Temporary Thyroid Dysfunction and Catecholamine Excess Due to Mercury Poisoning in 6 Cases

Abstract

Objective:

Mercury poisoning is a condition with multiple-organ dysfunction that has effects on the central nervous system, gastrointestinal system, cardiovascular system, skin, lungs, and kidneys. It can be fatal or may result in sequelae such as neurological disturbances, if treated late or left untreated. The endocrinological effects of mercury exposure are not well-known. We aimed to evaluate patients with mercury poisoning.

Materials and Methods:

A total of 6 cases of mercury poisoning from 3 families were included in the study. Clinical, laboratory, and follow-up data were recorded.

Results:

Thyroid dysfunction was presented as high thyroid hormones and normal thyrotropin level (unsuppressed) in 5 cases (83.3%). On the other hand, pheochromocytoma-like syndrome was detected in 5 cases (83.3%) with hypertension. The 4 cases were the first to use methimazole for mercury poisoning due to tachycardia and hypertension despite antihypertensive treatment due to catecholamine excess and thyroid dysfunction. Hyponatremia was detected in 3 cases (50%).

Conclusion:

Mercury poisoning is difficult to diagnose because it is rare and presents with nonspecific physical and laboratory findings. Early diagnosis and providing appropriate treatment are essential in order to prevent sequelae. Mercury poisoning should be considered in patients with unexplained hypertension and tachycardia suggesting the involvement of thyroid hormones and catecholamines.

What is already known on this topic?

• Mercury poisoning causes multiorgan dysfunction due to its toxic effects on the central nervous system, gastrointestinal system, cardiovascular system, skin, lungs, and kidneys.

• The endocrinological findings of mercury poisoning are less known.

• Non-specific clinical and laboratory test results may cause delay in diagnosis and initiation of treatment.

What this study adds on this topic?

• Thyroid dysfunction and catecholamine excess are endocrine findings of mercury poisoning.

• Mercury poisoning should be considered in patients with unexplained hypertension and tachycardia suggesting the involvement of thyroid hormones and catecholamines.

Introduction

Mercury is a heavy metal that can be found in organic, inorganic, and elemental forms in nature. All 3 forms are toxic to the human body as it is easily evaporated at room temperature. Mercury exposure mainly occurs through inhalation, but oral ingestion and dermal exposure are also possible routes. Mercury poisoning causes multiorgan dysfunction due to its toxic effects on the central nervous system, gastrointestinal system, cardiovascular system, skin, lungs, and kidneys.^1-3 The most common findings of mercury intoxication are acrodynia, limb pain, hypertension, tachycardia, irritability, sweating, fever, anorexia, and rashes. Early diagnosis and management of mercury poisoning are important because of its complications which can be irreversible when not treated or treated late.^1,4-7 The endocrinological findings of mercury poisoning are less known. Non-specific clinical and laboratory test results may cause delays in diagnosis and initiation of treatment.

Five of the patients we report here were previously reported because of the resemblance of non-specific multisystemic symptoms of mercury poisoning with rheumatological diseases.⁸ This report highlights the effects of mercury on sodium homeostasis, thyroid function, and catecholamine levels in 6 cases. All 6 patients with mercury poisoning were successfully treated with dimercaptosuccinic acid (DMSA) and supportive care.

Materials and Methods

Patients

The clinical files of 6 cases with mercury poisoning from 3 different families, who were followed up by İstanbul University-Cerrahpaşa, Pediatric Rheumatology and Pediatric Endocrinology departments between 2019 and 2020, were retrospectively evaluated. The patient’s demographic, clinical, laboratory, and radiologic findings were obtained from medical records. This report follows the chronological order of the referrals of the patients. Cases 1, 2, and 3 were admitted in February 2019, cases 4 and 5 were admitted in March 2019, and case 6 was admitted in March 2020.

This study was conducted in accordance with ethical standards. The parents of the patients were informed verbally and in writing and consent for publication was obtained. Signed consent was obtained from the parents of all cases. The study was approved by the İstanbul University-Cerrahpaşa, Cerrahpaşa Faculty of Medicine Clinical Research Ethics Committee (September 8, 2021-178214).

Statistical Analysis

Statistical analyses were performed using Statistical Package for the Social Sciences, version 21.0 (IBM Corp.; Armonk, NY, USA). Descriptive statistics for categorical variables were presented as frequencies and percentages. The continuous variables were given as mean ± SD.

