

Wichrowska

Kocięcki

Aflibercept versus Faricimab in the treatment of neovascular age-related macular degeneration and diabetic macular edema: a review. Int J Mol Sci. 2022;23(16):10.

27.

Walker

Nickolas

Kepley

, et al. Predictors of renal function in primary hyperparathyroidism. J Clin Endocrinol Metab. 2014;99(5):1885-1892.

28.

Ruwanpathirana

Dissanayaka

Munasinghe

, et al. Diagnostic pitfalls and therapeutic challenges of hypercalcaemia in chronic kidney disease: a case report and a narrative review. Egypt J Intern Med. 2024;36(1):14.

29.

Gan

Wang

Zhang

Metabolomic profile of secondary hyperparathyroidism in patients with chronic kidney disease stages 3–5 not receiving dialysis. Front Endocrinol. 2024;15:11.

30.

Nekoukar

Zakariaei

Taghizadeh

, et al. Methanol poisoning as a new world challenge: a review. Ann Med Surg. 2021;66:102445.