Easy and quite typical question. We are told about an HIV patient with irregular follow-up of antiretroviral treatment, presenting fever, hepatosplenomegaly, pancytopenia and polyclonal hypergammaglobulinemia. All these data are suggestive of visceral Leishmaniasis, so an OM biopsy should be performed to look for amastigotes and confirm the diagnosis.

A 53-year-old woman consults for a fever of 15 days of evolution, without symptoms of infectious focality. On examination, a painful hepatomegaly is detected at 5 cm from the costal margin and the spleen is palpated at 14 cm from the left costal margin. The blood count showed Hb 8.5 g/dL, leukocytes 630/ml (lymphocytes 63%, monocytes 20%, neutrophils 17%) and platelets 35,000/ml. Biochemistry shows moderate elevation of liver biochemistry, LDH is normal and polyclonal hypergammaglobulinemia (3.5 g/dL) is observed in the proteinogram. He has a history of known HIV infection for 10 years and irregular adherence to antiretroviral treatment, with recent determinations of CD4 lymphocytes 350 cells/mL and HIV viral load of 154 copies/mL. For the past 3 months she has been treated for seronegative symmetrical polyarthritis with 10-20 mg/day of prednisone. Which of the following statements is correct?

I would perform a bone marrow biopsy, since the most probable diagnosis is visceral leishmaniasis.

Pancytopenia is justified by C virus-associated cirrhosis and I would not perform further testing.

Probably a medullary toxicity due to prednisone that would be treated with drug withdrawal and filgastrim.

I would request an ANAs determination to rule out disseminated systemic lupus.

I would intensify antiretroviral therapy, as it is likely that all manifestations are due to HIV.

Pharmacology_Katzung

Sharon Safrin, MD A 35-year-old white woman who recently tested seropositive for both HIV and hepatitis B virus surface antigen is referred for evaluation. She is feeling well overall but reports a 25-pack-year smoking history. She drinks 3–4 beers per week and has no known medication allergies. She has a history of heroin use and is currently receiving methadone. Physical examination reveals normal vital signs and no abnormalities. White blood cell count is 5800 cells/mm3 with a normal differential, hemoglobin is 11.8 g/dL, all liver tests are within normal limits, CD4 cell count is 278 cells/mm3, and viral load (HIV RNA) is 110,000 copies/mL. What other laboratory tests should be ordered? Which antiretroviral medica-tions would you begin?

Gero Hütter

to express wildtype CCR5 (because they hadn't been replaced yet from bone marrow precursors), also had no detectable virus. After 600 days without antiretroviral drug treatment, the patient's blood, bone marrow and bowel HIV levels were below the limit of detection; the virus was thought to be present in other tissues. However, the patient actually had a brain biopsy, in addition to biopsies of his intestines, liver, lymph nodes, bone marrow—basically, every part of the body that can be biopsied. All were negative for virus. There is no virus in this person's body out to two and a half years off of all anti-HIV drugs. His antibody levels—called titers—are declining just the way expected if the patient was vaccinated against HIV and then the levels of antibodies were examined. They'd be very strong in the beginning, but would weaken if they are not re-exposed to the virus. It is believed this patient has no HIV in his body and therefore there is nothing to re-expose him, so the

Haemophagocytic syndrome and elevated EBV load as initial manifestation of Hodgkin lymphoma in a HIV patient: case report and review of the literature.

