A Case of Post-Malarial Postural Orthostatic Tachycardia Syndrome in a Young Woman of South Asian Origin

doi:10.21203/rs.3.rs-5085815/v1

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Case Report

A Case of Post-Malarial Postural Orthostatic Tachycardia Syndrome in a Young Woman of South Asian Origin

https://doi.org/10.21203/rs.3.rs-5085815/v1

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Postural orthostatic tachycardia syndrome (POTS) is a chronic and debilitating dysautonomic disorder characterized by impairments in autonomic control of cardiovascular, gastrointestinal, and thermoregulation functions, resulting in various symptoms of orthostatic intolerance. While POTS is increasingly being diagnosed as post-COVID sequelae and complications, it’s rarely being reported if caused by non-viral infections and other clinical conditions. This case study reports a 30-year-long medical history of a patient who developed POTS at the age of 21 after about 4-weeks following a complete recovery from malignant malaria when she was a first-year medical student. She was initially presented with tachycardia, dizziness, presyncope, several episodes of syncope, and dysautonomic symptoms and was diagnosed with POTS only four years later by a tilt table test. This is a rare and probably the first reported case of post-malarial POTS, although symptoms associated with severe orthostatic hypotension, such as tachycardia and insufficient peripheral vasoconstriction, that are very similar to the symptoms of POTS, have been previously described in cases with acute malignant malaria. The patient made a remarkable recovery from POTS as she responded well to pharmacotherapy, primarily beta-blockers, along with lifestyle modifications. However, mild dysautonomic symptoms such as lack of thermoregulation and decreased perspiration have persisted throughout, and the patient has managed to cope with these symptoms and could function well in her daily life. Based on this case study, we suggest that the non-viral etiology of POTS, particularly the post-malarial cases, should be studied in detail to further understand the pathophysiology and management of the disorder.

Internal Medicine

Preventive Medicine

Critical Care & Emergency Medicine

Allergy & Immune Disorders

Cardiac & Cardiovascular Systems

Postural orthostatic tachycardia syndrome (POTS)

orthostatic intolerance

malignant malaria

tachycardia

syncope

dyspnea

thermoregulation

tilt table testing

beta-blockers

vasoactive agents

Postural orthostatic tachycardia syndrome (POTS) is dysautonomic syndrome¹ characterized primarily by impairments in autonomic control of cardiovascular, gastrointestinal, and thermoregulation functions^2,3, resulting in symptoms of orthostatic intolerance, including anxiety/palpitation, dizziness/vertigo, pre-syncope/syncope, hyperventilation/dyspnea, tremulousness, sweating, headache, fatigue, sleep disorder, and weakness⁴. While POTS patients can present with a myriad of symptoms, the most commonly including lightheadedness (99%), tachycardia (97%), presyncope (94%), headache (94%), and difficulty concentrating (94%)⁵ (see Table 1 for a list of system-wise symptoms). Biometrically, POTS is diagnosed when there is a sustained heart rate increase of ≥ 30 bpm or an increase of heart rate to ≥ 120 bpm within the first 10 minutes of orthostatic intolerance and without significant orthostatic hypotension⁶. POTS can be chronic and debilitating³, and the symptoms can impact the patient's activities of daily living such as bathing, housework, and feeding⁴. The prevalence of POTS is proximately between 0.2% and 1% of the population, most commonly diagnosed in young and middle-aged women as well as in individuals with chronic fatigue syndrome or autoimmune disorders³. While POTS can occur spontaneously due to unknown or genetic etiology⁷, it can emerge in response to viral infections including COVID-19 and other medical conditions such as Ehlers-Danlos syndrome, Lyme disease, or autoimmune disorders⁸.

Table 1

Clinical symptoms of POTS involving different systems as described by Fedorowski⁹
General symptoms	General deconditioning, chronic fatigue, exhaustion, heat intolerance, fever, debility, bedriddenness
Cardiovascular system	Main: Orthostatic intolerance, orthostatic tachycardia, palpitations, dizziness, lightheadedness, presyncope, exercise intolerance Other frequent symptoms: dyspnea, chest pain/discomfort, acrocyanosis, Raynaud's phenomenon, venous pooling, limb edema
Nervous system	Headache/migraine, mental clouding (‘brain fog’), cognitive impairment, concentration problems, anxiety, tremulousness, light and sound sensitivity, blurred/tunnel vision, neuropathic pain (regional), sleeping disorders, involuntary movements
Musculoskeletal system	Muscle fatigue, weakness, muscle pain
Gastrointestinal system	Nausea, dysmotility, gastroparesis, constipation, diarrhea, abdominal pain, weight loss
Respiratory system	Hyperventilation, bronchial asthma, shortness of breath
Urogenital system	Bladder dysfunction, nycturia, polyuria
Skin	Petechiae, rashes, erythema, telangiectasias, abnormal sudomotor regulation, diaphoresis, pallor, flushing

