Kyawzaw Lin

Despite advanced diagnosis and treatment, infective endocarditis (IE) is a potentially life-threatening condition. Although recent studies have provided evidence of changing trends in IE epidemiology, few studies examine patterns within urban minority populations. Here we present the epidemiology, risk factors, and outcomes of IE among an underserved African American population in Brooklyn, New York, compared to the general population. This is a retrospective study which included 67 patients with IE diagnosed at The Brooklyn Hospital Center from 2009 to 2015. Patients were selected according to the modified Duke Criteria for definite IE. Various epidemiological parameters were examined via chi-square and Fisher’s exact test using SPSS 24 software (IBM Corp., Armonk, NY). The mean age of the 67 patients was 63 years and 46.3% of the patients were men. The majority of patients (70.1%) were African American while Hispanics and Caucasians were 17.9% and 7.5%, respectively. Healthcare-associated IE (58.2%, n=39) outnumbered community-acquired IE (41.8%, n=28). The sites of vegetation were the mitral valve (62.7%, n=42), tricuspid valve (22.4%, n=15), aortic valve (11.9%, n=8), and intravenous catheter (3%, n=2). In valves, 13.4% of the cases were found in prosthetic valves while the majority occurred in native valves. The most common pathogens of IE were the Staphylococcus (50.8%, n=34) species, followed by Streptococcus species (32.8%, n=22). Overall, the in-hospital mortality was 38.8% (n=26) with higher mortality observed for healthcare-associated IE than community-acquired IE (P = .049). Embolic complications were associated with significant mortality (P < .001). Our study demonstrated that the common causative pathogens for IE among African Americans trends towards Staphylococcus species followed by Streptococcus species, similar to the contemporary epidemiology of IE. Healthcare-associated IE outnumbered community-acquired IE and was associated with higher mortality. Embolic complications were significantly associated with high mortality. Therefore, efforts made to control healthcare-associated infections are expected to decrease the trend of IE.

Ginseng is commonly used as a medicinal herb for memory and concentration and general well-being. Drug-induced liver injury (DILI) is one of the most challenging disorders and trending events in the United States which are related to body building and weight loss supplements. Currently, herbal and dietary supplementation is the second most common cause of DILI. Here, we report on a 45-year-old healthy Chinese woman who presented with dull intermittent left upper quadrant abdomen pain for a month. Upon thorough history taking, she had been taking ginseng tea and supplementation for her menopausal symptoms for almost 3 months. Physical examination was unremarkable except mild tenderness in left upper quadrant of the abdomen. Liver function test showed aspartate transaminase (AST) 717 U/L, alanine transaminase (ALT) 343 U/L, total bilirubin 5 mg/dL, direct bilirubin 3.3 mg/dL, alkaline phosphatase 182 U/L, with international normalized ratio (INR) 1.2. Prior liver enzymes (6 months earlier) showed AST 21 U/L, ALT 18 U/L, total bilirubin 0.8 mg/dL, direct bilirubin 0.3 mg/dL, alkaline phosphatase 34 U/L, with INR 0.7. Viral serology for acute hepatitis B, C, E, cytomegalovirus, Epstein-Barr virus, and varicella zoster virus was negative. She was immune to hepatitis A. Her antinuclear antibody was positive. Her anti-Smith antibody, anti-smooth muscle antibody, HFE gene mutation, ceruloplasmin, alpha-1 antitrypsin serologies were within normal references. An abdomen sonogram showed fatty infiltration. Liver biopsy showed moderate to severe portal inflammation and marked lobular disarray. Portal and lobular inflammatory infiltrates consisted of a mixture of histiocytes, lymphocytes, plasma cells, eosinophils, and neutrophils with centrilobular necrosis and focal bridging necrosis, and necro-inflammation. After 6 weeks of follow-up, the patient improved physically, and the abdomen pain resolved. Ginseng has been widely used in the Chinese community as medicinal herb for a variety of conditions for decades. However, proper research has never been done regarding its pharmacokinetics, efficacy, and safety issues. In our case report, the idiosyncratic DILI resulted from ingestion of ginseng as herbal supplementation for premenopausal symptoms. Physicians should be aware of and suspect DILI in any patient with acute liver injury, and patients should be reminded that all medications and supplements have a potential to cause DILI.

