Letters to the Editor
271 *Corresponding author.
E-mail address: [email protected] Accepted 20 March 2015 http://dx.doi.org/10.1016/j.jinf.2015.03.005 ª 2015 The British Infection Association. Published by Elsevier Ltd. All rights reserved.
Cryoglobulinemic purpura in visceral leishmaniasis
KEYWORDS Cryoglobulinemia; Leishmaniasis; Purpura
Dear Editor, We read the spotlessly review on leishmaniasis1 published in your journal recently and would like to present an uncommon clinical manifestation of visceral leishmaniasis. An 85 year-old man was admitted to the emergency room of the hospital due to a 10-day history of macroscopic hematuria, as well as thrombocytopenia which had been found by a laboratory test. Moreover, he reported fever, perspiration during the night, fatigue, 10 kg weight loss during the last month, and appearance of a rash on his legs which had already regressed at the time of his admission to the hospital. His medical record includes coronary disease and coronary artery bybass surgery, hypertension, hypertrophy of the prostate gland and appendectomy. He was under medication, which included carvedilol 75 mg, isosorbite-5-mononitrate 60 mg, acetylsalicylic acid 100 mg and metoprolol 100 mg. He is neither a smoker nor a drinker, and he is the owner of a dog. On admission, physical examination disclosed splenomegaly, as well as hepatomegaly and lymphadenia of the left axilla. Abdominal sonography and the computed tomography scan confirmed the hepatic and splenic enlargement, both of which were measured to be 19 cm. Moreover, a small infarct was found in the middle of the spleen. Major laboratory findings included pancytopenia, hypoalbuminemia, elevated levels of C-reactive protein (CRP), lactate dehydrogenase (LDH), aspartate aminotransferase (AST) and g-gloutamyltraspeptidase (gGT), hypergammaglobulinemia, increased IgG globulin and b2-microglobulin and a positive rheumatoid factor (RF). Urine microscopy proved hematuria and proteinuria. The patient tested positive for antibodies against the K39 antigen of Leishmania and antibodies against Leishmania (1/320) in the serum. Furthermore, polymerase
chain reaction (PCR) was positive for the presence of protozoa of Leishmania in the blood, but negative for their presence at the bone marrow. However, contrary to expectations, Leismania was not found in the bone marrow biopsy. Because of the above findings, we initiated treatment with liposomal amphotericin B (3 mg/kg days 1e5, 14 and 21). However, on the 9th day of his hospitalization, the patient developed palpable purpura on both legs (Fig. 1). We checked for cryoglobulins, and a cryocrit of 3.5% was detected. Moreover, a remarkable renal dysfunction was noticed (glomerular filtration rate (GFR) was 69 ml/min on the day the patient was admitted to the hospital, but was found to be 34 ml/min on the 8th day of hospitalization). The patient tested negative for hepatitis B and C and human immunodeficiency virus infection. By the 14th day of the hospitalization, the purpura had completely regressed without any additional therapy. GFR was stable at 35 ml/min. We measured again the cryocrit and found out that it had noticeably decreased. Moreover, thrombopenia and leukopenia had regressed. The patient was discharged in a good performance status, after having taken 1500 mg of liposomal amfotericin B. He was advised to visit the hospital again, in order to receive two more doses of the treatment (on days 14 and 21 of the treatment). On the last day of the treatment (day 21) we noticed improved renal function (GFR: 51 ml/min), and also a significant reduction of the spleen (15 cm at the abdominal ultrasound). No purpura was detected (Table 1). In general, patients suffering from visceral leishmaniasis may exhibit fever, fatigue, anorexia, nausea, weight loss, pallor, abdominal discomfort, joint pain, arthralgia or cough, vomiting, diarrhea and bleeding. The clinical signs are hepatomegaly, splenomegaly, and more rarely lymphadenopathy and cutaneous vasculitis. Laboratory findings include pancytopenia, hypergammaglobulinaemia and absence of detectable cell-mediated immunity. More rarely, VL is also associated with manifestations of autoimmune diseases. These include low serum complement levels, increased titers of RF, antinuclear antibodies (ANA), anti-glomerular basement-membrane antibodies (GBM), anti-striated muscle antibodies (AMA) and anti-smooth
Figure 1
Cryoglobulinemic purpura.
272 Table 1
Letters to the Editor Evolution of serum laboratory and immunological parameters of the patient, on admission and during follow-up.
Laboratory variables
On admission
5th day of therapy
Followeup (9 days after the consummation of the treatment)
Hemoglobin (12e18 g/dl) White blood cell count (5.2e12.4 109/l) Platelet count (130e140 109/l) C-reactive protein (
271 *Corresponding author.
