Anaphylactic Food Allergy After Roux-en-Y Gastric Bypass.

The prevalence of obesity in the United States is projected to increase as high as 85% by 2030. Weight loss is associated with improved morbidity and mortality outcomes. Roux-en-Y gastric bypass (RYGB) is an effective procedure recommended for individuals with morbid obesity for weight loss. We report the case of a patient who developed worsening food allergic reactions after RYGB surgery that progressed to an anaphylactic reaction. A 36-year-old female developed an anaphylactic reaction to an ingredient in guacamole eight years after RYGB surgery. Prior to the surgery, she had symptoms consistent with oral allergy syndrome. After the gastric bypass, however, she experienced worsening symptoms. On this occasion, she developed throat tightness prompting a visit to the emergency department where she required emergent intubation for airway protection. Blood testing to assess for an immunoglobin E-mediated allergy to common foods was negative. Despite the negative test, the allergist maintained a high suspicion for the progression of food-pollen syndrome following gastric bypass. Disruption of protein digestion from stomach bypass surgery may result in dietary proteins large enough to elicit immune responses being presented to the immune-rich intestinal mucosa. Additional consideration should be given to patients with a preexisting history of food allergic reactions undergoing RGYB surgery.

A Rare Thrombophilic Occurrence: Dural Venous Sinus Thrombosis in a Patient with Significant Family History of Protein S Deficiency.

Protein S is a potent anticoagulant that downregulates thrombin formation and is a vitamin K-dependent glycoprotein which is primarily synthesized in the liver. A deficiency in this protein or decreased activity, as seen in hereditary protein S deficiency, can lead to life-threatening thrombosis. Hereditary protein S deficiency is a rare disease as listed by the National Organization for Rare Disorders (NORD). It is known to cause venous as well as arterial thromboembolic events commonly occurring in the deep leg and pelvic veins. Dural venous sinus thrombosis is a rare consequence of protein S deficiency and is associated with a risk of increased morbidity and mortality. We report a case of dural venous sinus thrombosis in a patient with a family history of protein S deficiency in nine family members. A 53-year-old female presented to the ED with a three-day history of persistent left-sided headache, left facial numbness with tingling, and photophobia. She denied any visual disturbances, slurring of speech, and/or unilateral weakness. Some 10 years prior to this episode, she was placed on warfarin therapy for deep vein thrombosis (DVT) of lower extremity, but she discontinued it after three years of treatment without consulting her treating physician. She was taking oral contraceptive pills (OCPs) for two years and discontinued one month ago. She has nine family members with protein S deficiency, but the patient was never screened for a hypercoagulable state. On admission, her vital signs were within normal limits. Pupils were round and reactive to light, neck was supple, there was a sensory deficit for pinprick on the left V2-V3 distribution, and remainder of the cranial nerves and neurologic examination was unremarkable. CT scan of the head demonstrated a hyper-density within the left transverse and sigmoid sinus suspicious for dural venous sinus thrombosis. This was confirmed by CT angiogram showing a filling defect throughout the transverse sinus and sigmoid sinus extending below the jugular bulb into the superior aspect of the jugular vein. Intravenous heparin and warfarin were initiated. As the patient had severe trypanophobia and IV heparin required frequent activated partial thromboplastin time (APTT) monitoring, this was later changed to subcutaneous low-molecular-weight heparin and warfarin. Subsequent thrombosis panel showed a reduced protein S activity of 15% and low levels of total and free protein S antigens. She was discharged home with life-long warfarin therapy. In conclusion, cerebral dural venous sinus thrombosis is a rare and potentially life-threatening condition that can be seen in hereditary protein S deficiency. A high degree of suspicion in young females with worsening headache and neurologic signs and symptoms will help with timely diagnosis and management avoiding serious consequences. In a patient with a family history of thrombophilia, as seen in our patient, screening is important in order to confirm an underlying thrombophilic state. Such testing may have helped our patient regarding education on avoiding potential risk factors for thrombophilia and importance of treatment adherence.

Infective Endocarditis Manifesting as Severe Elevation in Serum Aminotransferases in the Absence of Severe Tricuspid Regurgitation, Heart Failure, or Shock: A Diagnostic Challenge.

Infective endocarditis (IE) is a challenging condition to diagnose, given its protean clinical signs and symptoms, Elevation in serum aminotransferases in IE is associated with valvular regurgitation, acute heart failure, or congestive hepatopathy. Studies show co-existing liver failure portends worsening outcomes in IE and poses a challenge for successful surgical management. Here we report a diagnostic challenge in a 35-year-old man with IE presenting predominantly with gastrointestinal symptoms and severe elevation in serum aminotransferase. The degree of aminotransferase elevation in our patient prompted consideration of alternative causes like acetaminophen toxicity. Severe elevation in aminotransferases as an initial presentation in the absence of significant valvular regurgitation, acute right heart failure, or shock is uncommon. A high degree of suspicion is required to diagnose IE when patients present with atypical signs and symptoms to avoid delay in initiation of antibiotics and improve overall morbidity and mortality.

