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Letters to the Editor
was diagnosed. Treatment with methylprednisolone was initiated at 120 mg a day, leading to improvement both clinically and analytically. Twelve months treatment with interferon a2b at high dosage according to the Kirwood programme was well tolerated. A year later, two cervical lymphadenopathies were positive for metastatic melanoma; and 8 years after the first diagnosis of the tumour, she had bone metastases. One year later, the patient is alive and continues to experience flares of variable intensity of DM, which are partially controlled with oral corticosteroids. DM and CM is a rare association. We have reviewed all the published cases and out of all cases, 61.5% were women (12/26), and 69.2% had cutaneous and muscle involvement. Fifty-two per cent (13/25) were CM stage IV and survived less than a year (6.25 months median survival, range 2–11). Thirty-six per cent (9/25) were CM stage III, and 12% were stages I–II with a similar prognosis to that reported by AJCC2010 for CM (60% within first year). The time between CM and the appearance of the DM and CM stage were identified as independent prognostic factors (P < 0.02 and P < 0.004 respectively) in the survival rates. Cases with CM at stage IV and the emergence of DM up to 3 months after CM had a worse prognosis (Fig. 2). The cutaneous manifestations of DM can precede the neoplasm and thus be considered a marker of metastasis.4 However, the majority of cases
References 1 Barnes BE, Mawr B. Dermatomyositis and malignancy. A review of the literature. Ann Intern Med 1976; 84: 68–76. 2 Schiller M, Böhm M, Hensen P, Riemann H, Luger TA, Nashan D. Dermatomyositis associated with malignant melanoma –
develop DM and the neoplasm simultaneously, as did our patient. The symptoms of DM are often exacerbated by tumour relapse, which in some cases can be ameliorated with surgical treatment of the primary and recurrent tumour.5 Schiller et al.2 stated that DM is a poor prognostic factor for melanoma, but our case is an exception. According to our study, the time of appearance of DM and the stage of the CM have a significant influence. Long-term studies are required to clarify whether DM is a predictor of tumour relapse.
Acknowledgement We thank the patient for providing permission to share her story. Received 12 February 2014; accepted 28 April 2014. doi:10.1111/imj.12552
P. Fernández-Crehuet,1 A. Pérez-Gil,2 A. Herrera-Saval,3 C. Cantalejo-Rodríguez,4 J. J Ríos-Martín5 and F. M Camacho-Martínez6 1
Dermatology Department, Alto Guadalquivir Hospital. Andujar, Jaén, 2Dermatology Department, Hospital Universitario Nuestra Señora de Valme, 3Dermatology Department, Bonaderma Clinic, 4 Dermatology Department, Hospital de Utrera, 5Pathology Department, and 6Dermatology Department, Hospital Universitario Virgen Macarena, Sevilla, Spain
a marker of poor prognosis? J Am Acad Dermatol 2006; 54: 221–6. 3 Jouary T, Gracia C, Lalanne N, Vital A, Taieb A, Delaunay M. Rapidly lethal dermatomyositis associated with metastatic melanoma. J Eur Acad Dermatol Venereol 2008; 22: 399–401. 4 Shorr AF, Yacavone M, Seguin S, Jackson LW, Dennis GJ. Dermatomyositis and
Organophosphate poisoning with coronary artery vasospasm confirmed by angiography Organophosphate compounds are used worldwide as agriculture pesticides and have become one of the most common causes of poisoning.1 High incidence of mortality has been reported in the past because of delay of diagnosis and improper treatment.2 Respiratory failure has been the main cause of mortality.3 Cardiovascular effects of organophosphate poisoning are sometimes © 2014 The Authors Internal Medicine Journal © 2014 Royal Australasian College of Physicians
malignant melanoma. Am J Med Sci 1997; 313: 249–51. 5 Sais G, Marcoval J, Juggla A, Curco N, Servitje O. Dermatomyositis and metastatic malignant melanoma, with complete regression of the primary lesion. Br J Dermatol 1994; 130: 796–7.
