The Role of Impulsivity, Inattention and Comorbid ADHD in Patients With Bulimia Nervosa.
The Role of Impulsivity, Inattention and Comorbid ADHD in Patients with Bulimia Nervosa.
PLoS One. 2013; 8(5): e63891
Seitz J, Kahraman-Lanzerath B, Legenbauer T, Sarrar L, Herpertz S, Salbach-Andrae H, Konrad K, Herpertz-Dahlmann B
Little is known about the contribution of impulsivity, inattention and comorbid attention deficit/hyperactivity disorder (ADHD) in the development and maintenance of bulimia nervosa (BN). In particular, their specific contribution to disordered eating symptoms and whether they have additive effects to the general psychopathological burden remains unclear.Fifty-seven female patients seeking treatment for BN and 40 healthy controls completed diagnostic questionnaires and interviews that investigated: a) ADHD, b) impulsivity, c) eating disorders and d) general psychopathology. Attentional processes and impulsivity were assessed by a comprehensive computer-based neuropsychological battery.Twenty-one percent of patients with BN met the clinical cut-off for previous childhood ADHD compared to 2.5% of healthy controls. Adult ADHD according to DSM IV was also more prevalent in patients with BN, with an odds ratio of 4.2. Patients with BN and previous childhood ADHD were more impulsive and inattentive than patients with BN alone. These patients also displayed more severely disordered eating patterns and more general psychopathological symptoms compared with those without ADHD. Severity of eating disorder symptoms was better explained by inattentiveness than by either impulsivity or hyperactivity.Our data suggest an elevated rate of former childhood and current ADHD-symptoms in treatment-seeking patients with BN. Stronger impulsivity and inattention associated with more severe neuropsychological deficits and eating disorder symptoms indicate an additive risk that is clinically relevant for these patients. Thus, clinicians should identify comorbid patients who might profit from additional ADHD-specific treatments. HubMed – eating
Eating Out Without Overeating.
JAMA Intern Med. 2013 May 13; 1-2
Katz MH
True Beer Potomania Causing Critical Hyponatremia.
Chest. 2012 Oct 1; 142(4_MeetingAbstracts): 414A
Patel N, Sacks A
SESSION TYPE: Critical Care Cases IIPRESENTED ON: Wednesday, October 24, 2012 at 11:15 AM – 12:30 PMINTRODUCTION: Hyponatremia is a potentially fatal condition. Symptoms range from weakness and fatigue to seizures, coma, and even death. Causative circumstances are equally numerous and categorized on the associated volume status. Volume status, along with the degree of hyponatremia, determines the strategy to treat the patient. One such cause is excessive intake of a low-sodium liquid (i.e. beer) coupled with reduced intake of sodium, protein and other necessary nutrients, referred to as beer potomania. We present a case of profound hyponatremia.CASE PRESENTATION: A 56 year old female brought into the emergency department, for witnessed seizure activity and minimally responsive. Over the past several days, she has been progressively confused, somnolent and waning speech and orientation. In addition, she had nausea with multiple episodes of nonbloody emesis. Patient is a heavy alcoholic, partial to beer and has not been eating well. Physical exam showed an obtunded patient with diminished responsiveness and reflexes, upper extremities in a flexed posture and withdrawing to noxious stimulus. Laboratory studies revealed a sodium level of 97 mmol/L Due to an earlier seizure and the extreme degree of hyponatremia, the patient was started on a hypertonic saline infusion. Rate was calculated for goal correction rate of about 0.5 mmol/L/hour. Laboratory panels were followed frequently in the ICU, and the rate was adjusted accordingly. Patient recovered well during the hospitalization. Her mentation was near baseline after day two and by day 7 was discharged to home.DISCUSSION: Hyponatremia is common and often not life-threatening. Symptoms develop with levels below 125 with neurological complications occurring with sodium less than 115. However, acute and severe cases carry high mortality rates, greater than 50% when the level is less than 105. A thorough history is paramount; in this case the etiology was strongly suspected. Once the diagnosis of hyponatremia is made, the workup includes serum and urine osmolarity, urine sodium to determine volume status. In the case of beer potomania and polydypsia, sodium should correct shortly. Be wary of a rapid correction, which can result in osmotic demyelination syndrome. In cases of beer potomania, even conservative treatment can lead to this complication.CONCLUSIONS: With due diligence and appropriate treatment, severe hyponatermia can be a survivable disease entity and can have complete recovery.1) Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis. 2007;50(4):673-680.2) Campbell, M. Hyponatremia and Central Pontine Myelinolysis as a Result of Beer Potomania: A Case Report. Prim Care Companion J Clin Psychiatry. 2010; 12(4): PCC.09100936.DISCLOSURE: The following authors have nothing to disclose: Nimesh Patel, Andrew SacksNo Product/Research Disclosure InformationUniversity of Arizona, Sahuarita, AZ. HubMed – eating
Passive Transfer of Nut Allergy by Lung Transplantation.
