Cardiology in the Young (2015), 25, 261–266
© Cambridge University Press, 2013
doi:10.1017/S1047951113002023
Original Article Dilated cardiomyopathy secondary to rickets-related hypocalcaemia: eight case reports and a review of the literature Osman Yilmaz,1 Hasim Olgun,2 Murat Ciftel,1 Omer Kilic,3 Ibrahim Kartal,4 Nebahat Y. Iskenderoglu,4 Fuat Laloglu,5 Naci Ceviz2 1
Department of Pediatric Cardiology, Erzurum District Training and Research Hospital, Erzurum, Turkey; 2Department of Pediatrics, Division of Pediatric Cardiology, Ataturk University Medical Faculty, Erzurum, Turkey; 3Department of Pediatric Infectious Diseases, Erzurum District Training and Research Hospital, Erzurum, Turkey; 4Department of Pediatrics, Erzurum District Training and Research Hospital, Erzurum, Turkey; 5Department of Neonatal Intensive Care Unit, Nenehatun Obstetrics and Gynecology Hospital, Erzurum, Turkey Abstract Introduction: Dilated cardiomyopathy is usually idiopathic and may arise secondary to infections or metabolic or genetic causes. Another rare cause is hypocalcaemia. Owing to the fact that calcium plays an essential role in excitation and contraction of myocardial muscle, myocardial contractility may decline in patients with hypocalcaemia. Materials and Methods: Patients with symptoms of congestive heart failure and rickets-related hypocalcaemia were assessed clinically and by echocardiography in a paediatric cardiology clinic. Echocardiography was performed for all patients. Rickets was diagnosed according to the clinical, laboratory, and radiologic findings. Maternal lifestyle and living conditions were investigated, and the maternal 25-OH vitamin D3 blood level was measured. Results: We evaluated eight patients who developed heart failure as a result of severe hypocalcaemia associated with rickets between August, 1999 and June, 2012. The age distribution of the patients was 3–12 months. Laboratory results were consistent with advanced-stage rickets. Severe hypocalcaemia was detected in all patients. The maternal 25-OH vitamin D3 levels were low. Echocardiography revealed increased pre-treatment left ventricle end-systolic and end-diastolic diameters for age and reduced ejection fraction and fractional shortening. After clinical improvement, the patients were discharged. Conclusions: Severe hypocalcaemia associated with rickets must always be kept in mind among the causes of dilated cardiomyopathy and impaired cardiac function in infants. If diagnosed and treated in time, dilated cardiomyopathy and severe heart failure related to rickets respond well. Keywords: Rickets; hypocalcaemia; vitamin D3 deficiency; dilated cardiomyopathy Received: 15 August 2013; Accepted: 20 October 2013; First published online: 17 December 2013
D
ILATED CARDIOMYOPATHY IS USUALLY IDIOPATHIC
and may arise secondary to infections or metabolic or genetic causes. Another rare cause is hypocalcaemia.1–3 Owing to the fact that calcium plays an essential role in excitation and contraction of myocardial muscle, myocardial contractility may Correspondence to: O. Kilic, Department of Pediatric Infectious Diseases, Erzurum District Training and Research Hospital, Erzurum, Turkey. Tel: + 90 442 2325364; Fax: + 90 442 2325090; E-mail: [email protected]
decline in patients with hypocalcaemia.4 Many case reports of hypocalcaemia-related reversible dilated cardiomyopathy and heart failure in childhood have been published.5–12 Studies that took place in our region indicate that rachitis, which is an important cause of hypocalcaemia, remains to be a serious health problem.13,14 In this study, the clinical and laboratory features of patients with cardiomyopathy and congestive heart failure secondary to severe rickets diagnosed between 1999 and 2012 were evaluated.
