Henoch-Schonlein Purpura in a Disseminated Tuberculosis Patient / 대한소화기내시경학회지

Henoch-Schonlein purpura is a systemic leukoclastic vasculitis and involves small vessels resulting in vasculitis. Major pathogenetic mechanism of Henoch-Schonlein purpura has not been still elucidated. Possible causes, however, may be associated with viral infection, bacterial infection, exposure to drugs and toxins, systemic diseases and carcinomas. Henoch-Schonlein purpura rarely develops in patients with tuberculosis, though there have been some reports on the development of this syndrome during antituberculous therapy. A 24-year-old man was admitted to our hospital because of diffuse abdominal pain, lower leg purpura and disseminated tuberculosis involving lung, duodenum, colon and lumbar spine and diagnosed as Henoch-Schonlein purpura with disseminated tuberculosis. Henoch-Schonlein purpura developed before antibuberculous therapy and antituberculous treatment was effective both in disseminated tuberculosis and Henoch-Schonlein purpura. We concluded that disseminated tuberculosis might be a cause of Henoch-Schonlein purpura.

A Case of Waldenstrom's Macroglobulinemia Treated with 2-Chlorodeoxyadenosine (Cladribine) / 대한혈액학회지

Waldenstrom's macroglobulinemia is a low- grade lymphoproliferative disorder with monoclonal IgM protein. It is characterized by normocytic, normochromic anemia and lymphoplasmacytic marrow infiltration. Chemotherapy with alkylating agents and steroids has been the standard therapy for patients with symptomatic macroglobulinemia. The purine nucleoside analogues, either alone or in combination with other chemotherapeutic agents are increasingly used, and approximately 40% of patients who have received prior therapy with alkylating agents responded. We experienced a case of Waldenstrom's macroglobulinemia suc-cessfully treated with three courses of cladribine, who had previously received unsuccessful therapy using an alkylating agent, steroid and plasmapheresis. Treatment was well tolerated except for frequent upper respiratory infections with severe pancytopenia. A marked and sustained bone marrow suppression occurred in this patient but resolved in three months without any severe infection.

A Case of Gastric Injury by Acute Iron Intoxication / 대한소화기내시경학회지

Iron is a kind of corrosive agent. Iron overdose causes gastrointestinal complication such as mucosal ulceration, bleeding, intestinal perforation and may occur metabolic acidosis, hepatic dysfunction, hepatic failure, renal failure and cardiomyopathy. Delayed sequalae including gastric outlet obstruction develops 4 to 6 weeks after ingestion. The determination of serum iron and TIBC is an important factor in ascertaining the toxic potential in acute iron ingestion and more is the amount of ingested elemental iron, greater is a patient's toxicity. Supportive care is most important and patients who have severe symptom and abnormal vital sign should be treated with deferoxamine. We report the case that a 20-year-old pregnant female (33 weeks gestation) who had visited complaining of gastrointestinal symptom with iron overdose state was administrated with deferoxamine, therefore we removed iron loads within stomach with endoscopic suction and observed multiple gastric erosion with much old iron in endoscopic findings.