Chest. 2012 Oct 1; 142(4_MeetingAbstracts): 1039A
Polito C, Neujahr D, Bag R, Lodi U, Sullivan T, Force S, Lawrence EC
SESSION TYPE: Miscellaneous Cases IIIPRESENTED ON: Wednesday, October 24, 2012 at 11:15 AM – 12:30 PMINTRODUCTION: This case describes a patient who developed a nut allergy after lung transplantation.CASE PRESENTATION: A 71 year-old man with idiopathic pulmonary fibrosis underwent bilateral lung transplantation in August 2011. The donor was an 15 year-old male with a history of asthma and peanut allergy and died of anaphylaxis after eating a food that contained nuts. After transplantation, the patient underwent induction immunosuppression with methylprednisolone, basiliximab and azathioprine followed by an oral regimen of predisone, tacrolimus and azathioprine. The recipient had no history of food allergy prior to transplantation. He was discharged after an uncomplicated postoperative course on day seven. Two weeks after discharge the patient experienced a syncopal event at home. Bradycardia and expiratory wheezing were present on initial examination. He was admitted to the hospital, stabilized, and discharged the following day. Two days later the patient experienced a respiratory arrest at home after eating a pastry that contained a nut crust. He was intubated in the field and was again noted to have diffuse wheezing. He was treated for status asthmaticus which resolved with bronchodilators and corticosteroids. Additional food history was obtained after extubation and revealed that the patient had eaten the same dessert immediately prior to both episodes. Specific IgE titers were performed and positive for pistachio (1.49 kU/L) and cashew (0.84 kU/L). Peanut specific IgE was negative. Upon discharge, the patient was advised to avoid all nuts and was given a prescription for intramuscular epinephrine. Three months after transplantation repeat titers were undetectable except for pistachio (0.49kU/L). Five months after transplantation skin prick testing for nut allergens was positive for cashews.DISCUSSION: To our knowledge, this is only the fourth reported case of passive transfer of a nut allergy in a lung transplant recipient. In all cases, the donor allergy was documented prior to transplantation. Passive transfer of nut allergy is hypothesized to occur by one of two mechanisms. Donor lungs may contain previously sensitized B lymphocytes that produce nut-specific IgE. Alternatively, transfer of sensitized mast cells harboring nut-specific IgE may also occur with subsequent migration of mast cells into host tissues.CONCLUSIONS: Knowledge of donor allergies should be considered prior to lung transplantation. If an allergy is identified, transplant recipients should be educated prior to discharge.1) Bhinder, S et al. Development of transient peanut allergy following lung transplantation: a case report. Canadian Respiratory Journal 2011; 18(3):154-6.2) .3) .DISCLOSURE: The following authors have nothing to disclose: Carmen Polito, David Neujahr, Remzi Bag, Umbreen Lodi, Timothy Sullivan, Seth Force, E. Clinton LawrenceNo Product/Research Disclosure InformationEmory University, Decatur, GA. HubMed – eating