262
February 2015
Cardiology in the Young
Methods Patients with symptoms of congestive heart failure and rickets-related hypocalcaemia were assessed clinically and by echocardiography in a paediatric cardiology outpatient clinic. Heart failure was diagnosed with the help of clinical findings and chest radiography. Echocardiographic examination was performed for all patients. Rickets was diagnosed according to the clinical, laboratory, and radiologic findings. Clinical and laboratory data of the patients were digitally recorded and consistent with severe rickets. In all, eight patients with heart failure accompanied by dilated cardiomyopathy were identified. The following factors were investigated: total number of children in the family, feeding methods, ingestion of vitamin D supplements, and history of symptoms such as loss of appetite, frequent respiratory infections, and seizure without fever. Maternal lifestyle and living conditions were also evaluated. During physical examination of the 3-month-old patients, growth and development percentiles, presence of craniotabes, fontanel width, and rachitic rosary were evaluated. The blood glucose, urea, creatinine, sodium, potassium, chloride, calcium, phosphorus, alkaline phosphotase, complete blood count, C-reactive protein, 25-OH vitamin D3, and parathormone levels in the patients’ blood samples were analysed. Wrist X-rays were obtained. A paediatric cardiologist in an echocardiography laboratory performed echocardiographic examinations for all patients in the supine position with Vivid 5 and Vivid 7 echocardiography instruments (GE Medical Systems, Horten, Norway) and a 7 MHz probe. Left ventricle function and left ventricle end-systolic and end-diastolic diameters were measured. Carnitine levels were measured, and certain viral serologic studies – hepatitis A, B, and C; Epstein–Barr virus; cytomegalovirus; parvovirus; and mumps – were performed using blood samples of patients with dilated cardiomyopathy.
Results We evaluated eight patients who developed heart failure as a result of severe hypocalcaemia associated
with rickets between August, 1999 and June, 2012. The age distribution of the patients was 3–12 months. In all, six patients had growth development impairment. Examination of maternal lifestyles and living areas revealed that mothers were living at the edge of Erzurum City and tended to keep the children covered, limiting exposure to sunlight. Maternal age and sibling number were variable. Demographic, clinical and familial characteristics of our patients are shown in Table 1. All patients were breastfed and were not taking supplemental vitamin D. Owing to the fact that none of the patients was in good general health, all were admitted to the hospital for treatment. Although they were brought to the hospital mostly for respiratory difficulties, nutritional impairment, or seizures, signs of congestive heart failure were discovered during the first examination. Clinical features of the patients are summarised in Table 2. Laboratory results were consistent with advanced-stage rickets, and severe hypocalcaemia was detected in all patients (Table 3). The mothers of all patients were examined by an endocrinologist. The maternal blood 25-OH vitamin D3 levels were
© Cambridge University Press, 2013
doi:10.1017/S1047951113002023
Original Article Dilated cardiomyopathy secondary to rickets-related hypocalcaemia: eight case reports and a review of the literature Osman Yilmaz,1 Hasim Olgun,2 Murat Ciftel,1 Omer Kilic,3 Ibrahim Kartal,4 Nebahat Y. Iskenderoglu,4 Fuat Laloglu,5 Naci Ceviz2 1
Department of Pediatric Cardiology, Erzurum District Training and Research Hospital, Erzurum, Turkey; 2Department of Pediatrics, Division of Pediatric Cardiology, Ataturk University Medical Faculty, Erzurum, Turkey; 3Department of Pediatric Infectious Diseases, Erzurum District Training and Research Hospital, Erzurum, Turkey; 4Department of Pediatrics, Erzurum District Training and Research Hospital, Erzurum, Turkey; 5Department of Neonatal Intensive Care Unit, Nenehatun Obstetrics and Gynecology Hospital, Erzurum, Turkey Abstract Introduction: Dilated cardiomyopathy is usually idiopathic and may arise secondary to infections or metabolic or genetic causes. Another rare cause is hypocalcaemia. Owing to the fact that calcium plays an essential role in excitation and contraction of myocardial muscle, myocardial contractility may decline in patients with hypocalcaemia. Materials and Methods: Patients with symptoms of congestive heart failure and rickets-related hypocalcaemia were assessed clinically and by echocardiography in a paediatric cardiology clinic. Echocardiography was performed for all patients. Rickets was diagnosed according to the clinical, laboratory, and radiologic findings. Maternal lifestyle and living conditions were investigated, and the maternal 25-OH vitamin D3 blood level was measured. Results: We evaluated eight patients who developed heart failure as a result of severe hypocalcaemia associated with rickets between August, 1999 and June, 2012. The age distribution of the patients was 3–12 