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Abstract: This 62-year-old aunt presented with chest tightness and shortness of breath after intermittent exertion for up to one year. Examination revealed that the patient had decreased cardiac function, but the coronary angiography results were normal. Upon pursuing the medical history, it was found that the patient had a history of recurrent convulsions for many years. Combining the findings, it was clear that the patient had hypoparathyroidism with symptomatic epilepsy. After aggressive drug treatment, her symptoms resolved and her heart function and structure recovered.
[Basic information] Female, 62 years old
Disease Type】Hypoparathyroidism
【Visiting Hospital】Beijing Hospital
Consultation date】April 2019
Treatment plan】Intravenous drug therapy (furosemide injection, calcium gluconate injection) + oral drug therapy (calcium carbonate D3 tablets, vitamin D drops)
[Treatment period] 10 days of hospitalization and regular outpatient follow up
Treatment effect】The condition has been controlled, and all indicators are improving
I. Initial consultation
The patient is a 62-year-old female who was admitted to the hospital with the complaint of “intermittent chest tightness and shortness of breath for one year”. She reported that she had generalized weakness in the past year, and chest tightness and shortness of breath occurred intermittently after cold or exertion, without chest pain, wasting, low fever and night sweats, etc. The chest tightness and shortness of breath often improved slightly after resting on her own.
The patient’s vital signs were stable, his mental state was clear, and his spirit was fine. There were no special abnormalities in the neurological examination and cardiopulmonary and abdominal examination. The patient had mild depressible edema in both lower extremities.
The outpatient electrocardiogram showed prolonged QT interval. A chest X-ray examination showed no significant abnormalities, and the blood gas analysis was basically normal. The patient’s pulmonary function was checked and showed mild hypoventilation. Echocardiography showed a slightly enlarged left atrium, hypotonic left ventricular function, left ventricular ejection fraction of 45%, and no segmental ventricular wall motion abnormalities. Myocardial enzyme spectrum examination was performed, and the results were normal. Admitted to hospital with “cause of chest tightness to be investigated”.
II. Treatment history
After the patient was admitted to the hospital, further improvement of various tests showed that the patient’s blood potassium ion concentration was 3.23mmol/L; calcium ion concentration was 1.7mmol/L, which was low; phosphorus ion concentration was 2.21mmol/L, which was high; sodium ion concentration was 142mmol/L; chloride ion concentration was 91mmol/L; magnesium ion concentration was 0.79mmol/L. Liver and kidney The liver and kidney function was normal, and the thyroid function was normal. The whole segment parathyroid hormone measurement was 1.10ng/L, which was significantly low.
The patient started to have recurrent hand and foot twitches 15 years ago and was seen at the local hospital. On CT scan of the sexual head, bilateral basal ganglia, thalamus, dentate nucleus, and cerebral hemispheres were seen to be symmetrically distributed with patchy, striated, lunar, or punctate calcifications. The diagnosis of hypoparathyroidism with symptomatic epilepsy was considered in conjunction with the clinical presentation.
To clarify the cause of the patient’s chest tightness and shortness of breath, a cardiology consultation was requested and the patient was given a coronary angiogram, which suggested a myocardial bridge distal to the left anterior descending branch, with no remaining abnormalities. Combined with the patient’s cardiac ultrasound and electrocardiogram findings, previous history of hypocalcemia and extensive cranial calcification, hypocalcemic cardiomyopathy was considered to be caused by hypoparathyroidism.
After admission, the patient was given furosemide injection for diuresis, along with slow sedation of calcium gluconate injection and oral calcium carbonate D3 tablets and vitamin D drops for treatment.
III. Treatment effect
After 10 days of hospitalization, the patient’s lower limb edema disappeared and no further discomfort such as chest tightness and shortness of breath and limb twitching occurred, so the patient was given a discharge diagnosis and was instructed to continue to take oral calcium carbonate D3 tablets and vitamin D drops and to monitor the blood calcium level regularly to maintain it in the normal range. One year after discharge, a repeat cardiac ultrasound showed that the left ventricular ejection fraction was 55%, the left atrium returned to normal size, and the electrocardiogram QT interval returned to normal, suggesting that the patient’s cardiac function and structure had recovered.
IV. Notes
We are glad that after a series of medication treatment, the patient’s somatic symptoms improved significantly and the heart function and structure were restored. However, since there is no specific medication for hypoparathyroidism and primary hypoparathyroidism is difficult to cure, the patient was advised to adhere to regular medication for calcium supplementation after discharge and to monitor blood calcium levels to adjust medication dosage. Also, because of the patient’s age and the fact that chronic low calcium in middle-aged and elderly women can lead to severe osteoporosis and a high risk of fracture, the patient should also be careful to prevent falls and trauma to prevent fractures after discharge.
V. Personal insight
The patient in this case had a history of recurrent limb twitching for many years in the past without systematic examination and treatment, resulting in the presence of persistent hypocalcemia affecting brain function and structural function of the heart. There is no specific drug treatment for hypoparathyroidism, but with regular calcium supplementation, the progression of the disease and clinical symptoms can be effectively controlled.
Regarding the patient’s parathyroid etiology typing, considering that the patient has no previous history of neck surgery such as thyroid, no hypomagnesemia and other lesions, primary hypoparathyroidism is now considered a high possibility. More than 90% of patients with hypoparathyroidism have calcification in the brain parenchyma, the mechanism of which may be related to hypocalcemia and increased vascular permeability, or it may be due to pathological water retention in the brain tissue leading to calcification of calcium salts in the brain parenchyma. In contrast, the altered structural function of the heart caused by chronic hypocalcemia may be related to lower blood calcium affecting the excitation-contraction coupling of cardiac myocytes.
In addition, hypocalcemia can cause increased renal tubular sodium reabsorption, leading to water and sodium retention and increasing cardiac load. However, the signs and symptoms of hypocalcemic cardiomyopathy are not specific and can be easily misdiagnosed clinically as coronary artery disease and dilated cardiomyopathy. Therefore, the possibility of the disease should be considered when anti-heart failure therapy alone is ineffective and auxiliary tests do not reveal hypocalcemia that could explain the symptoms and signs.