Cases 1, 2, and 3

A 15-year-old boy (case 1) and his 9-year-old sister (case 2) were referred to our clinic with complaints of rashes for 5 months and widespread body pain, fatigue, and unexplained weight loss for 2 months. Their 8-year-old brother (case 3) was asymptomatic except for the rashes on his legs and arms, and these rashes had disappeared spontaneously before the admission of the older 2 siblings. Due to the simultaneous onset of the symptoms, all 3 patients had been evaluated in terms of a possible infectious disease, but the test results did not confirm the presence of an infection. Subsequently, the patients were referred to our pediatric rheumatology clinic with a suspicion of rheumatic disease due to their symptoms such as weight loss, erythematous rashes, hypertension, and myalgia. In addition to tachycardia and hypertension, case 1 had muscle weakness, widespread muscle tenderness, petechial rashes on the left forearm, and skin lesions compatible with vitiligo. Case 2 had agitation, irritability, muscle pain, maculopapular eruption, tachycardia, and hypertension (Figure 1A). Case 3 had normal heart rate and blood pressure. The laboratory results of cases 1 and 2 showed thrombocytosis, elevation of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), and normal urinalysis. The sodium levels of cases 1 and 2, which were initially 133 mEq/L and 134 mEq/L, decreased to 124 mEq/L and 123 mEq/L after initiation of the treatment, respectively. The ophthalmologic evaluation of the patients was normal except for case 2 who had bilateral grade 1 hypertensive retinopathy. The echocardiographic findings in Case 2 revealed normal systolic functions with an ejection fraction of 62% and a fractional shortening of 32%. However, left ventricular (LV) hypertrophy was detected with an interventricular septal end diastole dimension of 8.6 mm (z score = +2.0) and an LV posterior wall end diastole dimension of 8.2 mm (z score = +2.33). In addition, LV diastolic dysfunction was detected with an LV end-diastolic size of 26 mm (z score = −4.1) and an LV end-systolic size of 18 mm (z score = −2.4).

Figure 1.

(A) Maculopapular rash (case 2). (B) Plantar erythema and desquamation (case 4). (C) Maculopapular rash (case 6). (D) Cranial MRI (case 6).

The results of thyroid function tests showed slightly increased free triiodothyronine (FT3) and increased free thyroxine (FT4) levels with normal thyrotropin (TSH) levels in cases 1 and 2, and slightly increased FT3 level with normal TSH level in case 3. While the thyroid autoantibodies in cases 2 and 3 were negative, the thyroid autoantibodies in case 1 were positive [anti-thyroid peroxidase antibody (TPO) 41.23 IU/mL (<34), anti-thyroglobulin antibody (Tg) 149.9 IU/mL (<115)]. Thyroid ultrasonography was normal in all 3 patients. Renal and surrenal ultrasonography did not suggest pheochromocytoma. Due to the presence of neuropsychiatric symptoms, hypertension, tachycardia, and skin changes, differential diagnosis included poisoning. When a detailed history was taken, it was learned that the children had brought home a bright fluid from the schoolyard. They both had touched and played with it, and the 9-year old sister had even put it into her mouth to taste it. After the DMSA challenge test, elevated blood and urine mercury levels were detected in all 3 siblings. After a definitive diagnosis of mercury intoxication was made, DMSA treatment was initiated immediately. Later, doxazosin and propranolol were also added to the treatment in cases 1 and 2 who had tachycardia and hypertension. Hyponatremia was treated with oral and intravenous sodium supply. Methimazole was added for thyroid dysfunction because the 2 patients had tachycardia and hypertension despite treatment. After the symptoms subsided with DMSA treatment, all medications were gradually decreased and then discontinued. In cases 1, 2, and 3, thyroid function normalized in 24, 8, and 2 weeks, respectively (Tables 1 and 2).

Table 1.

