A high serum bromide level can cause erroneously high serum chloride levels measured through routine assays. Here, we describe a case of pseudohyperchloremia in which routine labs showed a negative anion gap and elevated chloride levels measured with ion-selective assay. The serum chloride level was found to be lower when measured with a chloridometer that employs a colorimetric method of quantification. The initial serum bromide level was elevated at 1100 mg/L that was confirmed by repeating the test that again showed an elevated level of 1600 mg/L and appeared to cause erroneous hyperchloremia when using conventional serum chloride quantification methods. Our case highlights lab errors and factitious hyperchloremia as a cause of the negative anion gap caused by bromism, even without a clear history of bromide exposure. The case also underscores the importance of chloride measurement using both colorimetric methods and ion-selective assay in the case of hyperchloremia.

INTRODUCTION:Gemcitabine is used for treatment of pancreatic cancer. Pulmonary toxicity is uncommon side effect of gemcitabine. We are presenting a case of gemcitabine induced pneumonitis. CASE PRESENTATION: A 73 year-old-female with history of pancreatic cancer, hypertension, chronic kidney disease and anemia presented to emergency department with complain of shortness of breath (SOB) for five days which got progressively worse after her 6th chemotherapy cycle. She was diagnosed with adenocarcinoma of pancreases with metastasis to liver about one and half year prior to presentation. She received treatment with gemcitabine and Nab-paclitaxel for a year and was only on gemcitabine for last six month. She was tachypneic and hypoxic requiring 2 L oxygen via nasal cannula (NC). Physical examination was notable for wheeze and rhonchi on both lung auscultation. Blood tests resulted troponin 10pg/mL, brain natriuretic peptide 370pg/mL, serum creatinine 1.69mg/dL, D-dimer 4.45mg/dL, hemoglobin 7.1g/dL, white blood cell count 6600 cells/microliter, platelet 86/microliter. Infectious work up including urine culture, blood culture and PCR from nasal swab for atypical pneumonia panel and MRSA were resulted negative. Chest radiograph showed bilateral interstitial and airspace opacities in the mid and lowers lung fields with small pleural effusion (fig 1). She had lung VQ scan without ventilation scan given which showed area of segmental perfusion defect (fig. 2) . Imaging of lower extremities was negative for deep venous thrombus. Echocardiogram was negative for cardiac cause. Arterial blood gas showed respiratory acidosis with pH 7.15 when oxygen requirement increased to 15 L via mask which required high flow nasal cannula then ultimately noninvasive positive pressure ventilation (NIPPV). Heparin infusion was started which later discontinued as perfusion defect correlated with opacities on chest x-ray and respiratory acidosis. She was stated on intravenous methyl prednisolone succinate as other potential causes were unlikely. Her symptoms improved dramatically in one day requiring 2L oxygen via NC. She was discharged on steroid taper dose. DISCUSSION: Gemcitabine induced pneumonitis is diagnosis of exclusion. Our patient received both paclitaxel and gemcitabine for a year but she was only on gemcitabine for six month prior to presentation. SOB was progressive correlating with chemotherapy. Life threatening as well as infectious causes were ruled out before starting treatment for drug toxicity. SOB improved dramatically from NIPPV to NC within 24 hour of treatment with steroid. This case emphasis on early detection of gemcitabine induced lung toxicity help to improve quality of life and choosing alternative therapy. CONCLUSIONS:Gemcitabine induced pneumonitis should be on differential diagnosis of hypoxia in patients on chemotherapy with gemcitabine. Physician should be aware of this uncommon but fatal side effect.

We report a morbidly obese 72-year-old man admitted with acute right-sided chest pain and hypoxemia following bouts of vigorous coughing. This case illustrates the need to consider unusual etiologies of a common clinical presentation.

Introducti on: Polyarthriti s is a common presentati on of pati ents att ending medicine outpati ent department. Among various causes Rheumatoid arthriti s is the commonest and a well established case has disti nct characteristi c features. However the early presentati on of this disease has not been clear thus leading to delay in treatment. The objecti ves of this study was to identi fy the various causes of polyarthriti s in our clinical practi ce, discuss the varied clinical presentati on of rheumatoid arthriti s including early Rheumatoid arthriti s and to evaluate the treatment response during one year follow up. Methods: Prospecti ve longitudinal study conducted in a teaching hospital over a two years periodResults: Rheumatoid arthriti s was the commonest cause of polyarthriti s (77.8%) with a period prevalence of 0.7%. Early presentati on included atypical features like asymmetry, unilateral presentati on, manifesti ng within 2 months to 2 years of diagnosis. 43% (n=18) of the pati ents had swelling and tenderness in overused joints 1.5 years prior to full clinical manifestati on. Flitti ng or migratory joint pain not considered to be a feature of rheumatoid arthriti s was also present in 14.3% (n=6) pati ents with mean durati on of 1.5 years prior to full blown presentati on. MCPJ (metacarpophalyngeal joints) and PIP (proximal interphalyngeal joints) were involved in 90%. Treatment response with Methotrexate as a single DMARD was good as compared with DAS 28 ESR score. Conclusions:RA is a common arthriti s with varied clinical presentati on. Recogniti on of early symptoms is needed for early diagnosis and initi ati on of DMARD. Methotrexate as a DMARD is eff ecti ve and should be initi ated early.

Hypertensive emergency is a common cause of emergency room (ER) visits. Scleroderma renal crisis (SRC) is one of the rare causes of hypertensive emergency. SRC is a life-threatening condition that presents with acute onset severe hypertension accompanied by retinopathy, encephalopathy, and rapidly worsening renal function. We present a case of hypertensive emergency and renal failure with positive anti-Scl 70 and RNA polymerase III which is characteristic of SRC. Despite appropriate supportive care and timely treatment with angiotensin-converting enzyme inhibitors, the patient progressed to end-stage kidney disease.