Plasmodium malariae causes uncommon benign malaria found in the malaria endemic regions mostly of Sub-Saharan Africa. As Plasmodium malariae does not have a continued liver stage in humans the only way to have reinfection without reexposure is through recrudescence. However, reports of its recrudescence after antimalarials are rare with only a handful of case reports in the literature. Research in this field to date has not been able to establish definitively an emergence of resistance in Plasmodium malariae to commonly used antimalarials. In the presented case, patient had a recrudescence of P. malariae after full treatment with quinine and clindamycin. This recrudescence was treated with full course of chloroquine with clearance of parasite from blood immediately after treatment and at two months' follow up. The recrudescence in this case cannot be explained by mechanisms explained in prior articles. We propose that the indolence of some of the Plasmodium malariae trophozoites in the blood can shield them from the effect of the toxic effects of antimalarials and enable them to produce recrudescence later. However, when recrudescence happens, this should not be considered a case of development of resistance and a course of chloroquine should be considered.

Patients with symptoms of opiate withdrawal, after the administration of opiate antagonist by paramedics, are a common presentation in the emergency department of hospitals. Though most of opiate withdrawal symptoms are benign, rarely they can become life threatening. This case highlights how a benign opiate withdrawal symptom of hyperventilation led to severe respiratory alkalosis that degenerated into tetany and cardiac arrest. Though this patient was successfully resuscitated, it is imperative that severe withdrawal symptoms are timely identified and immediate steps are taken to prevent catastrophes. An easier way to reverse the severe opiate withdrawal symptom would be with either low dose methadone or partial opiate agonists like buprenorphine. However, if severe acid-base disorder is identified, it would be safer to electively intubate these patients for better control of their respiratory and acid-base status.

Patient: Female, 49Final Diagnosis: Asystole with cardiac arrestSymptoms: —Medication: —Clinical Procedure: Peripheral inserted central catheter • lung biopsySpecialty: PulmonologyObjective:Rare diseaseBackground:Solitary fibrous tumors are rare tumors of mesenchymal origins, most commonly seen arising from the pleural lining of the lungs. These are generally benign tumors, which in rare cases have been identified to be associated with multiple paraneoplastic syndromes.Case Report:This is a case of a solitary fibrous tumor of the pleura in a 49 year old female which was found to be associated with elevated levels of serum beta human chorionic gonadotropin (β-hCG). Due to the lack of plausible causes for elevated β-hCG in the patient, immune-histochemical staining of the tumor specimen for β-hCG was obtained. This confirmed the patient’s solitary fibrous tumor as the source of the β-hCG. The patient was also found to have a possible paraneoplastic syndrome with irregular menstruation and hot flushes from the secreted β-hCG.Conclusions:This is the first reported case of solitary fibrous tumors of the pleura producing β-hCG. Multiple types of lung tumors have been associated with production of β-subunit of human chorionic gonadotropin. Production of βhCG by these tumors has been associated with a poor prognosis. In this case, we find an aggressive form of solitary fibrous tumor associated with production of β-hCG and associated paraneoplastic syndrome secondary to the β-hCG. Further study is required to identify the frequency of this phenomenon and the implications of β-hCG production in the prognosis of the solitary fibrous tumors.

INTRODUCTION: Tuberculosis (TB) and sarcoidosis are granulomatous diseases that challenge clinicians. We report a patient whose unusual presentation exemplified such a diagnostic dilemma. CASE PRESENTATION:A 26-year-old Pakistani female at 38 weeks gestation presented with transient right-sided weakness, aphasia and 2 weeks of headache. She was afebrile and appeared well. The fetus was in no distress. She experienced a brief recurrence of neurologic symptoms the next day. Examination was normal except during the episode. CTA was negative for stroke. Brain MRI (Fig. ) showed bilateral ring-like lesions consistent with inflammation or infection. Lung apices included in the CTA revealed bilateral nodular infiltrates. Recent CXR was clear. Chest CT (Fig. ) revealed adenopathy and lung nodules. On repeated questioning, the patient denied respiratory symptoms. Routine laboratory evaluation was unremarkable. LP yielded 455 WBCs with 78% lymphocytes; glucose 26; protein 121; low ADA. CSF AFB smear was negative. Vasculitis serology and HIV test were negative. QuantiferonÔ was previously positive. Bronchoscopic lung biopsy and placental tissue showed noncaseating granulomas with negative AFB stain. BAL smear was negative for AFB. The healthy appearance of the patient and fetus, lack of pulmonary symptoms, absence of fever, low ADA, presence of noncaseating granulomas, rarity of placental TB and immunocompetence all favored sarcoidosis over TB. Nevertheless, given her demographics, anti-TB therapy was initiated. Ultimately, BAL and lung biopsy cultures returned positive for M. tuberculosis. CSF AFB culture was negative.

A 49-year-old woman presented to the ED with sudden onset abdominal pain, nausea, and vomiting. Her medical history included an uncomplicated gastric lap band surgery 9 years ago and subsequent removal of lap band after 6 years. She had a Roux-en-Y gastric bypass and cholecystectomy 5 months prior to the current presentation. The patient had been diagnosed with asthma and was prescribed an inhaled corticosteroid that she used only as needed. The patient denied smoking and heavy alcohol consumption. She was currently employed as a scrub technician in a local surgical center.