of 1/1
in the decrease of white cells is statistically significant (p , 0.001); this points to leucopenia as an important side effect of combination therapy. Francesca Russo, M.D. Marco Bacosi, M.D. Lucia Miglioresi, M.B.Bs. Giovanni L. Ricci, M.D., Ph.D. Gastroenterology Unit Department of Clinical Sciences Univ. “La Sapienza” Rome, Italy REFERENCES 1. Davis GL, Esteban-Mur R, Rustgi V, et al. Interferon alfa-2b alone or in combination with ribavirin for the treatment of relapse of chronic hepatitis C. N Engl J Med 1998;339:1493–9. 2. Brillanti S, Migliolo M, Barbara L. Combination antiviral therapy with ribavirin and interferon a in interferon a relapsers and non- responders: Italian experience. J Hepatol 1995;23(suppl 2):13– 6. 3. Kakumu S, Yoshioka K, Wakita T, et al. A pilot study of ribavirin and interferon b for the treatment of chronic hepatitis C. Gastroenterology 1993;105:507–12. 4. Scotto G, Fazio V, Tantimonaco G. Pilot study of a short course of ribavirin and alfa interferon in the treatment of chronic active hepatitis C not responding to alfa interferon alone. Ital J Gas- troenterol 1996;28:505–11. Reprint requests and correspondence: Giovanni L. Ricci, M.D., Ph.D., Gastroenterology Unit, Department of Clinical Sciences, Policlinico, 00161 Rome, Italy. Received Nov. 17, 1999; accepted Nov. 30, 1999. Re: Drug-Resistant Falciparum Malaria With Bowel Symptoms TO THE EDITOR: I wish to bring to the notice of the readers of your esteemed journal the following clinicopath- ological experience, which deserves attention for the better management of cases of drug-resistant falciparum malaria with bowel symptoms. A 22-yr-old man developed intermittent fever of 5 days duration with peripheral blood smear positivity for plasmo- dium falciparum. Culture for Salmonella typhi was negative; Widal test and HIV were also negative. The patient was started on chloroquine and symptomatic therapy. The fever, as high as 103°F before institution of therapy, decreased to 100°F. CBC was noncharacteristic; but blood smear was still positive for falciparum rings on day 8. On day 8, he developed clinical features of acute abdomen, and an emer- gent exploratory laparotomy was performed because of sus- picion of bowel perforation. Because of concern that this may represent undiagnosed typhoid fever (endemic in this region), intravenous ciprofloxacin was started, along with gentamicin and metronidazole. Exploratory laparotomy re- vealed two discrete punched-out perforations of 1.5 cm and 1.0 cm in the last 6 inches of terminal ileum, close to the antimesenteric border, with markedly congested small bowel and enlarged, congested mesenteric nodes. Histopa- thology of the sites of perforations showed neutrophils and macrophage response with vascular congestion and serosi- tis. Lymph nodes showed marked congestion and areas of infarction also. Despite the continuation of broad spectrum antibiotics including ciprofloxacin, the patient developed recurrent features of acute abdomen on the second postop- erative day. The fever (100°F) continued to persist. A repeat blood smear revealed persisting parasite in the blood. Based on the suspicion that this represented chloro- quine-resistant falciparum malaria, a decision was made to give quinine 600 mg i.v. every 8 h instead of chloroquine. Dramatically, from the next morning onwards the patient was afebrile, and abdominal complaints also regressed com- pletely, without necessitating further surgery. The patient was discharged on day 14, afebrile and with normal wound healing. Gastrointestinal ischemia is a known problem with falci- parum malaria. However, small bowel perforation due to falciparum malaria infection has not been reported in the literature. This patient did not respond to antityphoid med- ications or chloroquine. Dramatic clinical improvement was noted with the institution of quinine. Subsequently, two other patients with an identical presentation were treated successfully with quinine, with minimal morbidity at our institution. It is our impression that drug-resistant strains of falcipa- rum malaria produce accelerated or aggressive ischemic changes of organs and, in particular, the gastrointestinal tract, because of microvascular occlusion, by the parasitized and nonparasitized RBC causing a local hyperviscosity of microvasculature that can lead to frank perforation instead of an ischemic ooze. Molecular biological events incited by the drug-resistant forms of falciparum deserve study in greater detail apart from the already known role of ICAM-1, CD 36, and thrombospondin receptors, red cell rosette for- mation, and vasculo-occulsion. CH.V. Ramana Murty, M.D. Y.V.S. Prabhakar, M.D. Guntur Medical College Guntur, India V. Bala Bhaskara Rao, M.S. Guntur, India Sreenivasa S. Jonnalagadda, M.D. Division of Gastroenterology Washington University School of Medicine St. Louis, Missouri Reprint requests and correspondence: CH.V. Ramana Murty, M.D., Professor of Pathology, Guntur Medical College, House No. 6, Pragati Apartments, 5/2 Chandramouli Nagar, Guntur, Andhra Pradesh, India 522007. Received Nov. 23, 1999; accepted Nov. 30, 1999. 1101 AJG – April, 2000 Letters to the Editor

Re: drug-resistant falciparum malaria with bowel symptoms

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  • in the decrease of white cells is statistically significant (p ,0.001); this points to leucopenia as an important side effectof combination therapy.