serious but not fully appreciated by physicians.4 Mechanisms underlying the cardiovascular effects of organophosphate compounds are still unclear. Possible mechanisms include sympathetic and parasympathetic overactivity, hypoxaemia, acidosis and a direct toxic effect on the myocardium.5 Here, we report a rare case of coronary artery vasospasm cause by organophosphate poisoning. A 57-year-old man was brought to our Emergency Department for being found unconscious at home. The patient had some wine the night before, and went to bed
1043
Letters to the Editor
Figure 1 ECG at different stages. (a) peaked T-wave in V1–V3 leads and inverted T-wave in II, III and aVF leads on admission; (b) ST-segment elevated in II, III and aVF leads; (c) ST-segment regressed after injection of nitroglycerine; (d) another ST-segment elevation and third degree atrioventricular block at end stage.
without any symptoms such as chest pain. His wife found him unconscious the next morning. He had no convulsion or mouth angle deflection, and no medicine bottle was found in the bedroom. Previous medical history included coronary heart disease diagnosed only by electrocardiography (ECG), but we did not get the report. On physical examination, the patient’s vitals were as follows: body temperature 36.9°C, heart rate 90 beats per minute, respirations 20 per minute, blood pressure 88/59 mmHg and oxygen saturation 99% (on supplemental oxygen, 3 L/min). The patient had no response to verbal command. Skin was mildly wet without any special smell. His pupils’ diameter was 1 mm, and light reflex was negative on both sides. Lung auscultation revealed some moist rales on the dorsum side at the supine position. Cardiac auscultation revealed no murmurs. His abdomen was soft and non-tender to palpation, with normoactive bowel sounds and no hepatosplenomegaly. Babinski sign was negative bilaterally. Cranial computed tomography scan showed no sign of cerebral haemorrhage or infarction. ECG showed peaked T-wave in V1∼V3 leads and T-wave inversion in II, III and augmented vector foot (aVF) leads (Fig. 1a). Then ST-segment elevated about 3∼5 mv in II, III and aVF leads in the next ECG about 30 min later (Fig. 1b). Blood test revealed some severe metabolic acidosis (Table 1). Thereafter, the patient underwent a percutaneous coronary artery angiography performed after administration of aspirin (300 mg) and clopidogrel hydrogen sulfate 1044
tablets (300 mg) through a stomach tube and subcutaneous injection of low-molecular-weight heparin calcium (0.6 mL, approximately 6000 U). Coronary angiogram demonstrated that the patient had small coronary plaques and irregularities, 75–90% stenosis in the left anterior descending and left circumflex and severe vasospasm in the right coronary artery. After intracoronary injection of nitroglycerine, coronary angiogram showed complete resolution of the coronary vasospasm with no residual lesion (Fig. 2), and ECG displayed regression of ST-segment elevation in II, III and aVF leads (Fig. 1c). We also found vasospasm in the right iliac artery during angiogram, which disappeared after another local injection of 200 μg of nitroglycerine (Fig. 3). After coronary angiogram, blood test showed troponin I 4000 μg/mL) in the blood. The patient was then treated with an intravenous injection of atropine 10 mg. Atropine was then given as an intermittent dosing (2–5 mg every 10–30 min) according to the patient’s heart rate, sweating, rales of lungs and size of pupils until atropinisation and dry secretion was achieved. Atropine was then given 0.5–1 mg every 2–6 h after atropinisation (40.5 mg in total). Pralidoxime chloride was also injected (1 g per 4 h). Gastric lavage was performed through stomach tube using warm water. Hemoperfusion was also performed for 4 h. The patient did not revive unconsciousness. About 14 h after admission, the ECG showed © 2014 The Authors Internal Medicine Journal © 2014 Royal Australasian College of Physicians
Letters to the Editor
Figure 2 Coronary artery angiography. (a) left coronary artery vasospasm; (b) resolution of left coronary artery vasospasm after injection of nitroglycerine; (c) right coronary artery vasospasm; (d) resolution of right coronary artery vasospasm after injection of nitroglycerine.
