Autoimmune gastritis as an unexpected cause of diarrhea in a young adult with type I diabetes: a case report.

BACKGROUND: Type 1 diabetes mellitus (T1DM) is a lifelong diagnosis that involves immune-mediated damage of pancreatic beta cells and subsequent hyperglycemia, manifesting as: polyuria, polydipsia, polyphagia, and weight loss. Treatment of type 1 diabetes centers on insulin administration to replace or supplement the body's own insulin with the goal of achieving euglycemia and preventing or minimizing complications. Patients with T1DM are at risk for developing other autoimmune conditions, most commonly thyroid or celiac disease. CASE PRESENTATION: A 20-year-old African American female with T1DM was referred by her endocrinologist to pediatric gastroenterology for 2 months of nocturnal, non-bloody diarrhea, left lower quadrant pain, and nausea; she was also being followed by neurology for complaints of lower extremity paresthesias and pain. The patient's initial lab-workup was remarkable for a low total Immunoglobulin A (IgA) level of < 6.7 mg/dL. As IgA deficiency is associated with an increased risk of celiac disease, the patient underwent upper and lower endoscopy, which was grossly unremarkable; however, histology revealed a pattern consistent with autoimmune gastritis. Subsequent serum evaluation was remarkable for an elevated fasting gastrin level and an elevated parietal cell antibody level without macrocytic anemia, iron deficiency, or vitamin B12 depletion. The patient was diagnosed with autoimmune gastritis (AIG) and subsequently initiated on parenteral B12 supplementation therapy with improvement in her neurologic and gastrointestinal symptoms. CONCLUSION: This case illustrates the importance of recognition of red flag findings in a patient with known autoimmune disease. Following well-established health maintenance recommendations for individuals with T1DM ensures that common comorbidities will be detected. Autoimmune gastritis, while a rarer pathology in the pediatric population, deserves consideration in patients with pre-existing autoimmune conditions and new gastrointestinal or neurologic symptoms, as AIG can be associated with poor outcomes and risk of malignancy. Initial lab findings associated with an eventual diagnosis of AIG typically include anemia, iron deficiency, or Vitamin B12 deficiency. However, as demonstrated in this case, symptoms of AIG can rarely present before anemia or Vitamin B12 deficiency develops. To prevent permanent neurological damage, parenteral Vitamin B12 therapy must be considered even in the absence of Vitamin B12 deficiency, especially in those patients already experiencing neurological symptoms.

Antibiotic resistance, molecular characterizations, and clinical manifestations of Campylobacteriosis at a military medical center in Hawaii from 2012-2016: a retrospective analysis.

Hawaii has one of the highest incidences of Campylobacteriosis in the United States, but there remains little published data on circulating strains or antimicrobial resistance. We characterized 110 clinical Campylobacter isolates (106 C. jejuni, 4 C. coli) processed at Tripler Army Medical Center in Honolulu, HI from 2012-2016. Twenty-five percent of C. jejuni isolates exhibited fluoroquinolone (FQ) resistance, compared with 16% for tetracycline (TET), and 0% for macrolides. Two of the four C. coli isolates were resistant to FQ, TET, and macrolides. C. jejuni isolates further underwent multilocus sequence typing, pulsed-field gel electrophoresis, and molecular capsular typing. Nineteen capsule types were observed, with two capsule types (HS2 and HS9) being associated with FQ resistance (p < 0.001 and p = 0.006, respectively). HS2 FQ-resistant isolates associated with clonal complex 21, possibly indicating clonal spread in FQ resistance. Macrolides should be considered for treatment of suspect cases due to lack of observed resistance.

The potential danger of eating wild lettuce: a brief review of human rat lungworm infection.

Angiostrongylus cantonensis, the causative agent of human rat lungworm disease, is the most common cause of eosinophilic meningitis worldwide and is endemic throughout Asia Pacific. It is acquired through the consumption of infected freshwater mollusks or contaminated produce. Human angiostrongyliasis is usually a self-limited disease presenting with headache and various neurologic sequelae varying from cranial nerve palsies to radiculitis and/or paresthesias. Fatal cases are rare, and manifest as fulminant meningomyeloencephalitis. The diagnosis is made through the use of clinical history, exam, and laboratory data including peripheral blood counts, cerebrospinal fluid (CSF) examinations, and serologic or molecular diagnostic techniques. Medical therapy is largely focused on symptomatic relief, and includes analgesics, lumbar puncture, and corticosteroids. In resource-limited settings, prevention is key, and the use of analgesics can provide symptomatic relief after infection. Efforts to increase disease awareness have been made in endemic areas, as evidenced by the recent Rat Lungworm Disease Scientific Workshop which was held in Honolulu in 2011. The proceedings of the workshop were published in a supplement to this journal (Hawaii J Med Public Health. Jun 2013;72(6):Supp 2). However, wilderness medicine and travel medicine specialists must also be aware of the disease, how it is contracted, its presentation, and treatment options should they encounter a patient who is in or has returned from an endemic area. This brief review highlights eosinophilic meningitis caused by A. cantonensis, including an example case, an overview of its clinical presentation, treatment options, and prevention.