Haptoglobin (Hp) is an inflammatory and adiposity marker, its expression during obesity being specifically induced in the white adipose tissue (WAT). We previously reported that when challenged with a high fat diet (HFD) Hp(-/-) mice are partially protected from the onset of insulin resistance and hepatosteatosis. The aim of the present study was to get further insights into Hp function in WAT. To this end, we performed histological and gene expression analysis of the Hp(-/-) WAT, both in standard and obesity conditions, and investigated how Hp deficiency impacts adipogenesis and WAT development. The average size and percentage of very large adipocytes were respectively smaller and reduced in HFD Hp(-/-) mice as compared with HFD WT. The expression of perilipin, HSL and angiogenesis related markers were increased in HFD Hp(-/-) mice. Lean adult Hp(-/-) showed significantly larger adipocytes and lower subcutaneous WAT expression of aP2 and LPL with respect to WT. Hp(-/-) young mice (P30) were characterized by larger adipocyte size and lower expression of adipocyte and adipogenesis markers. Comparison of adipocyte size distribution between young and adult mice revealed attenuated changes in Hp(-/-) mice compared with WT. Mouse embryonic fibroblasts from Hp(-/-) mice were less capable of accumulating triglycerides and exhibited lower expression of PPARγ, aP2, FAS, LPL and Leptin. In conclusion, Hp deficiency tends to blunt the effect of age and diet on the size of adipocytes, which show less susceptibility to develop hypertrophy during obesity and a reduced adipogenic/hyperplastic potential during youth. In addition, Hp deficiency impacts negatively on adipogenesis.

To determine the association between all-cause mortality and dietary protein intake in patients with chronic kidney disease, we performed a large-scale, 8-y prospective cohort study in 98,489 maintenance hemodialysis patients from a multicenter dialysis care provider. Compared with the reference level (60 to <70 g/d), patients with low protein nitrogen appearance (PNA) levels [<30 g/d, HR: 1.40 (95% CI: 1.30, 1.50); 30 to <40 g/d, HR: 1.33 (95% CI: 1.28, 1.39)] were associated with higher all-cause mortality and patients with high PNA levels [≥110 g/d, HR: 0.92 (95% CI: 0.88, 0.97); 100 to <110 g/d, HR: 0.87 (95% CI: 0.82, 0.91)] were associated with lower all-cause mortality in all analyses. This association was also found in subanalyses performed among racial and hypoalbuminemic groups. Hence, using PNA as a surrogate for protein intake, a low daily dietary protein intake is associated with increased risk of death in all hemodialysis patients. Whether the association between dietary protein intake and survival is causal or a consequence of anorexia secondary to protein-energy-wasting/inflammation or other factors should be explored in interventional trials.

SESSION TYPE: Cancer Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

The incidence of solid organ cancer with metastasis to bones of the digits (acrometastasis) is exceedingly rare, occurring in only 0.1% of cases with osseous involvement. We describe a 52 year-old female who was found to have metastatic lung adenocarcinoma with acrometastasis during evaluation of left thumb pain.

CASE PRESENTATION:

A 52 year-old female with history of migraines and 20 pack-year smoking was evaluated by orthopedics for left thumb swelling, pain, and absent flexion, and determined to have a trigger finger. Hand radiographs revealed no osseous abnormalities. She received a flexor sheath injection of corticosteroids, with subsequent improvement in pain and range of motion. However, 6 weeks later she developed new thumb erythema, relapse of symptoms, and a palpable mass. Surgical exploration revealed complete destruction of the proximal phalanx and no viable bone remaining. Histologic evaluation of the mass revealed a poorly differentiated adenocarcinoma, suggestive of a primary lung tumor by immunohistochemical staining. Survey imaging with CT chest revealed a large left upper lobe mass, extensive adenopathy of the mediastinum and left hilum, and suggestion of lymphangitic carcinomatosis. Additionally, PET imaging illustrated widespread disease, with involvement of the brain, adrenal glands, pelvis, and spine.

DISCUSSION:

Bony metastases are common and frequently occur from a wide array of primary tumors, including lung, prostate, kidney, breast, and gastrointestinal. However, bones of the hand rarely harbor metastatic disease, accounting for only 0.1% of metastatic osseous involvement. Acrometastasis was first identified in 1906 in a female with breast cancer and metastases to the metacarpals. The etiology of acrometastasis is almost exclusively a lung primary tumor, accounting for approximately 44% of all reported cases. The mechanism of spread to the digits is unknown, but hypotheses include increased blood flow and chemotaxis of prostaglandins during trauma. The high predilection towards a primary lung tumor among acrometastases is thought to be secondary to direct systemic arterial supply, whereas tumor emboli of other primary malignancies must first pass through capillary beds of the liver or the lung.