Renal Phosphate Wasting Due to Tumor-Induced (Oncogenic) Osteomalacia.

Osteomalacia is a widely prevalent bone disorder that is caused by an imbalance in body calcium and phosphate. Tumor-induced osteomalacia (TIO) is a rare form of osteomalacia that is associated with mesenchymal tumors. It is caused by overproduction of fibroblast growth factor 23 (FGF-23), a hormone involved in phosphate regulation. A 59-year-old male with a history of factor V Leiden mutation, pulmonary embolism, and deep vein thrombosis was diagnosed with oncogenic osteomalacia in 2008 following laboratory findings significant for low phosphorus and elevated FGF-23 levels. He underwent a resection of a right suprascapular notch mass with the biopsy confirming a phosphaturic mesenchymal tumor. He was maintained on oral phosphorus and calcitriol replacements with a regular follow-up with oncology and nephrology. Eight years later, the patient's phosphorus levels started declining despite replacement. A repeat test showed FGF-23 levels once again elevated. A whole-body magnetic resonance imaging (MRI) scan showed no significant findings. The patient was continued on oral replacement therapy with a close follow-up. Two years later, urine phosphorus excretion was elevated at 2494 mg per 24 hours with low plasma phosphorus (1.2 mg/dL) and an elevated FGF-23 level of 1005 relative units (RU)/mL. A repeat MRI of the right shoulder revealed a mass in the supraspinatus muscle and another in the spinal glenoid notch. The masses were resected and the biopsy was consistent with a recurrence of the phosphaturic mesenchymal tumor. Follow-up serum phosphate levels remained in the normal range. FGF-23 plays a critical role in bone mineralization through the regulation of phosphate levels. Overproduction, as seen in mesenchymal tumors, results in hyperphosphaturia, hypophosphatemia, and low calcitriol levels. While the definitive treatment of TIO involves the resection of the mesenchymal tumor, localization of the tumor is often challenging given its small size and slow growth. This leads to delayed diagnosis and treatment. For individuals whose tumor cannot be resected or detected, burosumab is the preferred form of therapy. Interestingly, FGF-23 is shown to have a potential cardiovascular (CV) morbidity and mortality through various mechanisms like activation of myocardial FGF-23 receptors, endothelial dysfunction, inflammation, and altered phosphorus and vitamin D metabolisms. While studies have shown possible FGF-23 effects on CV outcomes in patients with chronic kidney disease, this has not been proven in cases of TIO.

Falling Through the Cracks: The Need to Include Acute Pancreatitis in Risk Assessment Models for Acute Deep Venous Thrombosis.

Acute pancreatitis is an inflammatory condition caused by an insult to the pancreas. Pancreatitis is associated with local and systemic complications such as splenic vein thrombosis and systemic inflammatory response syndromes (SIRS), respectively. Pancreatitis increases the risk of deep vein thrombosis (DVT) through a combination of increased production of pro-inflammatory cytokines and systemic vascular injury. However, DVT and pulmonary embolism remain under-recognized and underappreciated complications of acute pancreatitis as they fall through the cracks in the commonly used venous thromboembolism (VTE) risk assessment model. We therefore propose that VTE prophylaxis needs to be considered by all clinicians when admitting and evaluating patients with acute pancreatitis and that acute pancreatitis needs to be included on the various VTE risk assessment calculators as it is a significant risk factor for the development of VTE.

Effect of maternal HIV infection on child survival in Ghana.

The purpose of this study was to measure the association between maternal HIV infection and infant mortality in Ghana. Using a censored synthetic cohort life table based on the birth history of 3639 childbirths during 1999-2003 obtained from the interviews of a nationally representative sample of 5691 women age 15-49 in 6251 households in the 2003 Ghana Demographic and Health Survey. The survey collected demographic, socioeconomic, and health data of the respondents as well as obtained voluntary counseling test for HIV infection from all eligible women. The effects of maternal HIV status and other factors on infant mortality were estimated using multivariate survival regression analysis and the results are presented as Hazard Ratios (HR) with 95% confident interval (95% CI). Children born to HIV infected mothers were three times as likely to die during infancy as those born to uninfected mothers (HR = 3.01; 95% CI: 1.64, 5.50). Controlling for other factors affecting infant mortality further sharpens this relationship (HR = 3.51; 95% CI: 1.87, 6.61). Not receiving antenatal care, low birth weight, and living in households that use high pollution cooking fuels were associated with a higher risk of infant mortality. Maternal HIV status is a strong predictor of infant mortality in Ghana, independent of several other factors. The results of this study suggest that HIV/AIDS epidemic has had great impact on child well-being and child survival. This impact tends to increase as the HIV/AIDS epidemic matures and infection in adults increases.