Clinical and Laboratory Findings of the Cases

Age (years)/Sex	Case 1	Case 2	Case 3	Case 4	Case 5	Case 6
	14/Male	9 /Female	7/Male	6/Female	4/Female	15/Male
Complaint	Fever, weight loss, rashes, fatigue, generalized myalgia, arthralgia	Fever, weight loss, rashes, fatigue, generalized myalgia, arthralgia	Asymptomatic	Rashes, burning pain in their hands and feet	Rashes, burning pain in their hands and feet	Fever, rashes, burning pain in their hands and feet
Physical examination
Heart rate	125/min	140/min	104/min	142/min	152/min	110/min
Blood pressure	145/90 mm Hg (95.p;129/80)	130/85 mm Hg (95.p;112/75)	90/64 mm Hg	128/78 mm Hg (95.p;111/73)	120/80 mm Hg (95.p;111/71)	160/100 mm Hg (95.p;133/83)
Skin	Erythematous papules/Maculopapular rash	Erythematous papules/Livedoid rash	–	Erythromelalgia	Erythromelalgia	Maculopapular rash
Hypertensive retinopathy	–	+	NE	NE	NE	–
Laboratory
CBC	Normal	WBC:17.400/mm3 Plt: 439.000/mm3	Normal	Normal	Normal	Normal
CRP (N < 0.5 mg/dL)	14.35
ESR (mm/h)	61	115
Na (initially) (mEq/L)	133	134	139	136	137	137
Na (lowest) (mEq/L)	124	123				124
FENa (%)	0.43	0.06				0.55
Renin (ng/mL/saat)	Normal	Normal		Normal	Normal	Normal
Aldosterone (ng/dL)	Normal	Normal		Normal	Normal	Normal
Urine analysis	Proteinuria (−)	Proteinuria (−)				Proteinuria (++)
	Glucosuria (−)	Glucosuria (−)				Glucosuria (−)
Proteinuria (gr/24 h)						7.8
Sinus tachycardia	+	+	–	+		+
Hypertensive cardiomyopathy	–	+	NE	–	–	–
Polyneuropathy	+	–	NE	NE	NE	–
TSH (uIU/mL)	3.21 (0.6-4.84)	1.6 (0.6-4.84)	2.17 (0.6-4.84)	1.01 (0.7-5.97)	0.93 (0.7-5.97)	1.11 (0.6-4.84)
fT4 (ng/dL)	2.7 (0.97-1.67)	2.2 (0.97-1.67)	1.45 (0.97-1.67)	2.12 (0.96-1.77)	1.91 (0.96-1.77)	2.07 (0.97-1.67)
fT3 (pg/mL)	5.3 (2.53-5.22)	5.43 (2.53-5.22)	5.32 (2.53-5.22)	4.74 (2.41-5.5)	4.32 (2.41-5.5)	3.58 (2.53-5.22)
Anti-TPO (IU/mL)	41.23 (<34)	14.3 (<34)	NE	0.31 (<5.6)	0.04 (<5.6)	13 (<34)
Anti-Tg (IU/mL)	149.9 (<115)	12.2 (<115)		0.65 (<4.1)	0.81 (<4.1)	12.48 (<115)
TRAB (IU/mL)	Negative	Negative		Negative	Negative	Negative
Thyroid US	Normal	Normal	NE	Normal	Normal	Normal
Urine metanephrine (mcg/24 h)	325 (<185)	111.5 (<185)	NE	NE	NE	512.21 (30-350)
Urine normetanephrine (mcg/24 h)	894 (<286)	521 (<286)
Urine noradrenaline (mcg/24 h)	144 (<80)	105.8 (<80)				314.11 (20-105)
Renal and surrenal imaging	Normal	Normal	NE	Normal	Normal	Normal
Blood mercury level (ug/L) (N<5)	77	27	30	2.3	2.8	47
Urine mercury level (ug/g creatinine) (N<5)	2666	2029	1526	207.8	332.1	1046.6
Treatment	DMSA Methimazole Doxazosin Propranolol Gabapentin	DMSA Methimazole Doxazosin Propranolol	DMSA	DMSA Methimazole Propranolol Amlodipine Gabapentin	DMSA Methimazole Propranolol Amlodipine Gabapentin	DMSA Doxazosin metoprolol Amlodipine Gabapentin Olanzapine
Remission period of thyroid dysfunction (week)	24	8	2	8	8	8

Cases 1, 2, 4, 5, and 6 were diagnosed with thyroid dysfunction. cases 1, 2, and 6 were detected with increased catecholamine levels.

Anti-Tg, anti-thyroglobulin antibodies; anti-TPO, anti-thyroid peroxidase antibodies; CBC, complete blood count; DMSA, dimercaptosuccinic acid;ESR, erythrocyte sedimentation rate; FENa, fractional excretion of sodium; fT3, free triiodothyronine; fT4, free thyroxine; Na, sodium; NE, not evaluated; Plt, platelet; TRAB, thyrotropin receptor antibodies; TSH, thyrotropin; WBC, white blood cell.

