Food safety is a major concern worldwide and human beings are frequently exposed to potentially toxic metals (PTMs) through consumption of vegetables, fruits, and cereal crops grown in contaminated areas. The present study investigates the concentrations of PTMs such as chromium (Cr), nickel (Ni), zinc (Zn), arsenic (As), cadmium (Cd), and lead (Pb) in the foodstuffs (fruits, vegetables, and cereals) collected from different markets of Khyber Pakhtunkhwa, Pakistan. Samples of fruits (banana, tangerine, apple, and guava), vegetables (tomato, onion, potato, pea, and lady finger), and cereals (rice, kidney beans, and chick peas) were acid-extracted and analyzed using ICP-MS. The concentrations of Cr, Zn, Pb, As, and Cd in fruits (54, 50, 50, 45, and 4% samples, respectively), vegetables (53, 43, 63, 80, and 46%), and cereals (37, 62, 25, 70, and 25%) exceeded their respective permissible limits set by FAO/WHO (2001). The results showed that the highest mean concentration was observed for Ni (14.95 mg/kg), Pb (0.57 mg/kg), and Cd (0.27 mg/kg) in vegetables followed by fruits and cereals. However, the highest mean concentration of As (0.44 mg/kg) was observed in cereal crops followed by vegetables and fruits. The individual health risk of PTMs via consumption of fruits, vegetables, and cereals were found within safe limits for adults and children. Nevertheless, the total HRI values (fruits + vegetables + cereals) for Ni, As, and Cd for both adults and children were observed > 1 and may posed potential risk for the community consuming these foodstuffs on a daily basis. Graphical abstract ᅟ.

Giant bullae often mimic pneumothorax on radiographic appearance. We present the case of a 55-year-old man admitted to a referring hospital with dyspnea, cough, and increasing sputum production; he refused thoracotomy for tension pneumothorax and presented to our hospital for a second opinion. A computed tomography (CT) scan at our hospital revealed a giant bulla, which was managed conservatively as an exacerbation of chronic obstructive pulmonary disease. Thoracic surgery was consulted but advised against bullectomy. Giant bullae can easily be misdiagnosed as a pneumothorax, but the management of the two conditions is vastly different. Distinguishing between the two may require CT scan. Symptomatic giant bullae are managed surgically. We highlight the etiology, presentation, diagnosis, and treatment of bullous lung disease, especially in comparison to pneumothorax.

CaseHospital Day 1: A 55-year-old man with chronic back pain was brought to the hospital by EMS after a cardiac arrest. The patient's brother stated that the patient had been drinking excessive amounts of alcohol and ingesting large quantities of oxycodone for the past 2-3 months. He was brought in to the Emergency Department approximately 20 minutes of ACLS in the field and started on a cooling protocol. The patient had continuous blinking and vertical eye movements, and an EEG showed status epilepticus. The patient was started on a propofol infusion, and the neurology service was consulted. Continuous EEG monitoring showed epileptiform activity; a MRI of the brain was consistent with anoxic brain injury. His neurological examination demonstrated intact brain stem reflexes. The family inquired about the patient's prognosis and were told that meaningful recovery was unlikely but that his prognosis could not be determined until his seizures were controlled and the sedatives were discontinued. The family wanted to withdraw care, but after the neurology consultant reiterated to them that we did not have sufficient data for a prognosis they agreed to observe the patient for 24 hours. Hospital Day 2:The next day we were informed that the patient's wife --with whom we had spoken only over the phone --wished to stop all medications and remove him from life support because the patient's wishes were to not be kept on life support. After several discussions we followed her wishes and discontinued all medications except those necessary for comfort. The patient was extubated using a termination of care protocol. Following extubation, sponta- Hospital Day 3:The following morning the patient showed significant neurological improvement; he was opening his eyes, recognizing family members, following commands, moving all extremities, and even vocalizing with a few words. Due to the change in clinical status the family decided to increase the level of support to maintain hydration and electrolytes and consider nutrition. Later that day his mental status again deteriorated, continuous EEG showed seizurelike activity, and anti-epileptic medications were restarted. He then developed respiratory distress with significant upper airway secretions, O 2 saturations in the 70s, and respiratory rates in 50s. The DNR/DNI status was resumed per family's wishes. His level of care was decreased to comfort measures only so that his respiratory distress and air hunger could be adequately treated. Hospital Day 4:The next morning he once again improved. He was more alert and making some effort to respond to commands. Once again his clinical status was reviewed with the family, and we increased some aspects of care, including routine labs and intravenous fluids with dextrose and multivitamins. That afternoon he became very agitated and received multiple doses of lorazepam, furosemide, and fentanyl which had little effect. Hospital Day 5:The following day he was in severe distress and was not responding to our commands. We started him on a fentanyl...

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Introduction: Postpartum Thyroiditis (PPT) is an autoimmune disorder characterized by destruction of the thyroid gland within the first year after delivery. Systemic Lupus Erythematosus (SLE), another autoimmune disease, has been associated with a spectrum of thyroid disorders. While the prevalence of thyroid diseases in patients with SLE is increased, the association between SLE and PPT is not well known. The infrequency of encountering SLE and PPT makes abnormal thyroid tests in the postpartum period a diagnostic challenge. Clinical Case: A 27-year-old G1P1001 who was five months postpartum and not breast feeding was referred to Endocrinology clinic for evaluation of abnormal thyroid function tests. Past medical history was significant for SLE with renal and pericardial involvement. SLE was well controlled, treated with hydroxychloroquine. Family history was significant for hypothyroidism in her mother. She was asymptomatic and appeared clinically euthyroid. Vitals were stable and physical exam was negative for goiter, nodule or orbitopathy. Lab results at two months postpartum showed an elevated TSH of 3.87 UIU/mL (Normal 0.40-3.8 UIU/mL) and at four months postpartum TSH was low at 0.012 UIU/mL. Repeat labs at five months postpartum continued to show a low TSH at 0.007 UIU/mL with mildly elevated Free T4 at 1.7 ng/dL (Normal 0.6-1.6 ng/dL) and elevated Free T3 of 6.0 pg/mL (Normal 2.1-3.8 pg/mL). Anti-thyroid peroxidase antibodies (TPO), thyroid stimulating antibodies (TSI) and TSH receptor antibodies (TRAb) were negative. Thyroid Ultrasound with Doppler was within normal limits. Radioactive Iodine Uptake and Scan, obtained at 6 months postpartum, showed high normal uptake (17% and 32% at 4 hours and 24 hours respectively), suggestive of recovery phase of PPT. The most recent TSH was elevated at 8.5 UIU/mL and Free T4 was low at 0.7 ng/dL. Disease course was consistent with PPT. Conclusion: The Th1 (T-helper) lymphocyte immune predominance in autoimmune thyroid disease and SLE is the immune-pathogenetic base of the association between both diseases. Postpartum thyroiditis is a variant of chronic autoimmune thyroiditis. Serum anti-TPO antibodies vary during pregnancy and tend to increase early and may decline later. Immunologic tolerance increases during pregnancy, fades in the postpartum period and makes interpretation of thyroid function tests and disease process challenging. Pregnant and postpartum patients who have SLE have increased prevalence of thyroid disease. Causes are multifactorial with a higher prevalence of hypothyroidism and thyroid autoantibodies. Hyperthyroidism is much less likely. One comparable study found 6 of 43 (14%) women with SLE developed PPT and only one of these patients had positive thyroid antibodies. These reports and our patient illustrate the variability of thyroid function tests in patients with SLE.