CONCLUSIONS:

Acrometastasis is a rare occurrence, and typically suggests concomitant widespread malignancy with poor prognosis. Our patient presented with thumb pain, and subsequent evaluation revealed metastatic lung adenocarcinoma. She died 6 weeks later. This emphasizes the importance of identifying non-benign causes of finger symptoms in a timely manner.1) Flynn CJ, et al. Two Cases of Acrometastasis to the Hands and Review of the Literature. Current Oncology 2008;15(5):51-58.DISCLOSURE: The following authors have nothing to disclose: David Ferraro, Pedro LuceroNo Product/Research Disclosure InformationSan Antonio Military Medical Center, Fort Sam Houston, TX.

SESSION TYPE: Critical Care Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Lactic acidosis is the most common cause of metabolic acidosis. Although generation of lactate is generally associated with hypoxia causing the body to shift towards anaerobic metabolism, the overproduction or underutilization of lactate is caused by more than just decreased tissue perfusion. We present a case of lactic acidosis with an ambiguous etiology.

CASE PRESENTATION:

An 86 year-old male was admitted to the medicine service for lower extremity DVT and infection of unknown etiology. He had a history of hypertension. Pertinent positives from the review of systems included weight loss, anorexia, constipation and fatigue. In the emergency room,he was found to have a lactate of 12. On the second day of his hospital course, he developed rectal bleeding and was transferred to our intensive care unit for further management. Upon arrival in the ICU, he was tachypneic, tachycardic with a blood pressure of 98/64 mmHg. His physical exam was significant for somnolence, blood-tinged stool on rectal exam and bilateral lower extremity edema. Laboratory studies revealed a three-gram decrease in hemoglobin, normal white count, an anion gap metabolic acidosis and mild hypoglycemia. After aggressive resuscitation, his vital signs and urine output normalized. Interestingly, his lactate increased to 19.9 and he developed a significant leukocytosis of up to 32,000. Ultimately, a peripheral smear showed what was thought to be mantle cell lymphoma or diffuse large B cell lymphoma. Flow cytometry studies and bone marrow or lymph node biopsies were necessary for more specific diagnosis but the patient quickly deteriorated. His family requested a withdrawal of life support and he died less than 24 hours later.

DISCUSSION:

The end product of glycolysis, pyruvate, reacts with NADH and lactate dehydrogenase to create lactate. Importantly, this process can occur despite ample supply of oxygen to the tissues. Epinephrine surges cause stimulation of the glycolytic pathway resulting in increased levels of blood lactate. Clearly, this process is at play in many ICU patients, albeit not necessarily in our patient. While insulin causes over-expression of glycolytic enzymes in healthy cells, IGF mimics insulin (with similar results) in malignant cells. Additionally, malignant cells often over-express insulin receptors, thereby creating two mechanisms for elevated lactate in some cancer states.

CONCLUSIONS:

It is important for physicians to recognize that in addition to ischemia or shock, lactic acidosis may be a result of liver disease, medications, epinephrine surge or, as in our patient, hematalogic malignancy.1) Sillos, E, et al. "Lactic Acidosis: A Metabolic Complication of Hematologic Malignancies." Cancer, 2001, 92: 2237-46.2) James, J H et al. "Lactate is an Unreliable Indicator of Tissue Hypoxia in Injury or Sepsis." Lancet, 1999, 354: 505-08.3) Madias, N. "Lactic Acidosis." Kidney International, 1986; 29: 752-74.DISCLOSURE: The following authors have nothing to disclose: Chandra Patel, James AnholmNo Product/Research Disclosure InformationLoma Linda University Medical Center, Loma Linda, CA.

SESSION TYPE: Bronchology Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Endobronchial tuberculosis is more common in children than adults. It can present as bronchial ulcerations, hyperemia and mass lesions with obstruction. In patients with pulmonary tuberculosis, endobronchial involvement can be seen in 20-30% of the patients, with a higher incidence in women and HIV positive patients. We report a rare case of endobronchial tuberculosis masquerading as refractory asthma.