Table 2.

Thyroid Function Tests and Treatment of the Cases

Case		1st Day	2nd Week	4th Week	8th Week	12th Week	24th Week
1	TSH (0.6-4.84 uIU/mL)	3.21	6.64	13.3	5.06	4.63	5.64
	FT4 (0.97-1.67 ng/dL)	2.31	2.12	1.76	2.26	1.85	1.44
	FT3 (2.53-5.22 pg/mL)	4.17	4.31	3.04	5.84	5.56	5.01
	Methimazole (mg/day)	30	15	10	5	5	–
2	TSH (0.6-4.84 uIU/mL)	1.6	2.79	4.04	6.65		1.44
	FT4 (0.97-1.67 ng/dL)	2.20	2.13	1.7	1.14		1.15
	FT3 (2.53-5.22 pg/mL)	5.43	4.97	3.27	4.45
	Methimazole (mg/day)	30	15	10	–
3	TSH (0.6-4.84 uIU/mL)	2.17	1.47
	FT4 (0.97-1.67 ng/dL)	1.45	1.34
	FT3 (2.53-5.22 pg/mL)	5.32	4.01
	Methimazole (mg/day)	–
4	TSH (0.7-5.97 uIU/mL)	1.01	0.45	1.83	2.23	1.34
	FT4 (0.96-1.77 ng/dL)	2.12	2.03	1.37	1.04	1.20
	FT3 (2.41-5.5 pg/mL)	4.74	2.67	1.94	4.89	5.07
	Methimazole (mg/day)	15	7.5	5	–
5	TSH (0.7-5.97 uIU/mL)	0.93	1.04	5.69	6.58	2.15
	FT4 (0.96-1.77 ng/dL)	1.91	1.99	1.55	1.34	1.62
	FT3 (2.41-5.5 pg/mL)	4.32	3.76	3.62	4.76
	Methimazole (mg/day)	15	7.5	5	–
6	TSH (0.6-4.84 uIU/mL)	2.7	2.11	2.04			1.39
	FT4 (0.97-1.67 ng/dL)	2.04	2.06	2.07			1.49
	FT3 (2.53-5.22 pg/mL)	2.78	3.83	3.61			4.14
	Methimazole (mg/day)	–

Thyroid function tests of the cases improved in 2-24 weeks. Abnormal results are shown in bold.

FT3, free triiodothyronine; FT4, free thyroxine; TSH, thyrotropin.

Cases 4 and 5

Two sisters, aged 4 and 6 years, were referred to our clinic due to complaints of irritability, redness, and pain in the hands and legs for 1 month. Tachycardia and hypertension were detected during physical examination. Both of the children had palmar and plantar macular rashes and peeling on their toes (Figure 1B). Despite high FT4 levels, TSH levels were normal (not suppressed). Thyroid autoantibodies were negative, and there were no abnormalities in thyroid ultrasound, renal, and adrenal imaging. These patients were referred for isolated Raynaud’s phenomenon. Mercury intoxication was considered in the differential diagnosis due to the hypertension, tachycardia, and acrodynia. Although blood mercury level was normal, elevated urine mercury levels were detected after the DMSA challenge test. However, a source of mercury could not be found. DMSA, propranolol, and nifedipine treatment was started in both patients. In their follow-up, methimazole was added to the treatment due to the persistence of tachycardia and hypertension. Their symptoms regressed and thyroid function tests of the patients were found to be normal after 8 weeks (Tables 1 and 2).

Case 6

A 15-year-old boy was referred to our clinic due to fever, rash, walking difficulty, and pain in the knees, fingers, and toes which had started 6 weeks ago (Figure 1C). He was agitated and had muscle sensitivity and fading purpuric rashes on his thigh. Focal tonic–clonic seizure, which involved the right arm and the head, was observed at admission. He was tachycardic and hypertensive. On cranial MRI, symmetric-subcortical edema was detected in the bilateral posterior parietal regions and the parasagittal area (Figure 1D). His cranial CT angiography and EEG findings were found to be normal, and levetiracetam was initiated. Free T3 and TSH values were found to be normal (non-suppressed), but the FT4 level was increased. Thyroid autoantibodies were negative and thyroid ultrasonography findings were normal. His initial sodium level was 137 mEq/L. A urinalysis revealed proteinuria (++) in the spot urine test and 7.8 g proteinuria in 24-hour urine. No additional treatment was added for proteinuria as he did not have edema and hypoalbuminemia. While evaluating the etiology of hypertension, urinary catecholamines were found to be elevated. Imaging of the surrenal gland did not suggest pheochromocytoma. When a detailed history in terms of intoxication was taken, mercury poisoning through inhalation of a substance, which probably contained mercury, was suspected, and the DMSA challenge test showed that blood and urine mercury levels were elevated. DMSA, gabapentin, doxazosin, and metoprolol treatment was initiated, and olanzapine was added after pediatric psychiatric consultation for agitation. Because the sodium level decreased to 124 mEq/L after DMSA treatment, sodium was replaced. A follow-up cranial MRI was performed 10 days later, and regression of the previous findings was observed. The patient’s thyroid function test results returned to normal without any antithyroid treatment in 8 weeks (Tables 1 and 2).