While there is a growing interest in POTS research³, especially after the COVID-19 pandemic¹⁰, there are significant challenges to studying POTS due to many reasons³, including its low prevalence rate, unsuccessful clinical trials, difficulty to diagnose due to variations of similar syndromes, and lack of consistency in outcome measures. Further, while there is a surge in interest in studying post-COVID manifestations of POTS¹⁰, studies related to other etiological factors, for example, post-malarial POTS, have not been reported although malaria-induced neural damage caused by Plasmodium falciparum has been previously reported¹¹. It is highly likely that such cases, which could have been otherwise diagnosed as POTS, have been under-reported as there is a severe lack of studies. With this background, we present here a case report about a 30-year-long clinical history of a woman who initially developed POTS symptoms (i.e., tachycardia, syncope, and dysautonomia) following an acute episode of malignant malaria and about her dramatic recovery from the major symptoms and near-normal functioning in many facets of her life.

First Hospital Visit (at Age 25)

A 25-year-old right-handed female medical student presented at a multispecialty hospital in south India with a history of recurrent attacks of palpitation associated with giddiness and syncope. These symptoms started after her recovery from a fatal episode of malignant malaria caused by Plasmodium Falciparum four years ago (at age 21) when she was a first-year medical student. She was treated with antimalarial therapy, primarily intravenous Quinine and IV fluids. Her malarial illness lasted about 3 weeks, and she lost 14 kg of body weight (from 48 kg to 34 kg). After about four weeks of her recovery from malaria, the patient started having recurrent attacks of palpitation which at times led to episodes of presyncope and syncope characterized by loss of consciousness and fainting or passing out. Her medical education was interrupted because of these symptoms. At times her heart rate went beyond 170 to 180/minute followed by a dizzy spell terminated by collapse (fall). Syncopal attacks became more frequent over the past year from her first hospital visit (7 times). On clinical examination, she had a structurally normal heart. Her thyroid function was normal and other blood investigations did not reveal any abnormality. The 24-hour ECG from the Holter monitor report showed evidence of atrial tachycardia.

With a provisional diagnosis of inappropriate atrial tachycardia, she was subjected to tilt table testing, during which she was continuously monitored for ECG rhythms and intra-arterial pressure. Her heart rate at rest was around 100–120/minute and it increased progressively, while the blood pressure response was normal. Thereafter, she was challenged with intravenous isoprenaline with which she developed sustained atrial tachycardia, and her blood pressure dropped after about 5 minutes of continuous tachycardia. Soon her symptom cluster was reproduced as she felt a dizzy spell and nearly collapsed. Her blood pressure response became normal after resting for about 10 minutes, and her heart rate settled to sinus rhythm with a rate of 100 per minute.

The cardiologist diagnosed the patient with POTS, which was considered a novel diagnosis as she was one among the very few people with POTS at that time. She was prescribed atenolol 25 mg twice a day (which is primarily used to treat angina and hypertension). The dosage could be increased to 50 mg twice a day if needed, along with salt therapy. If this regimen did not help her to a great extent, a small dose of Fludrocortisone (a steroid that would raise her BP to the normal range in the body) was prescribed, which can be supplemented with beta-blocker therapy as and when needed. Soon, Atenolol 25 mg BID was replaced with Metoprolol 50 mg twice daily as there was no significant improvement in controlling the heart rate. Since Midodrine was not available in India at that time, the patient was also prescribed oral Fludrocortisone (Florinef) to maintain her blood pressure. She was also prescribed Diltiazem XR 30 mg QD and Deriphyllin 150 mg for symptom control. With regular medication, the patient improved dramatically and without having major episodes of syncope, although mild symptoms of palpitation, dizziness, and hypersensitivity to extreme temperatures persisted. The patient was able to cope with these symptoms by implementing lifestyle changes as needed. She went on to complete her medical education and started working as a physician as these symptoms did not disrupt her daily activities and occupational functioning.