CASE PRESENTATION:

A 48 years old Guyanese female, non-smoker with history of hypertension and recently diagnosed mild intermittent asthma on albuterol MDI as needed, presented with complaints of worsening of her wheezing over four weeks. She denied weight loss, fever, chills or night sweats. No known Tuberculosis exposure. Her vitals were normal. Physical examination significant for diffuse bilateral expiratory wheezing. Laboratory investigations revealed normal complete blood count, kidney and liver functions. CXR showed bilateral upper lobe reticular nodular changes. A CT scan of the chest revealed bilateral cavitary lesions. Urine histoplasma antigen, ANCA, aspergillus antibody,HIV and hypersensitivity panel were negative. A tuberculin skin test and Quantiferon TB Gold test were positive. Three sputum samples for acid-fast smear were negative. High dose corticosteroids were started and a fiberoptic bronchoscopy was performed. Left bronchial inspection showed a large whitish fungating endobronchial lesion, occluding about 85% of the left main bronchus lumen. Inspection of the remaining bronchial tree similarly showed scattered whitish fungating patches that would not clear with normal saline washings. Biopsies of this large lesion showed necrotizing granuloma. Stains for acid-fast bacilli were positive.

DISCUSSION:

The association of endobronchial tuberculosis with hyperreactive airways has been described in patients with a known history of pulmonary tuberculosis. The differential diagnosis includes endobronchial tumors, wegener's granulomatosis, coccidiomycosis, histoplasmosis, and actinomycosis. Early introduction of antituberculous therapy is crucial to cure the patient. Endobronchial TB is treated with rifampin, isoniazid, ethambutol and pyrazinamide for nine months. Addition of corticosteroids is appropriate when airway compromise is present. Inhalation therapy with isoniazid or streptomycin was shown to be helpful in preventing stenosis in selected cases. For bronchial stenosis, bronchoscopic balloon dilatation with or without stent placement is needed. Our patient improved dramatically with her antituberculosis regimen. The corticosteroids she received initially may have had a role in preventing the complications of bronchial stenosis.

CONCLUSIONS:

We advocate including endobronchial tuberculosis in the differential diagnosis of immunocompetent patients presenting with a refractory wheeze.1) Hoheisel G, Chan BK, Chan CH, et al. Respir Med 1994; 88 : 593-97.2) Rikimaru T et al. Int J Tuberc Lung Dis 2001; 5: 769-74.DISCLOSURE: The following authors have nothing to disclose: Pankaj Kapadia, Amtinder Batth, Dipaben Modi, Karen Mrejen, Ricardo LopezNo Product/Research Disclosure InformationQueens Hospital Center affiliated with Mount Sinai School of Medicine, Jamaica, NY.

SESSION TYPE: Miscellaneous Student/Resident Cases IPRESENTED ON: Tuesday, October 23, 2012 at 11:15 AM - 12:30 PM

INTRODUCTION:

Tuberous sclerosis complex (TSC) is an inherited disorder that results in formation of benign hemartomas in multiple organs. We report a rare case highlighting the unique array of multiorgan involvement in TSC and the dilemma associated with management massive renal angiomyolipomas (AMLs).

CASE PRESENTATION:

A 28 year-old female with a history of seizure disorder and developmental delay presented with a two-week history of abdominal fullness, and two days of acute dyspnea and chest pain. Initial vital signs were normal. Examination was notable for decreased breath sounds at the left apex, a palpable mass in the left abdomen, and numerous ophthalmic and dermatologic findings consistent with TSC. Laboratory findings were within normal limits. Chest x-ray showed a moderate-sized left pneumothorax. CT chest, abdomen and pelvis was notable for diffuse cystic lung disease, a left-sided pneumothorax, and massive bilateral renal AMLs--the largest measuring 16 cm x 16 cm x 12 cm (Figures 1,2). Further imaging, including brain CT/MRI and echocardiography, revealed numerous manifestations characteristic of TSC. A chest tube thoracostomy was performed with resolution of the pneumothorax. The patient continued to experience significant abdominal pain. Therefore, a multidisciplinary approach was pursued--with input from numerous services--and the patient was placed on sirolimus for 12-months prior to consideration for embolization and debulking surgery.