Results

Three male cases and 3 female cases from 3 different families, who were diagnosed with mercury poisoning, were included in the study. The mean age of the cases was 9.17 ± 4.45 years. Hypertension was detected in 5 cases (83.3%). While the mean blood mercury level was 31.01 ± 28.31 ug/L and the mean mercury level in 24-hour urine was 1301.25 ± 963.57 ug/g creatinine. Thyroid dysfunction was presented as high thyroid hormones (THs) and normal TSH level (unsuppressed) in 5 cases (83.3%). The mean TSH, fT4, and fT3 values were found to be 1.67 ± 0.88 uIU/mL, 2.07 ± 0.4 ng/dL, and 4.78 ± 0.72 pg/mL, respectively. Four patients were the first patients to use methimazole in mercury poisoning because they had tachycardia and hypertension despite antihypertensive treatment due to catecholamine excess and thyroid dysfunction. The mean period of remission of thyroid dysfunction was 9.7 ± 7.4 weeks. Hyponatremia was detected in 3 of our cases. The clinical and laboratory findings at the time of diagnosis are presented in Table 1.

Discussion

Nonspecific signs and symptoms of chronic mercury poisoning can occur in a wide spectrum. Children are more affected by mercury poisoning because their blood–brain barriers are more permeable and their respiratory rate is higher than adults, and their nervous system is still developing. The mercury dose exposed is one of the important determining factors in terms of the severity of clinical symptoms.⁹ However, there is no correlation between blood and urine mercury concentrations and clinical findings.¹⁰ Mercury shows its effect by leading to enzyme inhibition, binding to hormone receptors, and affecting intracellular calcium metabolism and peroxidation.¹¹

Secondary hypertension and tachycardia were the main clinical findings in our cases. Symptoms mimicking pheochromocytoma, such as acrodynia, sweating, hypertension, and tachycardia, have been shown to result from the accumulation of catecholamines.^4,5,7 The cause of increased catecholamine levels is associated with the inhibition of catecholamine-O-methyltransferase (COMT). This enzyme plays a role in the catabolism of catecholamines. Mercury reduces the activity of S-adenosylmethionine which is a coenzyme activating COMT.^4,12-14

The association between Hg exposure and hyponatremia has been rarely reported in the literature.¹⁵ Although the exact mechanism is not known, increased renal perfusion pressure due to hypertension resulting from catecholamine excess may increase renal interstitial hydrostatic pressure, and hyponatremia develops as a result of decreased sodium reabsorption and increased sodium excretion.¹⁶ Torres et al⁴ reported that these findings were consistent with pressure natriuresis and stimulation of dopamine receptors in the kidney. Exaggerated process of pressure natriuresis and stimulation of dopamine receptors in the kidney may contribute to hyponatremia.^4,15 In our 3 patients, who developed hyponatremia, the sodium level was normal or close to normal at admission. During treatment, sodium levels decreased due to mercury passing from the tissues to the blood which resulted in increased levels of catecholamines, and hyponatremia was recovered with oral and intravenous sodium supplements. In case 6, nephrotic-range proteinuria was present. According to various case reports, kidney damage caused by mercury is known to cause dose-related tubular dysfunction and idiosyncratic nephrotic syndrome.¹⁷