Second Hospital Visit (at Age 33)

Following her dramatic improvements in her symptoms thanks to her correct diagnosis and treatment, the patient got married at the age of 31 and migrated to the United States. Within a year of her happy married life, she had a healthy child albeit undergoing a high-risk pregnancy and caesarian birth. However, around the age of 28 years, she suffered symptoms of severe gastroparesis, thrived mostly on a liquid diet, and lost about 15 pounds of her body weight. Further, she occasionally developed symptoms of mild dizziness and “near-syncope” experience during the summer months and developed pain in her fingers during the winter months akin to Raynaud's syndrome. After about two years of her married life in the US, she decided to go for a neurology consultation with a POTS expert.

History of Present Illness: The patient complains of dizziness with a change in position. She denies tinnitus, hearing loss, or vertigo. The patient does have nausea and dizziness. The patient feels vertigo inside of her body, but not outside. She sustained three episodes of near-syncope with a sensation of darkness in front of her eyes. The patient was able to avoid syncopal episodes. She has reportedly had 7–10 episodes of loss of consciousness (syncope) during her lifetime. She was diagnosed with postural orthostatic tachycardia syndrome (POTS) in India. The patient was evaluated with a tilt table test at that time. The patient has had palpitations early in the disease; however, it has resolved now. Overall, her condition had improved over the years. The patient reported that she has not been taking medications prescribed for her POTS symptoms. She has now sought medical help as she noticed worsening of her symptoms during the past 2 months. She was unable to stand for a prolonged period of time. The patient was afraid to take care of her 1-year-old child anticipating possible episodes of syncope. She denied numbness, tingling sensations, and balance problems. She also denied any falls but did complain of weakness in both lower extremities.

Neurological Examination: The Mental Status examination revealed that the patient was alert and oriented to time, place, and person. Memory examination revealed normal short-term memory with good recall. Attention span and concentration were normal. General knowledge and information were appropriate. Speech Articulation, fluency, and comprehension were normal. Naming and repetition were appropriate. The vocabulary was full. Cranial nerves examination revealed normal visual acuity and unrestricted vision fields. The color perception was normal. Pupils were rounded, equal, and reactive to light. There was no restriction of eye movements. Accommodation and conversion synkinesis were normal. There was no evidence of nystagmus. Muscles of mastication, facial muscles, sternocleidomastoid, trapezius, and tongue muscles were graded as 5/5. Facial sensation to temperature and pinprick was appropriate bilaterally. Hearing was normal bilaterally. Uvula was in the midline. Corneal, blink, jaw jerk, and gag reflexes were present bilaterally. The sensory examination was tested with pinprick and light touch and was found equal bilaterally. Vibration and proprioception were equal bilaterally. Neurological examination revealed diminished vibratory sense in both lower extremities.

Motor and Cerebellar functions: Muscle tone and bulk were normal. Muscle strength was graded as 5/5 in all muscle groups in the upper and lower extremities. Deep tendon reflexes were 2 at the biceps, triceps, knees, and ankles bilaterally. Plantar reflexes showed down-going toes bilaterally. Rapid alternating movement examination was normal. There was no ataxia or dysmetria. The finger-to-nose test and heel-knee-shin test were normal bilaterally. Gait was normal. The Romberg sign was normal with eyes open and closed. The patient was able to perform tandem gait, tip-toe walking, and heel walking.

Electrodiagnostic and neurophysiological evaluation: As the patient presents with long-standing symptoms of postural orthostatic tachycardic syndrome, lower extremity paresthesias, and diminished vibratory sense in both feet, it was necessary to rule out peripheral polyneuropathy. The neurophysiological evaluation did not reveal large fiber.

Other Details: Past medical history was unremarkable. Past surgical history was significant for cesarean section a year ago. No known allergy was reported. The patient was not on any medications currently. No history of alcohol, tobacco, or substances. The patient’s father had a history of myocardial infarction, and the mother had a history of kidney problems and removal of one kidney. A review of systems revealed palpitation, lightheadedness, constipation, and heat intolerance. Physical examination revealed a cooperative, well-nourished, afebrile patient. There was no evidence of carotid bruits. Funduscopic examination revealed flat discs without evidence of hemorrhage. Her other parameters were: supine blood pressure – 126/80, heart rate – 96, and standing blood pressure – 122/86.