months. Laboratory results were consistent with advanced-stage rickets. Severe hypocalcaemia was detected in all patients. The maternal 25-OH vitamin D3 levels were low. Echocardiography revealed increased pre-treatment left ventricle end-systolic and end-diastolic diameters for age and reduced ejection fraction and fractional shortening. After clinical improvement, the patients were discharged. Conclusions: Severe hypocalcaemia associated with rickets must always be kept in mind among the causes of dilated cardiomyopathy and impaired cardiac function in infants. If diagnosed and treated in time, dilated cardiomyopathy and severe heart failure related to rickets respond well. Keywords: Rickets; hypocalcaemia; vitamin D3 deficiency; dilated cardiomyopathy Received: 15 August 2013; Accepted: 20 October 2013; First published online: 17 December 2013
D
ILATED CARDIOMYOPATHY IS USUALLY IDIOPATHIC
and may arise secondary to infections or metabolic or genetic causes. Another rare cause is hypocalcaemia.1–3 Owing to the fact that calcium plays an essential role in excitation and contraction of myocardial muscle, myocardial contractility may Correspondence to: O. Kilic, Department of Pediatric Infectious Diseases, Erzurum District Training and Research Hospital, Erzurum, Turkey. Tel: + 90 442 2325364; Fax: + 90 442 2325090; E-mail: [email protected]
decline in patients with hypocalcaemia.4 Many case reports of hypocalcaemia-related reversible dilated cardiomyopathy and heart failure in childhood have been published.5–12 Studies that took place in our region indicate that rachitis, which is an important cause of hypocalcaemia, remains to be a serious health problem.13,14 In this study, the clinical and laboratory features of patients with cardiomyopathy and congestive heart failure secondary to severe rickets diagnosed between 1999 and 2012 were evaluated.
262
February 2015
Cardiology in the Young
Methods Patients with symptoms of congestive heart failure and rickets-related hypocalcaemia were assessed clinically and by echocardiography in a paediatric cardiology outpatient clinic. Heart failure was diagnosed with the help of clinical findings and chest radiography. Echocardiographic examination was performed for all patients. Rickets was diagnosed according to the clinical, laboratory, and radiologic findings. Clinical and laboratory data of the patients were digitally recorded and consistent with severe rickets. In all, eight patients with heart failure accompanied by dilated cardiomyopathy were identified. The following factors were investigated: total number of children in the family, feeding methods, ingestion of vitamin D supplements, and history of symptoms such as loss of appetite, frequent respiratory infections, and seizure without fever. Maternal lifestyle and living conditions were also evaluated. During physical examination of the 3-month-old patients, growth and development percentiles, presence of craniotabes, fontanel width, and rachitic rosary were evaluated. The blood glucose, urea, creatinine, sodium, potassium, chloride, calcium, phosphorus, alkaline phosphotase, complete blood count, C-reactive protein, 25-OH vitamin D3, and parathormone levels in the patients’ blood samples were analysed. Wrist X-rays were obtained. A paediatric cardiologist in an echocardiography laboratory performed echocardiographic examinations for all patients in the supine position with Vivid 5 and Vivid 7 echocardiography instruments (GE Medical Systems, Horten, Norway) and a 7 MHz probe. Left ventricle function and left ventricle end-systolic and end-diastolic diameters were measured. Carnitine levels were measured, and certain viral serologic studies – hepatitis A, B, and C; Epstein–Barr virus; cytomegalovirus; parvovirus; and mumps – were performed using blood samples of patients with dilated cardiomyopathy.
Results We evaluated eight patients who developed heart failure as a result of severe hypocalcaemia associated
with rickets between August, 1999 and June, 2012. The age distribution of the patients was 3–12 months. In all, six patients had growth development impairment. Examination of maternal lifestyles and living areas revealed that mothers were living at the edge of Erzurum City and tended to keep the children covered, limiting exposure to sunlight. Maternal age and sibling number were variable. Demographic, clinical and familial characteristics of our patients are shown in Table 1. All patients were breastfed and were not taking supplemental vitamin D. Owing to the fact that none of the patients was in good general health, all were admitted to the hospital for treatment. Although they were brought to the hospital mostly for respiratory difficulties, nutritional impairment, or seizures, signs of congestive heart failure were discovered during the first examination. Clinical features of the patients are summarised in Table 2. Laboratory results were consistent with advanced-stage rickets, and severe hypocalcaemia was detected in all patients (Table 3). The mothers of all patients were examined by an endocrinologist. The maternal blood 25-OH vitamin D3 levels were