Acute pancreatitis (AP) is an inflammatory disease presenting from mild localized inflammation to severe infected necrotic pancreatic tissue. In the literature, there are a few cases of hypothermia-induced AP. However, the association between hypothermia and AP is still a myth. Generally, mortality from acute pancreatitis is nearly 3–6%. Here, we present a 40-year-old chronic alcoholic female who presented with acute pancreatitis induced by transient hypothermia. A 40-year-old chronic alcoholic female was hypothermic at 81°F on arrival which was improved to 91.7°F with warming blanket and then around 97°F in 8 h. Laboratory tests including complete blood count, lipid panel, and comprehensive metabolic panels were within the normal limit. Serum alcohol level was 0.01, amylase 498, lipase 1,200, ammonia 26, serum carboxyhemoglobin level 2.4, and β-HCG was negative. The entire sepsis workup was negative. During rewarming period, she had one episode of witnessed generalized tonic-clonic seizure. It was followed by transient hypotension. Fluid challenge was successful with 2 L of normal saline. Sonogram (abdomen) showed fatty liver and trace ascites. CAT scan (abdomen and pelvis) showed evidence of acute pancreatitis without necrosis, peripancreatic abscess, pancreatic mass, or radiopaque gallstones. The patient was managed medically and later discharged from the hospital on the 4th day as she tolerated a normal low-fat diet. In our patient, transient hypothermia from chronic alcohol abuse and her social circumstances might predispose to microcirculatory disturbance resulting in acute pancreatitis. Early and aggressive fluid resuscitation prevents complications.

Gastrointestinal stromal tumors (GISTs) are rare neoplasms of the digestive tract. The clinical behavior of GISTs varies greatly, has extended follow-up, and almost all of the tumors have malignant potential. The introduction of imatinib has led to extraordinary improvements in the treatment of individuals with GISTs (as well as those with Philadelphia chromosome-positive chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia (ALL)). However, there have been notable postmarketing reports of adverse drug reactions of hepatotoxicity with the use of imatinib. By our search, among individuals taking imatinib for the treatment of GIST, only six cases of drug-induced liver injury (DILI) have been reported. Here, we present an interesting case of an elderly woman who developed DILI after taking imatinib for the treatment of GIST. As the liver function tests (LFTs) initially did not improve, it was decided to proceed with an interventional radiology (IR)-guided liver biopsy, which showed a histologic pattern of acute hepatitis, consistent with DILI. Ultimately, discontinuation of the antineoplastic agent led to recovery in the patient’s clinical condition along with normalization of her LFTs over the next several weeks. Thus, it is essential that physicians remain alert for and suspect DILI for any patient being treated with imatinib who presents with a sudden elevation of LFTs. The key to making the diagnosis is stopping the offending agent and closely monitoring the liver enzymes for improvement. When discontinuation of imatinib alone does not lead to improvement in LFTs and the patient’s clinical status, a detailed history should be taken and initial diagnostic testing performed to exclude other etiologies. And, if they are negative, a liver biopsy should be considered.

Splenic infarction is an unusual cause for a patient to present with left upper abdomen pain. A 47-year-old woman presented to the emergency department with left upper abdomen pain. She reported that she stopped taking warfarin two days prior to presentation. A physical examination revealed fine crackles within the left lower lobe and significant tenderness within the left upper abdomen. Computed tomography of the abdomen showed mild cardiomegaly with a 2.3 cm calcified thrombus in the left ventricular apex. We noted infarction in the spleen and right kidney with bilateral renal scarring. The patient was initially started on a heparin drip and later bridged to warfarin on the third day. She was discharged after seven days with complete resolution of the abdominal pain. The decision to prescribe an anticoagulant should include a consideration of underlying causes, comorbidities, an assessment of risks and benefits, and chances of recurrence. In our patient, her new splenic infarct and renal infarction were most likely embolic in origin due to her left ventricular apical aneurysm with thrombus and nonadherence to her prescribed anticoagulation medication.