Diagnostic Impression: After reviewing abundant medical records from India, the following impressions were made: (i) Confirmation of the diagnosis of POTS; (ii) There was no evidence for large fiber peripheral polyneuropathy; and (iii) Consideration should be given to autonomic neuropathy.

Recommendation: For further evaluation and the specialist’s opinion, the patient was referred to a cardiologist and a neurologist who was an autonomic disorders specialist. The patient was given prescriptions for Midodrine 5 mg to take at 8 am for blood pressure below 100 systolic. The patient was advised to record her blood pressure on a daily basis using a blood pressure monitor. In addition, she was advised to continue lower extremity exercises and increase oral fluid and salt intake. The patient was also advised that she might benefit from pressure stockings and abdominal binders as well as from sleeping in Trendelenburg position with her head elevated. As advised, the patient consulted the cardiologist and the neurologist, but no significant symptoms or findings other than those noted in the history of present illness were identified.

Current Status (at Age 51)

Over the past 18 years in the US, since her previous hospital visit at about age 33, the patient has been continuously on Metoprolol 50 mg/day and maintaining well. Apart from her mild symptoms related to thermoregulation (vasodilation to warm weather and vasoconstriction similar to the Reynolds phenomenon and chilblains in her feet during cold weather), she has been functioning optimally in all activities of daily living and occupation. For example, she could drive her car and do household chores, in addition to her successful completion of her USMLE exams and occupational functioning in various medical settings.

We report on a 21-year-old young woman who developed symptoms of POTS four weeks after complete recovery from acute malignant malaria that lasted for 3 weeks. She had palpitations, low blood pressure, dysautonomia, and syncope. She was diagnosed with POTS during her first visit to a multispecialty hospital at age 25. Due to continuous treatment, she recovered well from POTS symptoms and managed to live with mild symptoms of dysautonomia until age 31. She was off medication for the next two years and her persisting dysautonomic symptoms prompted her to seek another hospital visit and further referrals as they were becoming less tolerable. She was back on regular medication and continued to maintain well until now at age 51. This case was one of the first among the POTS cases in India when it was diagnosed over 25 years ago. Unlike the widely reported cases of post-viral POTS diagnosis, this is one of the rare cases of POTS due to post-malarial infection.

Interestingly, similar to the post-viral POTS, malaria-related POTS may suffer neurological damage. Severe orthostatic hypotension associated with tachycardia and insufficient peripheral vasoconstriction, as often manifested in POTS, has been widely reported in acute malignant malaria caused by Plasmodium falciparum¹² although very rarely described in uncomplicated malaria due to Plasmodium vivax¹³. To our knowledge, while malaria-related POTS has not been reported so far, post-malaria neurological syndrome with acute disseminated encephalomyelitis (ADEM) has been reported in a case report of a 30-year-old woman¹¹, who had a multifocal, monophasic, demyelinating disease akin to a post-viral infection. It is also possible that antimalarial drugs such as Quinine might cause neural damage. A rat study reported that Mefloquine, a quinoline-methanol derivative of Quinine, caused profound alterations in autonomic and respiratory control systems¹⁴. A human cell-culture study found that antimalarial drugs quinine, chloroquine, and mefloquine acted as antagonists at 5-HT3 receptors¹⁵. Therefore, it is highly likely that acute neural damage followed by chronic dysfunction of the autonomic nervous system following infection caused by Plasmodium falciparum and anti-malarial treatment is a possibility in our patient although there were no MRI and other imaging studies done to support this claim.

In one of the largest studies on 4835 participants with POTS, Shaw et al.⁵ reported that most of the patients with POTS were identified as female (80–94%), ages between 12–50 years with a median age 17 years, and 47% developed first symptoms after the age of 18. The major causes reported were infection (41%), surgery (12%), pregnancy (9%), vaccination (6%), accident (6%), puberty (5%), post-concussion (4%), and emotional stress or trauma (3%). The study also reported that patients waited a median 2 years to get a diagnosis with a mean of 4.9 ± 7.1 years, reflecting extraordinarily long waits. Further, 21% (n = 627) of patients reported having seen more than 10 doctors until they were diagnosed with POTS. In our patient, the symptoms started at age 21, following an acute malignant malaria and it took over 4 years to get the diagnosis of POTS, as it is understandable that 75% of patients reported being misdiagnosed before receiving the diagnosis of POTS even in recent times⁵. Although orthostatic tachycardia, the cardinal feature of POTS, was first described in 1940¹⁶, it was systematically described as a diagnostic category by Schondorf and Low in 1993¹⁷, just two years before our patient received the diagnosis. POTS is a heterogeneous dysautonomic disorder with various subtypes¹⁸, which is often underdiagnosed because symptoms mimic many related disorders including vasovagal syndrome⁴. Interestingly, to our knowledge, there are no studies or case reports available for the post-malarial POTS, as described in our case study.