(a)
(b)
(c)
(d)
ST-segment elevation in II, III and aVF leads again (Fig. 1d), complicated with third-degree atrioventricular block and serious bradycardia (heart rate 30–50 beats per minute). The patient died soon without chance of cardiac pacing or angiography (approximately 10 h from diagnosing to death). The history and manifestation of this patient showed few specific clues of organophosphate poisoning, such
Figure 3 Iliac artery angiography. (a) right iliac artery vasospasm; (b) resolution of right iliac artery vasospasm after injection of nitroglycerine.
(a)
© 2014 The Authors Internal Medicine Journal © 2014 Royal Australasian College of Physicians
as toxic exposure or smell of garlic, except for pinpoint pupils, slightly wet skin and mild rales in lungs. ST-segment elevation of ECG led to a misdiagnosis of acute myocardial infarction on admission. Coronary artery vasospasm, which could be responsible for ST-segment elevation, was then revealed by coronary artery angiography. ST-T change has been described as non-specific alteration in organophosphate poisoning
(b)
1045
Letters to the Editor
Table 1 Results of blood test Blood test Arterial blood gas analysis pH pCO2 (mmHg) pO2 (mmHg) Lactic acid (mmol/L) Standard bicarbonate (mmol/L) K+ (mmol/L) Na+ (mmol/L) Anion gap (mmol/L) Blood routine (vein) White blood cell (/L) Neutrophil (%) Haemoglobin (g/L) Haematocrit (%) Platelet (/L) Biochemical analysis (vein) Troponin I (ng/mL) Brain natriuretic peptide (pg/mL) D-dimer (ng/mL) Alanine transaminase (U/L) Aspartate transaminase (U/L) Creatinine (mmol/L) Blood urea nitrogen (mmol/L) K+ (mmol/L) Na+ (mmol/L) Cl− (mmol/L) Glucose (mmol/L) Cholinesterase (U/L) Carbon dioxide combining power (mmol/L)
Result
Reference range
6.86 43 100 0.8 4.5 5.9 132 31
7.35–7.45 35–45 80–100 0–1 22–27 3.5–5.5 135–145 8–16
27.99 × 109 78 185 52.31 278 × 109
4 × 109–10 × 109 50–70 120–160 40–50 100 × 109–300 × 109
Letters to the Editor
was diagnosed. Treatment with methylprednisolone was initiated at 120 mg a day, leading to improvement both clinically and analytically. Twelve months treatment with interferon a2b at high dosage according to the Kirwood programme was well tolerated. A year later, two cervical lymphadenopathies were positive for metastatic melanoma; and 8 years after the first diagnosis of the tumour, she had bone metastases. One year later, the patient is alive and continues to experience flares of variable intensity of DM, which are partially controlled with oral corticosteroids. DM and CM is a rare association. We have reviewed all the published cases and out of all cases, 61.5% were women (12/26), and 69.2% had cutaneous and muscle involvement. Fifty-two per cent (13/25) were CM stage IV and survived less than a year (6.25 months median survival, range 2–11). Thirty-six per cent (9/25) were CM stage III, and 12% were stages I–II with a similar prognosis to that reported by AJCC2010 for CM (60% within first year). The time between CM and the appearance of the DM and CM stage were identified as independent prognostic factors (P < 0.02 and P < 0.004 respectively) in the survival rates. Cases with CM at stage IV and the emergence of DM up to 3 months after CM had a worse prognosis (Fig. 2). The cutaneous manifestations of DM can precede the neoplasm and thus be considered a marker of metastasis.4 However, the majority of cases
References 1 Barnes BE, Mawr B. Dermatomyositis and malignancy. A review of the literature. Ann Intern Med 1976; 84: 68–76. 2 Schiller M, Böhm M, Hensen P, Riemann H, Luger TA, Nashan D. Dermatomyositis associated with malignant melanoma –
develop DM and the neoplasm simultaneously, as did our patient. The symptoms of DM are often exacerbated by tumour relapse, which in some cases can be ameliorated with surgical treatment of the primary and recurrent tumour.5 Schiller et al.2 stated that DM is a poor prognostic factor for melanoma, but our case is an exception. According to our study, the time of appearance of DM and the stage of the CM have a significant influence. Long-term studies are required to clarify whether DM is a predictor of tumour relapse.