DISCUSSION:

Angiomylolipomas are slow growing tumors often associated with TSC. While benign, these tumors can become symptomatic when they achieve extremely large sizes. Tumor size is correlated with increased risk of aneurysm and rupture. In addition, tumors can undergo malignant transformation and is associated with renal cell carcinoma. There are several indications for treatment, including suspicion of malignancy, alleviation of refractory pain and hemorrhage. The goal of therapy is to spare the kidneys. Transcatheter embolization has been shown to reduce tumor size by &gt;50 percent, with preserved renal function. The use of sirolimus, an immunosuppressant that targets mTOR, has also been shown to be effective in reducing tumor size by half. In our patient, given the extreme size of her AMLs, the treatment decision was based on using a multi-modal approach with sirolimus followed by embolization and/or surgical resection.

CONCLUSIONS:

The management of massive renal AMLs associated with TSC is complex and requires a multidisciplinary approach. This includes numerous treatment modalities aimed at achieving reduction in tumor size and ultimately decreasing the risk of untoward complications.1) Yamakado Y, Naoshi T, et al. Renal angiomyolipoma: relationships between tumor size, aneurysm formation, and rupture. Radiology 2002; 225(1):78-82.2) Williams JM, Racaidio JM, et al. Embolization of renal angiomyolipomata in patients with tuberous sclerosis complex. Am J Kidney Dis 2006; 47(1):95-102.DISCLOSURE: The following authors have nothing to disclose: Kelvin Chan, Nader KamangarNo Product/Research Disclosure InformationOlive View-UCLA Medical Center, Sylmar, CA.

SESSION TYPE: Critical Care Student/Resident CasesPRESENTED ON: Monday, October 22, 2012 at 01:45 PM - 03:00 PM

INTRODUCTION:

Sinus histiocytosis with massive lymphadenopathy is a rare histiocytic disorder (1969). The etiology is unknown although suspected occult infection or exaggerated immune response to infectious agent is possible.

CASE PRESENTATION:

A 27 yo AA female presenting with 1 week of worsening dyspnea & chest pressure. She reports having similar episodes for 1year. She reports palpitations, nausea and cough. CT Chest demonstrated a pericardial effusion, right pleural effusion, and extensive bilateral air space opacity in a tree and bud configuration and enlargement of the medisastinal and bihilar soft tissue mass impinging on the pulmonary artery. TTE showed markedly dilated RA/RV & reduced systolic function. PA systolic pressure was 85-90mmHg. She was treated with IV steroids and required high concentration oxygen. VAT with lymph node and lung biopsy was performed before pulmonary artery stenting and radiation therapy without significant therapeutic response. Pathology concluded "sinus histiocytosis with massive lymphadenopathy". Histiocytes showed emperipolesis and were CD68+, variably S100+, and CD1a negative.

DISCUSSION:

SHML occurs in any age group but most frequently in young children/adults, Males&gt; Females, in those of African or Caribbean decent. Potential causative agents include Post-viral (HHV6 or EBV), Hodgkins/non-hodgkins, and auto-immune disease although exact etiology is unclear. Typically SHML presents as massive bilateral cervical lyphadenopathy with fever, night sweats, & weight loss. Common extranodal sites include skin, upper respiratory tract, and bone but rarely include lung, spleen and bone marrow. Kidney, lower respiratory tract and liver involvement are poor prognostic factors. These patients typically have leukocytosis, elevated ESR, and polyclonal hypergammaglobulinemia. On pathology lymph nodes show pericapsular fibrosis with dilated sinuses, heavily infiltrated with large histiocytes, lymphocytes and plasma cells. Emperipolesis is the engulfment of lymphocytes and erythrocytes by histiocytes that express S100 and is considered the hallmark of SHML/RDD. Cells stain positive for S100, CD68 and negative for CD1a. We report a rare presentation of sinus histiocytosis with massive lymphadenopathy which presents as a mediastinal mass with lung involvement. Majority of patients have a benign course and do not require treatment. Therapy is reserved for patients with extranodal disease with vital organ involvement causing life-threatening complications. Systemic corticosteroids can decrease nodal size and symptoms. Radiotherapy and chemotherapy have limited efficacy.

CONCLUSIONS:

We report an aytpical presentation on a rare histiocytic disorder of biopsy proven Rosai-Dorfman disease (SHLM) resulting in hypoxic respiratory failure and death.1) Y. Shi et al. Sinus histiocytosis with Massive Lymphadenopathy (Rosai-Dorfman Disease): A case report and review of 49 cases with fine needle aspiration cytology. Cytojournal 2011:8:3DISCLOSURE: The following authors have nothing to disclose: Sajeet Sawhney, Edison Gavilanes, George Haralambou, Melvin HochmanNo Product/Research Disclosure InformationNew York Hospital Queens, Flushing, NY.