    Francesca Russo, M.D.Marco Bacosi, M.D.

    Lucia Miglioresi, M.B.Bs.Giovanni L. Ricci, M.D., Ph.D.

    Gastroenterology UnitDepartment of Clinical Sciences

    Univ. La SapienzaRome, Italy

    REFERENCES

    1. Davis GL, Esteban-Mur R, Rustgi V, et al. Interferon alfa-2balone or in combination with ribavirin for the treatment ofrelapse of chronic hepatitis C. N Engl J Med 1998;339:14939.

    2. Brillanti S, Migliolo M, Barbara L. Combination antiviral therapywith ribavirin and interferon a in interferon a relapsers and non-responders: Italian experience. J Hepatol 1995;23(suppl 2):136.

    3. Kakumu S, Yoshioka K, Wakita T, et al. A pilot study ofribavirin and interferon b for the treatment of chronic hepatitisC. Gastroenterology 1993;105:50712.

    4. Scotto G, Fazio V, Tantimonaco G. Pilot study of a short courseof ribavirin and alfa interferon in the treatment of chronic activehepatitis C not responding to alfa interferon alone. Ital J Gas-troenterol 1996;28:50511.

    Reprint requests and correspondence: Giovanni L. Ricci, M.D.,Ph.D., Gastroenterology Unit, Department of Clinical Sciences,Policlinico, 00161 Rome, Italy.

    Received Nov. 17, 1999; accepted Nov. 30, 1999.

    Re: Drug-Resistant FalciparumMalaria With Bowel SymptomsTO THE EDITOR: I wish to bring to the notice of thereaders of your esteemed journal the following clinicopath-ological experience, which deserves attention for the bettermanagement of cases of drug-resistant falciparum malariawith bowel symptoms.

    A 22-yr-old man developed intermittent fever of 5 daysduration with peripheral blood smear positivity for plasmo-dium falciparum. Culture for Salmonella typhi was negative;Widal test and HIV were also negative. The patient wasstarted on chloroquine and symptomatic therapy. The fever,as high as 103F before institution of therapy, decreased to100F. CBC was noncharacteristic; but blood smear wasstill positive for falciparum rings on day 8. On day 8, hedeveloped clinical features of acute abdomen, and an emer-gent exploratory laparotomy was performed because of sus-picion of bowel perforation. Because of concern that thismay represent undiagnosed typhoid fever (endemic in thisregion), intravenous ciprofloxacin was started, along withgentamicin and metronidazole. Exploratory laparotomy re-vealed two discrete punched-out perforations of 1.5 cm and

    1.0 cm in the last 6 inches of terminal ileum, close to theantimesenteric border, with markedly congested smallbowel and enlarged, congested mesenteric nodes. Histopa-thology of the sites of perforations showed neutrophils andmacrophage response with vascular congestion and serosi-tis. Lymph nodes showed marked congestion and areas ofinfarction also. Despite the continuation of broad spectrumantibiotics including ciprofloxacin, the patient developedrecurrent features of acute abdomen on the second postop-erative day. The fever (100F) continued to persist.

    A repeat blood smear revealed persisting parasite in theblood. Based on the suspicion that this represented chloro-quine-resistant falciparum malaria, a decision was made togive quinine 600 mg i.v. every 8 h instead of chloroquine.Dramatically, from the next morning onwards the patientwas afebrile, and abdominal complaints also regressed com-pletely, without necessitating further surgery. The patient wasdischarged on day 14, afebrile and with normal wound healing.

    Gastrointestinal ischemia is a known problem with falci-parum malaria. However, small bowel perforation due tofalciparum malaria infection has not been reported in theliterature. This patient did not respond to antityphoid med-ications or chloroquine. Dramatic clinical improvement wasnoted with the institution of quinine. Subsequently, twoother patients with an identical presentation were treatedsuccessfully with quinine, with minimal morbidity at ourinstitution.

    It is our impression that drug-resistant strains of falcipa-rum malaria produce accelerated or aggressive ischemicchanges of organs and, in particular, the gastrointestinaltract, because of microvascular occlusion, by the parasitizedand nonparasitized RBC causing a local hyperviscosity ofmicrovasculature that can lead to frank perforation insteadof an ischemic ooze. Molecular biological events incited bythe drug-resistant forms of falciparum deserve study ingreater detail apart from the already known role of ICAM-1,CD 36, and thrombospondin receptors, red cell rosette for-mation, and vasculo-occulsion.

    CH.V. Ramana Murty, M.D.Y.V.S. Prabhakar, M.D.Guntur Medical College

    Guntur, IndiaV. Bala Bhaskara Rao, M.S.

    Guntur, IndiaSreenivasa S. Jonnalagadda, M.D.

    Division of GastroenterologyWashington University School of Medicine

    St. Louis, Missouri

    Reprint requests and correspondence: CH.V. Ramana Murty,M.D., Professor of Pathology, Guntur Medical College, House No.6, Pragati Apartments, 5/2 Chandramouli Nagar, Guntur, AndhraPradesh, India 522007.

    Received Nov. 23, 1999; accepted Nov. 30, 1999.

    1101AJG April, 2000 Letters to the Editor