Acknowledgement We thank the patient for providing permission to share her story. Received 12 February 2014; accepted 28 April 2014. doi:10.1111/imj.12552
P. Fernández-Crehuet,1 A. Pérez-Gil,2 A. Herrera-Saval,3 C. Cantalejo-Rodríguez,4 J. J Ríos-Martín5 and F. M Camacho-Martínez6 1
Dermatology Department, Alto Guadalquivir Hospital. Andujar, Jaén, 2Dermatology Department, Hospital Universitario Nuestra Señora de Valme, 3Dermatology Department, Bonaderma Clinic, 4 Dermatology Department, Hospital de Utrera, 5Pathology Department, and 6Dermatology Department, Hospital Universitario Virgen Macarena, Sevilla, Spain
a marker of poor prognosis? J Am Acad Dermatol 2006; 54: 221–6. 3 Jouary T, Gracia C, Lalanne N, Vital A, Taieb A, Delaunay M. Rapidly lethal dermatomyositis associated with metastatic melanoma. J Eur Acad Dermatol Venereol 2008; 22: 399–401. 4 Shorr AF, Yacavone M, Seguin S, Jackson LW, Dennis GJ. Dermatomyositis and
Organophosphate poisoning with coronary artery vasospasm confirmed by angiography Organophosphate compounds are used worldwide as agriculture pesticides and have become one of the most common causes of poisoning.1 High incidence of mortality has been reported in the past because of delay of diagnosis and improper treatment.2 Respiratory failure has been the main cause of mortality.3 Cardiovascular effects of organophosphate poisoning are sometimes © 2014 The Authors Internal Medicine Journal © 2014 Royal Australasian College of Physicians
malignant melanoma. Am J Med Sci 1997; 313: 249–51. 5 Sais G, Marcoval J, Juggla A, Curco N, Servitje O. Dermatomyositis and metastatic malignant melanoma, with complete regression of the primary lesion. Br J Dermatol 1994; 130: 796–7.
serious but not fully appreciated by physicians.4 Mechanisms underlying the cardiovascular effects of organophosphate compounds are still unclear. Possible mechanisms include sympathetic and parasympathetic overactivity, hypoxaemia, acidosis and a direct toxic effect on the myocardium.5 Here, we report a rare case of coronary artery vasospasm cause by organophosphate poisoning. A 57-year-old man was brought to our Emergency Department for being found unconscious at home. The patient had some wine the night before, and went to bed
1043
Letters to the Editor
Figure 1 ECG at different stages. (a) peaked T-wave in V1–V3 leads and inverted T-wave in II, III and aVF leads on admission; (b) ST-segment elevated in II, III and aVF leads; (c) ST-segment regressed after injection of nitroglycerine; (d) another ST-segment elevation and third degree atrioventricular block at end stage.
without any symptoms such as chest pain. His wife found him unconscious the next morning. He had no convulsion or mouth angle deflection, and no medicine bottle was found in the bedroom. Previous medical history included coronary heart disease diagnosed only by electrocardiography (ECG), but we did not get the report. On physical examination, the patient’s vitals were as follows: body temperature 36.9°C, heart rate 90 beats per minute, respirations 20 per minute, blood pressure 88/59 mmHg and oxygen saturation 99% (on supplemental oxygen, 3 L/min). The patient had no response to verbal command. Skin was mildly wet without any special smell. His pupils’ diameter was 1 mm, and light reflex was negative on both sides. Lung auscultation revealed some moist rales on the dorsum side at the supine position. Cardiac auscultation revealed no murmurs. His abdomen was soft and non-tender to palpation, with normoactive bowel sounds and no hepatosplenomegaly. Babinski sign was negative bilaterally. Cranial computed tomography scan showed no sign of cerebral haemorrhage or infarction. ECG showed peaked T-wave in V1∼V3 leads and T-wave inversion in II, III and augmented vector foot (aVF) leads (Fig. 1a). Then ST-segment elevated about 3∼5 mv in II, III and aVF leads in the next ECG about 30 min later (Fig. 1b). Blood test revealed some severe metabolic acidosis (Table 1). Thereafter, the patient underwent a percutaneous coronary artery angiography performed after administration of aspirin (300 mg) and clopidogrel hydrogen sulfate 1044
