Shahid Ahmed

Low-grade B-cell bronchial associated lymphoid tissue (BALT) lymphoma.

Low-grade B-cell bronchial associated lymphoid tissue (BALT) lymphoma is a distinct subgroup of nonHodgkins lymphoma. Chronic antigen stimulation, triggered by autoimmune process or persistent infection may precede the development of BALT lymphoma. The lymphoma cells originate from the marginal zone and by invading the bronchial epithelial tissue, give rise to the lymphoepithelial lesion. BALT lymphoma shares the morphologic, immunophenotypic, and cytogenetic characteristics of other mucosa associated lymphoid tissue lymphomas. A majority of the patients are asymptomatic and pulmonary lesions are incidentally discovered on a routine chest radiograph. However, the clinical and radiographic features of BALT lymphoma are nonspecific. The disease is often localized at the time of diagnosis and responds favorably to local treatment, but the optimal management is not clearly defined. Overall, BALT lymphoma has a favorable prognosis and is associated with long-term survival.

Interferon in the treatment of hairy-cell leukemia

The introduction of alpha interferon in 1984 initiated a new and exciting turnaround in the treatment of hairy-cell leukemia. Until that time splenectomy was the only known effective therapy for this disease. Interferon proved to benefit hairy-cell leukemia patients with active disease, whether or not they had undergone prior splenectomy. However, most interferon-induced responses were partial and were of relatively short duration. Purine analogues such as cladribine and pentostatin have since been found to be more effective than alpha interferon and, therefore, have now replaced interferon as first-line therapy for hairy-cell leukemia. At the present time, interferon has a relatively limited role in the treatment of hairy-cell leukemia and it is reserved for a group of selected patients who have failed nucleoside analogue therapy. In this chapter, we discuss the efficacy of interferon and its response duration, toxicity and possible mechanism of action in patients with hairy-cell leukemia.

Interstitial Pneumonitis in a Patient Treated with α-Interferon and Ribavirin for Hepatitis C Infection

Hepatitis C is a common infection with worldwide prevalence. It has a variable course and can lead to chronic hepatitis, cirrhosis and hepatocellular carcinoma. Until recently alpha-interferon (IFN-alpha) was the only effective treatment available. Combination therapy with IFN-alpha and ribavirin has been found to be more efficacious than IFN-alpha alone. Various side effects have been ascribed to interferon, such as arthralgias, myalgias, fatigue, and gastrointestinal and neuropsychiatric symptoms. Interstitial pneumonitis is a rare but known complication of IFN-alpha when given at a high dosage of 6 to 10 million units per day. Ribavirin is associated with dose-dependent hemolytic anemia, cough, dyspnea, rash, depression, and dyspepsia, although a potential role in interferon-induced interstitial pneumonitis has not been described. We describe a patient with an excellent clinical response of chronic hepatitis C to combination therapy with IFN-alpha at a dosage of 3 million units per day and ribavirin. The patient developed interstitial pneumonitis that resolved after discontinuation of IFN-alpha and ribavirin. Given that interstitial pneumonitis has previously been reported with high-dose IFN-alpha, this case suggests that this complication may occur with lower dosages of IFN-alpha, although a potential role for ribavirin in this disorder at present remains speculative.

Possible Levofloxacin-Induced Acute Hepatocellular Injury in a Patient with Chronic Obstructive Lung Disease

Levofloxacin is one of the most commonly prescribed antibiotics for both inpatient and outpatient care of respiratory tract infection. It is generally well tolerated, and it has an excellent safety profile. We report a case of severe acute liver toxicity that apparently complicated intravenous administration of levofloxacin, which resolved after discontinuation of the drug.

Paradoxical Arterial Emboli Causing Acute Limb Ischemia in a Patient with Essential Thrombocytosis

Acute arterial occlusion can be the result of acute thrombosis or systemic embolism. Paradoxical embolism of a venous thrombosis through a right-to-left shunt is an important cause of acute limb ischemia. We describe a young patient with acute limb ischemia who was found to have multiple deep venous thromboses causing arterial embolization through a patent foramen ovale. Essential thrombocytosis was found to be the risk factor for venous thromboses in this patient. The patient was managed with embolectomy and anticoagulation along with chemotherapeutic cytoreduction of platelet count. This case illustrates the importance of considering the systemic embolism as a cause of acute arterial occlusion. The presence of a hypercoagulable status such as chronic myeloproliferative disorder does not eliminate the possibility of systemic embolism in the event of acute arterial occlusion. Patients presenting with acute limb ischemia should be evaluated for embolic sources. The presence of deep venous thrombosis in such a patient should prompt the evaluation for a patent foramen ovale.

Low-molecular weight heparin: treatment failure in a patient with primary antiphospholipid antibody syndrome.

Antiphospholipid antibody syndrome is an acquired autoimmune disorder characterized by vascular thrombosis and/or recurrent pregnancy losses along with laboratory evidence of antiphospholipid antibodies. Anticoagulation rather than immunosuppression is the mainstay of treatment. Despite the effectiveness of oral anticoagulation for the prevention of recurrent thromboembolic episodes, thrombotic complications in the setting of apparently therapeutic oral anticoagulation have been observed; this may at times be due to difficulties in maintaining a consistently therapeutic level of anticoagulation. Low-molecular-weight heparin has been a useful alternative for long-term anticoagulation when there is difficulty in managing oral anticoagulant therapy and has the advantage of a consistent anticoagulant effect. In this report, we describe a woman with primary antiphospholipid antibody syndrome who developed extensive pulmonary embolism despite receiving a proven therapeutic dosage of low molecular weight heparin.

Dexamethasone attenuates oxidation of extracellular matrix proteins by human monocytes.

In response to infection or in immune complex-mediated diseases, inflammatory cells may oxidatively damage extracellular matrix (ECM) proteins. In this study we evaluated whether human monocytes could oxidize ECM and whether this could be modulated by exposure to LPS, IgG complexes, and dexamethasone (DEX). Wells in tissue culture plates were coated with the ECM preparation Matrigel. Porous inserts with or without the human monocyte cell line THP-1 were placed into ECM-containing wells and cells were exposed to control conditions or to LPS (10 ng/ml), IgG complexes (200 and 500 microg/ml), or DEX (10(-7) and 10(-6) M). ECM was then subjected to Western blot analysis using an antibody to oxidized protein. In addition, Western blot analysis was carried out on DEX-treated cells to evaluate expression of the NADPH oxidase components p67-phox and gp91-phox. THP-1 cells enhanced ECM oxidation and this effect was augmented by LPS and by IgG aggregates. Preincubation of cells with DEX attenuated ECM oxidation and was also associated with decreased expression of p67-phox and gp91-phox. These findings suggest that human monocytes can oxidize ECM proteins and that this may be modulated by IgG complexes and LPS. Dexamethasone appears to attenuate ECM oxidation and a better understanding of this mechanism might allow for interventions to minimize oxidative damage to ECM proteins by monocytes in infectious and inflammatory states.