E-mail address: [email protected] Accepted 20 March 2015 http://dx.doi.org/10.1016/j.jinf.2015.03.005 ª 2015 The British Infection Association. Published by Elsevier Ltd. All rights reserved.
Cryoglobulinemic purpura in visceral leishmaniasis
KEYWORDS Cryoglobulinemia; Leishmaniasis; Purpura
Dear Editor, We read the spotlessly review on leishmaniasis1 published in your journal recently and would like to present an uncommon clinical manifestation of visceral leishmaniasis. An 85 year-old man was admitted to the emergency room of the hospital due to a 10-day history of macroscopic hematuria, as well as thrombocytopenia which had been found by a laboratory test. Moreover, he reported fever, perspiration during the night, fatigue, 10 kg weight loss during the last month, and appearance of a rash on his legs which had already regressed at the time of his admission to the hospital. His medical record includes coronary disease and coronary artery bybass surgery, hypertension, hypertrophy of the prostate gland and appendectomy. He was under medication, which included carvedilol 75 mg, isosorbite-5-mononitrate 60 mg, acetylsalicylic acid 100 mg and metoprolol 100 mg. He is neither a smoker nor a drinker, and he is the owner of a dog. On admission, physical examination disclosed splenomegaly, as well as hepatomegaly and lymphadenia of the left axilla. Abdominal sonography and the computed tomography scan confirmed the hepatic and splenic enlargement, both of which were measured to be 19 cm. Moreover, a small infarct was found in the middle of the spleen. Major laboratory findings included pancytopenia, hypoalbuminemia, elevated levels of C-reactive protein (CRP), lactate dehydrogenase (LDH), aspartate aminotransferase (AST) and g-gloutamyltraspeptidase (gGT), hypergammaglobulinemia, increased IgG globulin and b2-microglobulin and a positive rheumatoid factor (RF). Urine microscopy proved hematuria and proteinuria. The patient tested positive for antibodies against the K39 antigen of Leishmania and antibodies against Leishmania (1/320) in the serum. Furthermore, polymerase
chain reaction (PCR) was positive for the presence of protozoa of Leishmania in the blood, but negative for their presence at the bone marrow. However, contrary to expectations, Leismania was not found in the bone marrow biopsy. Because of the above findings, we initiated treatment with liposomal amphotericin B (3 mg/kg days 1e5, 14 and 21). However, on the 9th day of his hospitalization, the patient developed palpable purpura on both legs (Fig. 1). We checked for cryoglobulins, and a cryocrit of 3.5% was detected. Moreover, a remarkable renal dysfunction was noticed (glomerular filtration rate (GFR) was 69 ml/min on the day the patient was admitted to the hospital, but was found to be 34 ml/min on the 8th day of hospitalization). The patient tested negative for hepatitis B and C and human immunodeficiency virus infection. By the 14th day of the hospitalization, the purpura had completely regressed without any additional therapy. GFR was stable at 35 ml/min. We measured again the cryocrit and found out that it had noticeably decreased. Moreover, thrombopenia and leukopenia had regressed. The patient was discharged in a good performance status, after having taken 1500 mg of liposomal amfotericin B. He was advised to visit the hospital again, in order to receive two more doses of the treatment (on days 14 and 21 of the treatment). On the last day of the treatment (day 21) we noticed improved renal function (GFR: 51 ml/min), and also a significant reduction of the spleen (15 cm at the abdominal ultrasound). No purpura was detected (Table 1). In general, patients suffering from visceral leishmaniasis may exhibit fever, fatigue, anorexia, nausea, weight loss, pallor, abdominal discomfort, joint pain, arthralgia or cough, vomiting, diarrhea and bleeding. The clinical signs are hepatomegaly, splenomegaly, and more rarely lymphadenopathy and cutaneous vasculitis. Laboratory findings include pancytopenia, hypergammaglobulinaemia and absence of detectable cell-mediated immunity. More rarely, VL is also associated with manifestations of autoimmune diseases. These include low serum complement levels, increased titers of RF, antinuclear antibodies (ANA), anti-glomerular basement-membrane antibodies (GBM), anti-striated muscle antibodies (AMA) and anti-smooth
Figure 1
Cryoglobulinemic purpura.
272 Table 1
Letters to the Editor Evolution of serum laboratory and immunological parameters of the patient, on admission and during follow-up.
Laboratory variables
On admission
5th day of therapy
Followeup (9 days after the consummation of the treatment)
Hemoglobin (12e18 g/dl) White blood cell count (5.2e12.4 109/l) Platelet count (130e140 109/l) C-reactive protein (