SESSION TYPE: Miscellaneous Case Report Posters IPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Fat emboli have been known as part a syndrome associated with pelvic or long bone fractures, and patients usually present with neurologic, hematologic, dermatologic, and respiratory manifestations. Other types of pulmonary emboli represent dislodgements from thrombi or lesions originating in the venous circulation.

CASE PRESENTATION:

A 70 year-old non-smoker woman with a history of hypertension was evaluated for slightly worsening kidney function. Abdominal renal ultrasound followed by computed tomography (CT), showed a 12 cm left renal mass consistent with fat density (-69 Hounsfield Unit) and invasion of the left renal vein. Chest CT scan revealed a large pulmonary embolus of fat density within the right pulmonary artery. Left radical nephrectomy followed by histopathological examination demonstrated the diagnosis of benign angiomyolipoma (AML). The patient was discharged home on no anticoagulation. Follow-up chest CT scan 4 weeks later showed no extension of the pulmonary embolism.

DISCUSSION:

AML rarely extends into the renal vein, inferior vena cava or up to the right atrium. Moreover, only four cases of renal AML were reported in association with fat emboli. They were all symptomatic with significant respiratory or cardiovascular manifestations and treatment varied from observation to surgical embolectomy. Tan, Yip (1) described a patient who presented with acute dyspnea two months post nephrectomy for AML and was found to have fat pulmonary embolus that diminished in size 4 months later. Turowski et al reported a 20 year-old patient that developed cardiac arrest secondary to fat pulmonary embolus that occurred intra-operatively during nephrectomy for AML. In addition, Shinohara et al encountered the worst-case scenario where an 83 year-old woman presented with acute hemodynamic shock and died a few days later. There are no reported cases in the literature of renal AML that was associated with asymptomatic fat embolus. Further literature review found no evidence to support the use of anticoagulation to treat pulmonary fat emboli. Our case is unique as the patient was asymptomatic and the diagnosis was based on the incidental finding of right lung base density on abdominal CT scan. Unless symptomatic, the long-term implication of diagnosing asymptomatic fat emboli remains unclear. Furthermore, when invading the renal vein or the inferior vena cava (IVC), renal AML should be surgically removed even if asymptomatic. Some surgeons elect to use temporary balloon occlusion of the IVC during renal carcinoma resection to prevent fatal intraoperative pulmonary emboli.

CONCLUSIONS:

Benign renal angiomyolipoma with renal vein extension can be associated with incidental diagnosis of an asymptomatic fat embolism.1) Tan YS, Yip KH, Tan PH, Cheng WS. A right renal angiomyolipoma with IVC thrombus and pulmonary embolism. International urology and nephrology. 2010;42(2):305-8. Epub 2009/07/18.DISCLOSURE: The following authors have nothing to disclose: Kassem Harris, Elie Hatem, Rabih Maroun, Theodore ManiatisNo Product/Research Disclosure InformationStaten Island University Hospital, Staten Island, NY.

SESSION TYPE: Heart FailurePRESENTED ON: Sunday, October 21, 2012 at 10:30 AM - 11:45 AM

PURPOSE:

Intravenous (IV) diuretics are commonly used for the treatment of hospitalized patients with decompensated heart failure (HF), and can induce electrolyte abnormalities, acute kidney injury, and tinnitus. Extracorporeal ultrafiltration (UF) is an invasive therapy that has shown some promise for the treatment of decompensated HF with improvement in extracellular fluid volume and reduction in hospital readmissions. We conducted a meta-analysis of on the potential benefits of UF vs. IV diuretics in patients with decompensated HF.

METHODS:

We performed a literature search in PubMed, Cochrane Database, EMBASE (inception through February 15, 2012) using predefined criteria and specific terms, and reviewed proceedings from relevant scientific meetings. Randomized controlled trials (RCTs) comparing the efficacy of UF vs. IV diuretics on clinical, hemodynamic, and humoral parameters in patients with DHF were included. Random-effects (for continuous outcomes) and (Peto) fixed-effect (for binary outcomes) model meta-analyses were performed. Heterogeneity among individual study effect estimates was assessed using the I2 index.

