Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Subcutaneous fat necrosis (SCFN) of the newborn is an uncommon dermatologic disorder characterized by firm, palpable subcutaneous nodules or plaques with or without erythema. Despite its benign course, SCFN may become complicated by extracutaneous manifestations. Hypercalcemia is considered a rare complication, but it is potentially fatal if unrecognized. During the last several years therapeutic hypothermia (TH) became an essential new therapeutic modality for severe neonatal asphyxia. We report a neonate who presented with SCFN and hypercalcemia following hypothermia therapy for hypoxic ischemic encephalopathy (HIE) and provide a review of the contemporary literature on the topic. We believe that this is important since the use of TH is rapidly increasing, and therefore, the possible side effects including SCFN and hypercalcemia may also become more prevalent. This prompts the need for awareness by treating physicians for this complication.
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PMID:Subcutaneous fat necrosis and hypercalcemia following therapeutic hypothermia--a patient report and review of the literature. 2128 34

When an ECG shows (or is suspicious for) a Brugada pattern, i.e., the association of a positive terminal deflection and ST segment elevation in the right precordial leads, the cardiologist often faces several problems. Three important questions are raised by this ECG pattern: (1) is this really a Brugada ECG pattern? (2) How can be determined whether this patient is at risk for sudden death? and (3) Should this patient receive an implantable cardioverter-defibrillator (ICD)? The term "Brugada syndrome" should be restricted to patients who have diagnostic ECG changes, as well as a history of symptoms. Asymptomatic subjects, in contrast, should be categorized as having a "Brugada ECG pattern" rather than the syndrome. Diagnostic ECG (type 1) is characterized by a J wave (a terminal positive wave) whose amplitude is > or =2 mm, and a "coved" type ST segment elevation located in the right precordial leads. These signs are usually present in leads V1 and/or V2 (lead V3 is more rarely involved, and is never the only affected one), but occasionally also can be observed in some of the limb leads. Types 2 and 3 ECGs, which are not truly diagnostic of Brugada pattern, are characterized by a "saddle back" ST segment elevation, that is > or =1 mm in type 2 and <1 mm in type 3. In Brugada ECG pattern, the QRS complex characteristically shows a positive terminal deflection that mimics an r' prime wave (the wave occurring in right bundle branch block), in the right precordial leads. Actually, it is a J wave that is very similar to the "Osborn" one observed during hypothermia. The J wave of Brugada ECG pattern is generated by a voltage gradient across the myocardial wall of the right ventricular outflow tract. This abnormal potential can be recorded only by electrodes located very close to the site where that phenomenon is originating. Displacement of the right precordial leads electrodes one or two intercostal spaces above their normal positions may, at times, disclose the diagnostic pattern when conventional leads, recorded at the fourth intercostal space, are non-diagnostic or even normal. High right precordial leads should be recorded whenever standard V1-V3 leads raise the suspicion of Brugada pattern. For example, when a relatively large positive terminal wave, even of low amplitude, is recorded, placing high right precordial leads is an option that should be considered. The ECG may show a marked variation over time, ranging from the typical pattern to a completely normal ECG and back again. In subjects with a non-diagnostic ECG, a pharmacological test with sodium channel blockers may disclose the typical Brugada pattern. In order to establish the diagnosis, several conditions that can mimic Brugada pattern must be excluded. These include right bundle branch block, early repolarization, acute myocardial ischemia, pericarditis, hypercalcemia, hyperkalemia, hypothermia and primary right ventricular diseases, particularly arrhythmogenic right ventricular dysplasia. Some drugs (e.g., some antiarrhythmic drugs, psychotropic agents or antihistamines), hyperthermia and enhanced vagal tone, as it occurs after a full meal, may render Brugada pattern more evident on the ECG. Typical ventricular arrhythmia in Brugada syndrome is a polymorphic ventricular tachycardia, that can evolve into ventricular fibrillation; its mechanism is assumed to be phase 2 reentry. Monomorphic ventricular tachycardia is rarely seen. Atrial fibrillation occurs more frequently in patients with the Brugada ECG pattern than in the general population. A mutation in the SCN5A gene, which encodes the alpha subunit of the cardiac sodium channel, is found in about 20% of the subjects with Brugada pattern; mutations in other genes have less frequently been described. Genetic testing is not very helpful in formulating the diagnosis, but when a mutation is found it could be useful to extend testing to first degree relatives, enabling early detection of abnormal gene carriers. Patients who have experienced an aborted sudden death have a high risk of recurrence and should receive an ICD. A history of syncope, spontaneous type 1 ECG and male sex, not family history of sudden death, are independent risk factors. The role of programmed ventricular stimulation in risk stratification remains the subject of debate. Asymptomatic patients with a Brugada ECG pattern should: (1) receive adequate information on current knowledge concerning this topic, (2) be given the list of forbidden drugs, (3) be informed to promptly treat hyperthermia, (4) be informed that clinical evaluation should be extended to their first degree relatives, 5) undergo regular cardiology follow-up. Also in this group the role of programmed ventricular stimulation in risk stratification is debated. Subjects showing a Brugada pattern after a pharmacological challenge should be followed-up with ECG and 12-lead Holter monitoring, if available, to identify the appearance of spontaneous type 1 ECG. Symptoms should be promptly reported.
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PMID:[Doubts of the cardiologist regarding an electrocardiogram presenting QRS V1-V2 complexes with positive terminal wave and ST segment elevation. Consensus Conference promoted by the Italian Cardiology Society]. 2156 Apr 82