The three most common symptoms of POTs were lightheadedness, tachycardia, and presyncope, a symptom triad that was present in 91% of the patients⁵. Our patient had all three symptoms, along with headache, nausea, vomiting, blurry vision, dizziness, and syncope, until she was diagnosed and treated with medication. Shaw et al.’s study⁵ reported only 16% (N = 610) of POTS patients with Raynaud's phenomena, which was present in our patient and persisted for about 30 years even after being on continuous medication with metoprolol, a beta-blocker, as these medications have no role in controlling excessive vasoconstrictions. However, Nifedipine was prescribed to counteract Raynaud’s phenomena as needed. Although there are no FDA-approved drugs to treat patients with POTS, individualized treatment strategies are typically based on different subtypes of POTS, such as hypovolemic, neuropathic, and hyperadrenergic. A systematic review³ reported that the pharmacological approach for POTS is usually specific to its symptom clusters: (i) midodrine for reducing orthostatic symptoms, (ii) bisoprolol and fludrocortisone for orthostatic intolerance, and (iii) beta-blockers such as metoprolol for palpitations and tremors (see Table 2 for a list of most widely used pharmacological treatment for POTS). These pharmacological treatments help improve blood flow and reduce symptoms such as lightheadedness, dizziness, and fatigue that are common in patients with POTS by regulating the autonomic nervous system which controls involuntary functions of the body, including heart rate, blood pressure, and digestion³. Non-pharmacological and lifestyle changes, such as salt intake, exercise training, food regulation, compression stockings/garments, and avoiding prolonged standing, exertion, and extreme temperatures, are also important in controlling the symptoms of POTS⁹. Interestingly, 52% of the POTS patients attributed symptom improvements to nonpharmacological treatments⁵. Our patient, who is a medical doctor, properly followed both pharmacological and non-pharmacological treatments with the guidance of her clinical team, and therefore she has been able to function optimally in various life settings over the past 30 years.

Table 2

The most widely used pharmacological treatment in POTS (as reported by Fedorowski⁹)
Drug	Comments
Heart rate-controlling agents
Beta-blockers (propranolol, 10–40 mg TID; bisoprolol, 2.5-5 mg BID; metoprolol, 25–100 mg daily; atenolol, 12.5–50 mg daily)	Beta-blockers are especially recommended in the ‘hyperadrenergic’ subtype associated with sinus tachycardia > 120 bpm on standing. Beta-blockers may aggravate orthostatic intolerance in low-BP phenotype, asthma, and paroxysmal chest pain.
Ivabradine (2.5–7.5 mg BID)	This drug is effective in low-BP phenotype or when beta-blockers are not well tolerated. It is usually seen as an alternative to beta-blockers.
Verapamil (40–80 mg BID/TID)	This calcium channel blocker with a negative chronotropic effect can be tested in the ‘hyperadrenergic’ type associated with higher BP, migraine, and chest pain.
Vasoactive and volume-expanding agents
Clonidine (0.2–0.6 mg BID)	Centrally acting α2-adrenoreceptor agonist with overall sympatholytic effect. It is generally recommended for the ‘hyperadrenergic’ subtype and hypertensive tendency on standing.
Midodrine (2.5–10 mg TID)	Direct α1-adrenoreceptor agonist. One of the few pharmacological agents positively tested in placebo-controlled studies for orthostatic hypotension. It may be effective in the ‘hypovolemic’ subtype and low-BP phenotype with pronounced orthostatic intolerance.
Droxidopa (100–600 mg TID)	Peroral norepinephrine precursor. The drug has been empirically used off-label in severe POTS.
Pyridostigmine (30–60 mg BID/TID)	Acetylcholinesterase inhibitor. It might be considered in the POTS phenotype associated with suspected autonomic neuropathy, gastrointestinal dysfunction, and non-specific muscle weakness. The effect on BP is small.
Fludrocortisone (0.1–0.2 mg daily)	Mineralocorticoid. Volume expander. Increases sodium reabsorption and enhances the sensitivity of α-adrenoreceptors. The drug may worsen supine hypertension and hypokalemia. It is recommended in the ‘hypovolemic’ subtype and low-BP phenotype.
Ephedrine and pseudoephedrine (25/30–50/60 mg TID)	Direct and indirect α1-adrenoreceptor agonist. Efficacy is controversial.
Desmopressin (0.1–0.4 mg BID)	Vasopressin analogue. Volume expander. Increases water reabsorption and reduces nycturia. Sparse evidence exists. Efficacy is uncertain.
In-hospital acute 1–2 L physiological saline infusion (during consecutive 3–5 days)	In acute decompensated POTS, this method should be considered to alleviate the short-term symptoms.