RESULTS:

5 RCTs (343 analyzable patients) were included. UF (average duration 31±3 hours) resulted in a significant net fluid removal of 1609 ml (95% confidence interval [CI] -1006, -2212 ml; P &lt; 0.001; I2 = 2%) relative to IV diuretics, but a non-significant net weight loss of 2.9 kg (95% CI -6.6, 0.9 kg; P = 0.13, I2 = 98%). UF was also associated with a net reduction in circulating NT-proBNP level of 1192 pg/ml (95% CI -1748, -636 pg/ml; P &lt; 0.001, I2 = 0%) relative to IV diuretics. There was no observed effect of UF on mortality relative to IV diuretics (odds ratio 1.033; 95% CI 0.512, 2.083, P = 0.93 I2 = 0%).

CONCLUSIONS:

Compared to IV diuretics, extracorporeal UF is associated with more fluid removal, which is paralleled by a predictable decrease in circulating NT-proBNP levels. Although UF did not have an effect on mortality, analyses of other potential adverse effects of the therapy could not be ascertained.

CLINICAL IMPLICATIONS:

Based on this meta-analysis of a small number of RCTs, extracorporeal UF appears to be more effective than IV diuretics at removing extracellular fluid volume and improving circulating NT-proBNP levels in patients with decompensated HF. Ongoing large multicenter studies are expected to provide insights into the short- and long-term benefits and potential harms of this invasive extracorporeal therapy.DISCLOSURE: The following authors have nothing to disclose: Khagendra Dahal, Cristian Riella, Fouad Chebib, Diana Revenco, Paweena Susantitaphong, Lana Tsao, Michael Maysky, Bertrand JaberNo Product/Research Disclosure InformationSt. Elizabeth's Medical Center, Department of Medicine, Tufts University School of Medicine, Boston, MA.

SESSION TYPE: Critical Care Student/Resident Case Report Posters IPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Central diabetes insipidus is a condition characterized by excretion of large volumes of dilute urine secondary to either a deficiency in the production or release of arginine vasopressin. Glucocorticoids are necessary for the kidneys to excrete salt free water. Symptoms of central diabetes insipidus may be masked by concomitant ACTH deficiency. Polyuria may appear when corticosteroid replacement is instituted. We present a case of a woman who developed shock and was given dexamethasone for secondary adrenal insufficiency subsequently unmasking diabetes insipidus.

CASE PRESENTATION:

A 40-year-old Caucasian female with a remote history of pituitary surgery, presented with a 2-month history of recurrent vomiting, diarrhea and generalized weakness. Physical examination demonstrated drowsiness, tachycardia and hypotension. Initial labs revealed hyponatremia of 130 mmol/dl, hypokalemia 3.1mmol/dl, urine specific gravity of 1.030 and normal renal function. She was started on normal saline boluses but subsequently required vasopressors for refractory shock. Her work up included a serum cortisol which was found to be very low at 0.9 mcg/dl (normal cortisol level 5-25 mcg/dl). Cosyntropin stimulation test was positive for secondary adrenal insufficiency, and dexamethasone was initiated. The patient's symptoms resolved, however she subsequently developed polyuria. Further workup now revealed a low urine osmolality of 209 mOsmol/kg, plasma osmolality of 307 mOsmol/kg and hypernatremia of 149 mmol/dl. She was started on desmopressin for a new diagnosis of central diabetes insipidus. The patient improved and was discharged home on dexamethasone and desmopressin.

DISCUSSION:

Diabetes insipidus is defined as the excessive urinary loss of solute-free water demonstrated by polyuria (&gt; 2 ml/kg/hr). Cortisol plays a role in maintaining blood pressure and volume. When its levels are decreased, blood pressure decreases, which stimulates the release of vasopressin. Vasopressin increases water reabsorption in the kidney. If a person has diabetes insipidus concomitant with adrenal insufficiency and is treated with cortisol, the previously masked diabetes insipidus can rapidly manifest. As seen our case, polyuria ensued when dexamethasone was started for shock due to adrenal insufficiency. Desmopressin is the drug of choice for the treatment of central diabetes insipidus.

CONCLUSIONS:

Although rare, polyuria after initiating steroids is concerning for the unmasking of diabetes insipidus. Evaluation of urine and serum osmolality, as well a water deprivation test is the best ways to make the diagnosis, while desmopressin should be used for treatment.1) Baylis, PH, Cheetham, P, Diabetes Insipidus. Arch Dis Child 1998;79:84-89DISCLOSURE: The following authors have nothing to disclose: Hetalben Patel, Phillip Augustine, Richard FremontNo Product/Research Disclosure InformationMeharry Medical College, Nashville, TN.