Therapeutic moderate hypothermia in newborns with hypoxic-ischemic encephalopathy is rapidly becoming standard clinical practice. We report here 12 cases of subcutaneous fat necrosis among 1239 cases registered with a national registry of newborns treated with moderate whole-body hypothermia. All the infants suffered from perinatal asphyxia and hypoxic-ischemic encephalopathy. Moderate-to-severe hypercalcemia was identified in 8 of 10 infants with blood calcium measurements. In all cases the skin lesions appeared after completion of the cooling treatment. Our data suggest that prolonged moderate hypothermia is an actual risk factor for subcutaneous fat necrosis. Because the lesions often develop several days after birth, physicians need to be aware of this condition as a possible complication in infants treated with moderate hypothermia after asphyxia. Blood calcium levels need to be monitored in affected infants.
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PMID:Subcutaneous fat necrosis after moderate therapeutic hypothermia in neonates. 2172 10

Subcutaneous fat necrosis of the newborn is a form of panniculitis that most often occurs in full-term infants with predisposing risk factors. Three neonates with hypoxic ischemic encephalopathy were treated with therapeutic hypothermia and developed extensive subcutaneous fat necrosis. All three infants developed extensive subcutaneous fat necrosis, involving the back, scalp, and arms. Mild, asymptomatic hypercalcemia was noted in one infant in the weeks following the subcutaneous fat necrosis. Hypothermia as a risk factor for subcutaneous fat necrosis is reviewed. Clinicians should be aware of subcutaneous fat necrosis as a possible risk factor and complication associated with asphyxiated newborns who may undergo therapeutic hypothermia. Future studies for therapeutic hypothermia should evaluate neonates for the development of subcutaneous fat necrosis.
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PMID:Extensive subcutaneous fat necrosis of the newborn associated with therapeutic hypothermia. 2190 37

Subcutaneous fat necrosis is an inflammatory disorder of adipose tissue. Although patients need long-term follow-up to prevent hypercalcemia, the prognosis is generally favorable. We herein present a case of a newborn who developed subcutaneous fat necrosis-related hypercalcemia after hypothermia treatment for hypoxic ischemic encephalopathy. Widespread use of hypothermia treatment for hypoxic ischemic encephalopathy in the neonatal intensive care unit may increase the risk of developing subcutaneous fat necrosis and subsequently hypercalcemia. Great care should be taken to recognize skin findings early in newborns receiving hypothermia treatment, and those diagnosed with subcutaneous fat necrosis require close follow-up because they are at risk for developing hypercalcemia.
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PMID:Hypercalcemia due to subcutaneous fat necrosis in a newborn after total body cooling. 2235 80