In our subjects who had thyroid dysfunction, FT4 and/or FT3 were increased, but TSH levels were normal (Table 2). Unfortunately, total T4 concentrations could not be measured because this test was not covered by the social security and the family had limited sources. Previous studies have shown the effect of mercury on thyroid function, but the effect remains unclear. Mercury binds to sulfhydryl-containing ligands in the thyroid gland and reduces the production of THs by affecting TSH production, thyroid peroxidase production and iodination of thyroglobulin.¹⁸ In addition to the publications reporting that mercury suppresses the secretion of T4,¹⁹ it has been reported that it impairs thyroid functions by affecting both the production of THs and the conversion of T4 to T3.²⁰ In the study of Khan et al,²¹ it was reported that the hypothalamic–pituitary–thyroid (HPT) axis and enzymes involved in TH metabolism were affected leading to a decrease in serum T4 levels and an increase in TSH levels. On the other hand, it was suggested that inhibition of type I iodothyronine deiodinase by mercury might result in an increase in the total T4 level and the T4 : T3 ratio in the study of chlor-alkali workers.^22,23 The increase in FT4 rather than FT3 in our cases with thyroid dysfunction may be due to the inhibition of deiodinase leading to a decrease in the peripheral conversion of T4 to T3. Sun et al²⁴ suggested that exposure of zebrafish embryos to mercury might impair normal development and TH levels of their larvae by increasing the transcription levels of the genes located in the HPT axis. This was demonstrated by the analysis of the mRNA levels of the genes associated with thyroid development and TH synthesis, showing increased expression of HEX, NKX2.1, NIS, and TG. In addition, while the transcription of the deio2 gene increased, the unchanged deio1 expression was partially responsible for the increase in T3 level. According to the results of the study, it was revealed that the different effects of mercury on the thyroid may vary according to the dose, exposure route, and exposure time. Chronic exposure is more important than acute exposure in terms of thyrotoxicity of mercury.¹¹ There is no data regarding the initiation of antithyroid therapy in patients with symptomatic mercury poisoning with thyroid dysfunction. Antithyroid treatment has been reported in only 1 case. In this report, carbimazole was started in a 13-year-old patient who had a low TSH level and elevated T3 and T4 levels due to mercury poisoning.²⁵ Thyroid dysfunction in our 5 cases was characterized with increased THs and normal TSH. The unsuppressed TSH levels may be explained by the accumulation of mercury in the pituitary and thyroid gland leading to a disruption of the HHT axis.^21,26 Although TSH levels were not suppressed, methimazole was started in 4 cases due to tachycardia and hypertension that persisted despite antihypertensive treatment. In 1 case, treatment was not initiated despite slight T4 elevation. Remission of thyroid dysfunction occurred in 2-24 weeks.

Measurement of mercury serum concentrations is the most accurate way to evaluate exposure. However, normal blood levels do not exclude the diagnosis. Commonly used tests (blood, urine, and/or hair levels) may not show the total body load. Tests conducted with DMSA provocation are recommended, because they are more reliable and precise. It was observed that urinary mercury excretions increased after DMSA provocation, although the blood mercury level was normal in cases 4 and 5. Evaluation of catecholamine levels may be useful to confirm the diagnosis and evaluate the treatment response.^1,27

DMSA is highly bound to albumin through a disulfide bond, which increases the elimination of mercury. It is recommended to use DMSA at a dose of 10 mg/kg every 8 hours for 8 days, then every 12 hours for 14 days.³ Clinical and laboratory benefits were observed in all of our cases after DMSA administration (Figure 2). However, we observed a decrease in sodium levels in the blood, an increase in neuropsychiatric symptoms, and inability to control blood pressure as a result of the temporary increase in blood mercury and catecholamine levels due to mercury released from tissues during chelation therapy.

Figure 2.

Urine mercury levels of the cases. Urinary mercury levels of the cases decreased dramatically after dimercaptosuccinic acid treatment.

Regarding preference of antihypertensive agents, alpha- and beta-adrenergic blockers, such as labetalol should be preferred since the symptoms are known to occur mostly due to high catecholamine levels. Selectively blocking either alpha- or beta-adrenoreceptors can lead to overstimulation of the unblocked path. Therefore, it is recommended to inhibit both adrenoreceptors. In cases in which vasculitis is considered and without a detected tumor, calcium channel blockers can be added to the antihypertensive regimen.⁷

The main limitation of our study was that it was conducted with a small number of patients.

In conclusion, difficulties arise in the diagnosis of mercury poisoning due to its rarity, and nonspecific physical and laboratory findings. Mercury poisoning should be considered in patients with unexplained hypertension and tachycardia due to increases in THs and catecholamines.

Funding Statement

This study received no funding.