While POTS has been a highly recognized diagnostic category, especially after the COVID-19 pandemic due to its high prevalence following the SARS-CoV-2 infection¹⁰, it is also important to study malaria-related POTS, especially in tropical and poor countries where malarial infections are common. Although there were no obvious manifestations observed due to malignant malaria and/or malarial treatment in our patient, both animal and human studies have demonstrated neuronal damage following severe malarial illness. Our case study highlights the fact that post-malarial POTS seems to be a neglected area of research as there is a lack of data and a paucity of literature on this topic. While the diagnosis and management of POTS symptoms, irrespective of causal factors, are practically the same in current practice, we propose that the pathophysiology and manifestations of these symptoms may vary subtly due to specific etiological mechanisms. We also recommend that strategies aimed at both preventing and treating POTS symptoms should include both pharmacological and non-pharmacological measures, as both domains have been shown to reduce the symptoms and improve functioning, as our case report suggests.

POTS is a chronic and debilitating dysautonomic disorder characterized by impairments in autonomic control of cardiovascular, gastrointestinal, and thermoregulation functions, resulting in various symptoms of orthostatic intolerance. While POTS is increasingly being diagnosed as post-COVID sequelae and complications, it’s rarely being reported if caused by other infections and clinical conditions. This case study reports a 30-year clinical history of a woman patient who developed tachycardia, syncope, and dysautonomic symptoms at the age of 21 four weeks after her complete recovery from malignant malaria when she was a first-year medical student about 30 years ago. She was diagnosed with POTS four years after her first symptoms. This is a rare and probably the first reported case of post-malarial POTS, although symptoms associated with severe orthostatic hypotension, such as tachycardia and insufficient peripheral vasoconstriction, that are very similar to the symptoms of POTS, have been previously reported in acute malignant malaria. The patient was treated with pharmacotherapy, primarily beta-blockers, and Fludrocortisone along with lifestyle modifications. She responded well to medications and made a dramatic recovery from her major symptoms, although mild dysautonomic symptoms such as lack of thermoregulation and decreased perspiration have persisted. The patient has managed to live with these symptoms and to optimally function in her day-to-day life as well as in her medical career. We suggest that manifestations and pathophysiology of POTS caused by a non-viral etiology, including post-malarial onsets as illustrated in our case report, should be studied in detail to further understand the pathophysiology and management of the disorder.

Acknowledgments

I am grateful to Dr. Chella Kamarajan, PhD, for teaching me the basics of research methods and for his technical assistance during the preparation of this manuscript.

Data Availability Statement: Anonymized clinical data and reports regarding the case study will be made available by the author upon request.

Ethics Statement: The family members of the patient, who is deceased, provided consent for publishing this case report.

Conflicts of interest: The author declares no conflicts of interest for this case study.

Funding: The author declares that no financial support was received from any organization for this case study.

Author contributions: Mousumi Barua was involved in all aspects of the study, including the conception and design of the work, the acquisition and interpretation of data, and writing and editing the manuscript.