Calcification or ossification of the auricle, also referred to as petrified ear, is a rare diagnosis in dermatology. In medical literature, it has most often been attributed to trauma, hypothermia and frostbite, or hypercalcemia secondary to a metabolic or endocrine disorder, such as Addison's disease. Here, we report the clinical and radiologic findings of a 79-year-old African American male whose unilateral petrified auricle was an incidental finding. He had a preceding history of hyperparathyroidism and subsequent hypercalcemia treated with a subtotal parathyroidectomy three years prior to presentation. In addition to laboratory analysis, a history and physical examination was performed which revealed no other signs of hypercalcemia. Radiologic studies demonstrated partial ossification of the external auricular cartilage on the left side. The patient was diagnosed with the rare occurrence of a petrified ear. In light of this case, we provide a discussion concerning the possible etiologies of this diagnosis including appropriate patient evaluation and possible treatment recommendations.
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PMID:A rare case of petrified ear. 2325 82

THIS CASE REPORT EXPOSES A PHENOMENON WHICH, ALTHOUGH PROPOSED, HAS NOT BEEN DESCRIBED IN CLINICAL LITERATURE: transient postictal hemiplegia (Todd's paralysis) with concomitant electrocardiographic J-point deflection (Osborn waves). Although typically associated with hypothermia, a prominent J-wave on the electrocardiogram (ECG) results from a transmyocardial voltage gradient during ventricular repolarization. Rarely, the Osborn wave may be observed in a non-hypothermic setting such as hypercalcemia or cerebral hemorrhage. Transient postictal hemiplegia has been attributed to localized cerebral hypoperfusion resulting from motor cortex exhaustion following an epileptic seizure. The same central nervous system autonomic dysfunction has been theorized to produce subendocardial hypoperfusion with electrocardiographic change and cardiac troponin T elevation. This is the first described ECG evidence of a dynamically displaced J-point in the setting of postictal hemiplegia.
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PMID:Dynamic J-Point Elevation Associated with Epileptic Hemiplegia: The Osborn Wave of Todd's Paralysis. 2346 97

A 4-year-old female neutered British Shorthair cat was presented as an emergency owing to progressive apathy, anorexia, adipsia, weight loss and weakness. Clinical findings showed severe weakness, collapse, weak pulse, bradycardia, hypovolaemia and hypothermia. Blood examinations revealed marked metabolic acidosis, hyponatraemia, hyperkalaemia, hyperphosphataemia, hypercalcaemia, hypochloraemia and azotaemia. The diagnosis of feline hypoadrenocorticism was based on low cortisol and aldosterone plasma levels before and after synthetic adrenocorticotropic hormone administration. Initial treatment consisted of intravenous fluid therapy. After stabilisation a combination of fludrocortisone and prednisolone was given orally. One year after diagnosis the cat is free of clinical signs and in good condition.
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PMID:Addisonian crisis and severe acidosis in a cat: a case of feline hypoadrenocorticism. 2348 53

Subcutaneous fat necrosis of the newborn (ScFN) is an uncommon and transient disease characterized by defined areas of fat necrosis and overlying cutaneous nodule lesions. It usually becomes apparent within the first 6 weeks of life in full-term or post-term infants. It is caused by generalized and/or local tissue hypoperfusion. The skin lesions of ScFN tend generally to improve spontaneously in a few weeks. We present a full-term newborn with birth distress. After therapeutic hypothermia, she presented voluminous and numerous subcutaneous fat necrosis with extensive calcifications. Surgical management was decided at her ninth month because of a total lack of regression. Hypercalcaemia, the most threatening complication, appeared only after this delayed surgery.
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PMID:Surgical management of subcutaneous fat necrosis of the newborn required due to a lack of improvement: a very rare case. 2435 90

Subcutaneous fat necrosis of the newborn (SCFN) is a rare, benign, and self-limiting panniculitis of neonates that presents in the first few weeks of life and is most commonly associated with birth asphyxia and meconium aspiration. There have been few case reports of SCFN following therapeutic hypothermia. With the increasing use of therapeutic whole-body hypothermia, SCFN may become more prevalent. The differential diagnosis of SCFN can be broad, and clinicopathologic correlation is essential to make the correct and timely diagnosis. Clinicians should be aware of this rare disease and its potential serious complication hypercalcemia.
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PMID:Subcutaneous fat necrosis of the newborn associated with hypercalcemia after therapeutic hypothermia. 2507 24


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