We identified 114 patients with neurocysticercosis admitted to Ben Taub General Hospital in Houston, Texas between January 1994 and June 1997. Most of these patients were born in Mexico (78%) or Central America (16%), but 6% were born in the United States. Review of neurology clinic records identified 54 patients diagnosed with neurocysticercosis, representing 2% of all neurology clinic patients and 16% of all Hispanics diagnosed with seizures. Forty-one patients were interviewed and all reported significant risk factors for infection, including ingestion of undercooked pork, pig husbandry, immigration from and frequent travel to villages in disease-endemic areas, or personal/family history of taeniasis. Among Mexican immigrants, most were born in rural areas in Central (31%) or north central Mexico (38%). Significantly fewer of the patients were from the border states (15%). The median period from immigration to diagnosis was 58 months, but it was 28 months for the 13 patients who had not left the United States after immigration. Although neurocysticercosis is being diagnosed with increasing frequency in the United States, acquisition of infection is still strongly associated with pig husbandry in rural Latin America, with little evidence of local transmission. Even among urban immigrants to the United States and United States-born cases, there is close ongoing contact with disease-endemic villages.
Primary gastric chorioadenocarcinoma (PGC) is an exceedingly rare neoplasm which is often misdiagnosed as gastric adenocarcinoma at presentation. A markedly elevated serum beta human chorionic gonadotrophin (Beta HCG) level is a characteristic feature of this tumor. A 44 year old white male presented with generalized abdominal pain and fullness, tarry black stools and weight loss of 3 months duration. Medical work-up including imaging with CT scans revealed the presence of a gastric mass and multiple liver metastases. Tumor markers were significant for a Betahuman chorionic gonadotrophin (Beta HCG) of 23717.5 MIU/ML. Scrotal ultrasound did not show the presence of a testicular mass. Upper GI endoscopy with biopsy was positive for a poorly differentiated adenocarcinoma with Beta HCG staining on immunohistochemistry. The patient was diagnosed with metastatic PGC. He received four cycles of chemotherapy with Bleomycin, Etoposide and Cisplatinum. At the end of the fourth cycle, Beta HCG was 23 MIU/ML. CT scan for restaging, however showed an increase in the size of the metastatic lesions. The patient subsequently became profoundly pancytopenic, developed disseminated intravascular coagulation (DIC) and expired 12 months after initial presentation. PGC genetically and morphologically represents an adenocarcinoma and a choriocarcinoma. The significance of an elevated serum Beta HCG is controversial and it may have a role in evaluating response to treatment and tumor recurrence. Curative resection, appropriate chemotherapy and the absence of metastatic lesions is associated with improved survival. Hence, a high index of suspicion must be maintained to diagnose this tumor correctly at presentation and tailor therapy accordingly.
Immune thrombocytopenic purpura (ITP) is an autoimmune disease characterized by the production of antibodies to circulating platelets. Traditionally it has been regarded as a disorder of increased platelet destruction, so therapies have targeted this mechanism, including corticosteroids, IVIG, splenectomy and rituximab. More recently, it has become clear that decreased platelet production importantly contributes to the thrombocytopenia. The isolation of thrombopoietin (TPO), the ligand for the mpl receptor and the major hormone regulating platelet production, has shed new light on platelet homeostasis and facilitated the development of new therapeutic approaches. First generation TPO-mimetics were removed from clinical trials when some healthy volunteers and patients with cancer developed antibodies against these drugs that cross-reacted with native TPO, causing paradoxical thrombocytopenia. Two second generation TPO-mimetics, romiplostim and eltrombopag, share no structural homology with endogenous TPO and are being studied in a variety of thrombocytopenic states. Romiplostim was approved by the US FDA in August 2008 for the treatment of patients with ITP who had failed at least one prior therapy. This was based on randomized, placebo-controlled phase III studies that showed increased platelet counts in more than 80% of treated patients, with a durable platelet response by stringent criteria in 38% of splenectomized and 61% of non-splenectomized patients compared to 0%–5% in patients receiving placebo. Being non-immunosuppressive, the toxicity profile is favorable, although there are concerns with this class of drugs with thrombotic risks, “rebound thrombocytopenia,” marrow reticulin fibrosis, or even hematopoietic clonal proliferation. Romiplostim may gain an increasing niche in the treatment of ITP.
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