Grubb BP, Kosinski DJ, Boehm K, Kip K (1997) The postural orthostatic tachycardia syndrome: a neurocardiogenic variant identified during head-up tilt table testing. Pacing Clin Electrophysiol 20(9 Pt 1):2205–2212. 10.1111/j.1540-8159.1997.tb04238.x
Hasan B, Almasri J, Marwa B, Klaas KM, Fischer PR (2020) Treatment of Postural Orthostatic Tachycardia Syndrome With Medication: A Systematic Review. J Child Neurol 35(14):1004–1016. 10.1177/0883073820948679
Vasavada AM, Verma D, Sheggari V et al (2023) Choices and Challenges With Drug Therapy in Postural Orthostatic Tachycardia Syndrome: A Systematic Review. Cureus 15(5):e38887. 10.7759/cureus.38887
Agarwal AK, Garg R, Ritch A, Sarkar P (2007) Postural orthostatic tachycardia syndrome. Postgrad Med J 83(981):478–480. 10.1136/pgmj.2006.055046
Shaw BH, Stiles LE, Bourne K et al (2019) The face of postural tachycardia syndrome - insights from a large cross-sectional online community-based survey. J Intern Med 286(4):438–448. 10.1111/joim.12895
Stewart JM, Weldon A (2000) Vascular perturbations in the chronic orthostatic intolerance of the postural orthostatic tachycardia syndrome. J Appl Physiol (1985) 89(4):1505–1512. 10.1152/jappl.2000.89.4.1505
Boris JR, Huang J, Shuey T, Bernadzikowski T (2020) Family history of associated disorders in patients with postural tachycardia syndrome. Cardiol Young 30(3):388–394. 10.1017/S1047951120000165
Kucharik AH, Chang C (2020) The Relationship Between Hypermobile Ehlers-Danlos Syndrome (hEDS), Postural Orthostatic Tachycardia Syndrome (POTS), and Mast Cell Activation Syndrome (MCAS). Clin Rev Allergy Immunol 58(3):273–297. 10.1007/s12016-019-08755-8
Fedorowski A (2019) Postural orthostatic tachycardia syndrome: clinical presentation, aetiology and management. J Intern Med 285(4):352–366. 10.1111/joim.12852
Mallick D, Goyal L, Chourasia P, Zapata MR, Yashi K, Surani S (2023) COVID-19 Induced Postural Orthostatic Tachycardia Syndrome (POTS): A Review. Cureus 15(3):e36955. 10.7759/cureus.36955
Mohsen AH, McKendrick MW, Schmid ML, Green ST, Hadjivassiliou M, Romanowski C (2000) Postmalaria neurological syndrome: a case of acute disseminated encephalomyelitis? J Neurol Neurosurg Psychiatry 68(3):388–389. 10.1136/jnnp.68.3.388a
Butler T, Weber DM (1973) On the nature of orthostatic hypotension in acute malaria. Am J Trop Med Hyg 22(4):439–442. 10.4269/ajtmh.1973.22.439
Sivakorn C, Wilairatana P, Krudsood S et al (2021) Severe orthostatic hypotension in otherwise uncomplicated Plasmodium vivax infection. Malar J 20(1):28. 10.1186/s12936-020-03564-3
Lall VK, Dutschmann M, Deuchars J, Deuchars SA (2012) The anti-malarial drug Mefloquine disrupts central autonomic and respiratory control in the working heart brainstem preparation of the rat. J Biomed Sci 19(1):103. 10.1186/1423-0127-19-103
Thompson AJ, Lochner M, Lummis SC (2007) The antimalarial drugs quinine, chloroquine and mefloquine are antagonists at 5-HT3 receptors. Br J Pharmacol 151(5):666–677. 10.1038/sj.bjp.0707238
Medow MS (2011) Postural tachycardia syndrome from a pediatrics perspective. J Pediatr 158(1):4–6
Schondorf R, Low PA (1993) Idiopathic postural orthostatic tachycardia syndrome: an attenuated form of acute pandysautonomia? Neurology 43(1):132–137. 10.1212/wnl.43.1_part_1.132
Zadourian A, Doherty TA, Swiatkiewicz I, Taub PR (2018) Postural Orthostatic Tachycardia Syndrome: Prevalence, Pathophysiology, and Management. Drugs 78(10):983–994. 10.1007/s40265-018-0931-5

The authors declare no competing interests.

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A Case of Post-Malarial Postural Orthostatic Tachycardia Syndrome in a Young Woman of South Asian Origin

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Abstract

Introduction

Case Presentation

First Hospital Visit (at Age 25)

Second Hospital Visit (at Age 33)

Current Status (at Age 51)

Discussion

Conclusions

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References

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