Hypoparathyroidism and heart failure in thalassemic patients: a case report

Hypocalcemic cardiomyopathy due to primary or secondary hypoparathyroidism is usually refractory to conventional treatment for cardiac failure but responds favorably to the restoration of normocalcemia. We report on a thalassemic patient with severe cardiac failure due to hypocalcemia. Cardiac echocardiography showed impaired biventricular performance and laboratory analyses revealed hypoparathyroidism due to hemosiderosis. Concomitant treatment for heart failure and calcium supplementation was initiated. Thereafter, clinical and laboratory improvement was achieved. In the literature of thalassemic disorders, this is the first case of heart failure associated with hypoparathyroidism in which the patient recovered significantly after the correction of hypocalcemia, providing strong evidence to support our hypothesis of hypocalcemic myocardiopathy.     

Outbreak of infections caused by Enterobacter cloacae producing the integron-associated beta-lactamase IBC-1 in a neonatal intensive care unit of a Greek hospital

Nineteen of 27 ceftazidime-resistant Enterobacter cloacae isolates from a neonatal intensive care unit in Thessaloniki, Greece, had genes coding for the novel extended-spectrum beta-lactamase IBC-1; 18 of those 19 harbored similar conjugative plasmids and belonged to two distinct genetic lineages. A synergy test with ceftazidime and imipenem enabled us to identify five unrelated bla(IBC-1)-carrying E. cloacae isolates from other wards of the hospital. It seems that this integron-associated gene is capable of dispersing both by clonal spread and by gene dissemination.     

Clinical review: severe asthma

Severe asthma, although difficult to define, includes all cases of difficult/therapy-resistant disease of all age groups and bears the largest part of morbidity and mortality from asthma. Acute, severe asthma, status asthmaticus, is the more or less rapid but severe asthmatic exacerbation that may not respond to the usual medical treatment. The narrowing of airways causes ventilation perfusion imbalance, lung hyperinflation, and increased work of breathing that may lead to ventilatory muscle fatigue and life-threatening respiratory failure. Treatment for acute, severe asthma includes the administration of oxygen, beta2-agonists (by continuous or repetitive nebulisation), and systemic corticosteroids. Subcutaneous administration of epinephrine or terbutaline should be considered in patients not responding adequately to continuous nebulisation, in those unable to cooperate, and in intubated patients not responding to inhaled therapy. The exact time to intubate a patient in status asthmaticus is based mainly on clinical judgment, but intubation should not be delayed once it is deemed necessary. Mechanical ventilation in status asthmaticus supports gas-exchange and unloads ventilatory muscles until aggressive medical treatment improves the functional status of the patient. Patients intubated and mechanically ventilated should be appropriately sedated, but paralytic agents should be avoided. Permissive hypercapnia, increase in expiratory time, and promotion of patient-ventilator synchronism are the mainstay in mechanical ventilation of status asthmaticus. Close monitoring of the patient's condition is necessary to obviate complications and to identify the appropriate time for weaning. Finally, after successful treatment and prior to discharge, a careful strategy for prevention of subsequent asthma attacks is imperative.     

Determination of UVA protection factors using the persistent pigment darkening (PPD) as the end point. (Part 1). Calibration of the method

BACKGROUND/AIMS: The accuracy and reliability of any method to assess the UVA protection effectiveness of sunscreens needs to be demonstrated. The aim of the present study was to calibrate the effectiveness of a biological end point (Persistent Pigment Darkening, PPD) to assess UVA photoprotection, METHODS: Persistent Pigment Darkening was selected as the end point because its action spectrum extends across the UVA. A broad UVA source was chosen to challenge all UVA wavelengths. Attenuation of UVA was performed with neutral density filters (equally absorbing at all wavelengths). Human subjects were tested with a series of UVA beams attenuated by the neutral density filters. The UVA protection effectiveness of a standard sunscreen was also tested with four panels of volunteers to assess the reproducibility of the method. RESULTS: The attenuation factors of the neutral density filters were found to correspond to the UVA protection factors arrived at with PPD as the end point. The repetitive tests showed a good internal consistency of the method. CONCLUSIONS: The calibration procedure proposed shows threshold PPD, used as an end point in a UVA-PF test method, to be a reliable endogenous dosimeter for UVA radiation that enters the skin.