tablets (300 mg) through a stomach tube and subcutaneous injection of low-molecular-weight heparin calcium (0.6 mL, approximately 6000 U). Coronary angiogram demonstrated that the patient had small coronary plaques and irregularities, 75–90% stenosis in the left anterior descending and left circumflex and severe vasospasm in the right coronary artery. After intracoronary injection of nitroglycerine, coronary angiogram showed complete resolution of the coronary vasospasm with no residual lesion (Fig. 2), and ECG displayed regression of ST-segment elevation in II, III and aVF leads (Fig. 1c). We also found vasospasm in the right iliac artery during angiogram, which disappeared after another local injection of 200 μg of nitroglycerine (Fig. 3). After coronary angiogram, blood test showed troponin I 4000 μg/mL) in the blood. The patient was then treated with an intravenous injection of atropine 10 mg. Atropine was then given as an intermittent dosing (2–5 mg every 10–30 min) according to the patient’s heart rate, sweating, rales of lungs and size of pupils until atropinisation and dry secretion was achieved. Atropine was then given 0.5–1 mg every 2–6 h after atropinisation (40.5 mg in total). Pralidoxime chloride was also injected (1 g per 4 h). Gastric lavage was performed through stomach tube using warm water. Hemoperfusion was also performed for 4 h. The patient did not revive unconsciousness. About 14 h after admission, the ECG showed © 2014 The Authors Internal Medicine Journal © 2014 Royal Australasian College of Physicians
Letters to the Editor
Figure 2 Coronary artery angiography. (a) left coronary artery vasospasm; (b) resolution of left coronary artery vasospasm after injection of nitroglycerine; (c) right coronary artery vasospasm; (d) resolution of right coronary artery vasospasm after injection of nitroglycerine.
(a)
(b)
(c)
(d)
ST-segment elevation in II, III and aVF leads again (Fig. 1d), complicated with third-degree atrioventricular block and serious bradycardia (heart rate 30–50 beats per minute). The patient died soon without chance of cardiac pacing or angiography (approximately 10 h from diagnosing to death). The history and manifestation of this patient showed few specific clues of organophosphate poisoning, such
Figure 3 Iliac artery angiography. (a) right iliac artery vasospasm; (b) resolution of right iliac artery vasospasm after injection of nitroglycerine.
(a)
© 2014 The Authors Internal Medicine Journal © 2014 Royal Australasian College of Physicians
as toxic exposure or smell of garlic, except for pinpoint pupils, slightly wet skin and mild rales in lungs. ST-segment elevation of ECG led to a misdiagnosis of acute myocardial infarction on admission. Coronary artery vasospasm, which could be responsible for ST-segment elevation, was then revealed by coronary artery angiography. ST-T change has been described as non-specific alteration in organophosphate poisoning
(b)
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Letters to the Editor
Table 1 Results of blood test Blood test Arterial blood gas analysis pH pCO2 (mmHg) pO2 (mmHg) Lactic acid (mmol/L) Standard bicarbonate (mmol/L) K+ (mmol/L) Na+ (mmol/L) Anion gap (mmol/L) Blood routine (vein) White blood cell (/L) Neutrophil (%) Haemoglobin (g/L) Haematocrit (%) Platelet (/L) Biochemical analysis (vein) Troponin I (ng/mL) Brain natriuretic peptide (pg/mL) D-dimer (ng/mL) Alanine transaminase (U/L) Aspartate transaminase (U/L) Creatinine (mmol/L) Blood urea nitrogen (mmol/L) K+ (mmol/L) Na+ (mmol/L) Cl− (mmol/L) Glucose (mmol/L) Cholinesterase (U/L) Carbon dioxide combining power (mmol/L)
Result
Reference range
6.86 43 100 0.8 4.5 5.9 132 31
7.35–7.45 35–45 80–100 0–1 22–27 3.5–5.5 135–145 8–16
27.99 × 109 78 185 52.31 278 × 109
4 × 109–10 × 109 50–70 120–160 40–50 100 × 109–300 × 109