In HIV patients, haemophagocytic syndrome (HPS) may occur in the presence of cancer, concomitant viral infection, HIV primo-infection or at the initiation of highly active antiretroviral therapy (HAART). Hodgkin lymphoma remains a rare cause of HPS. We describe a case of HPS with very high Epstein Barr virus (EBV) load in a HIV patient as initial manifestation of Hodgkin lymphoma. A 29-year-old HIV positive man, successfully treated with HAART with an undetectable viral load and CD4 cells count of 438/µl, was admitted for high fever of unknown origin. Laboratory results showed a pancytopenia with haemoglobin at 82 g/l, lymphocyte count at 0.36G/l and platelets count at 47G/l; a highly elevated ferritine >7500 µg/l; increased lactate dehydrogenase at 885U/l and soluble IL2 receptor (CD25) >60 ng/ml. EBV load was measured and confirmed at 2,600,000 copies/ml. A PET-CT imaging showed diffuse elevated metabolic activity in the bone marrow and in two lesions in the spleen without lymphadenopathy. Bone marrow and liver biopsies revealed images of haemophagocytosis and lymphocyte depleted Hodgkin lymphoma. Treatment consisted in etoposid, steroids, and R-ABVD (rituximab, doxorubicin, bleomycin, vinblastine, dacarbazine) chemotherapy. The patient completed six cycles of chemotherapy. We reviewed the literature in PubMed with the following keywords: HPS, HIV, EBV, Hodgkin lymphoma. We identified four publications and two reviews reporting cases of HPS associated with Hodgkin lymphoma in HIV patients with either a positive EBV load either the presence of encoded EBV RNA in tumour cells. Twenty-two cases (including one pediatric case) were described. Among adults, mostly men, the median age was <50 years and immune suppression was marked with a median CD4 cell count<100 cells/µl, even in patients receiving HAART. When measured, EBV load in the serum was high. Prognosis was poor with a high mortality despite adequate treatment consisting in steroids and chemotherapy, with or without etoposide (Table 1). Our case report and the review of literature suggest that physicians should be aware of the association between EBV infection/reactivation and Hodgkin lymphoma as a cause of HPS in HIV patients, even if successfully treated with HAART. The pathogenesis of these three interrelated conditions (viral infection, oncogenesis and immunologic reaction) remains unclear.

[Parvovirus B19 infection in HIV-infected patients].

Here we provide a review of the literature and a description of our own clinical case. The patient was a 32-year-old woman who had been infected with HIV for 6 years without antiretroviral therapy. The test results showed CD4 87 cells/l, viral load 3750 copies/ml. Normochromic normocytic anemia and reticulocytopenia developed soon. In the myelogram, all erythroblasts were 0.5%. The viral load of parvovirus B19 DNA according to PCR was more than 9 million IU/ml. Pure red cell aplasia associated with parvovirus B19 was diagnosed. We started antiretroviral therapy with efavirenz, lamevudine and tenofovir. In addition to blood transfusions, we administered intravenous donor immunoglobulin with a dose increase from 5000 mg to 20 000 mg per day. After discontinuing of intravenous immunoglobulins, the laboratory test results were stable over the next 5 months: hemoglobin was more than 115 g/L, reticulocytes more than 3%, in the myelogram all erythroblasts were 21%. However, the elimination of parvovirus B19 wasnt achieved. The maximum decrease in viral load for parvovirus B19 was down to 720 IU/ml. A typical feature of the case was the lack of pure red cell aplasia of the bone marrow with the existing viral load of parvovirus B19. HIV infection progressed: 44 cells/l, viral load not determined. The case ended lethally.

[Visceral leishmaniasis with an unusually long incubation time].

A 25-year-old woman of Yugoslavian origin came to Germany two years before and did not leave Germany since this time. She developed a phlebothrombosis during pregnancy which was treated surgically and with subsequent heparinisation. The pregnancy had to be terminated by section because of abnormal liver functions and increased blood pressure. These values returned to normal within two months. Further tests again showed raised liver function tests (GOT 57 U/l, GPT 71 U/l) and antibodies against smooth muscle and actin. Autoimmune hepatitis was diagnosed and prednisolone given (100 mg daily). In the subsequent 4 months the patient progressively lost more weight and a pancytopenia developed. Suspected of having a systemic haematological syndrome she was admitted to hospital. Physical examination was unremarkable except for hepato- and splenomegaly (spleen 15.6 cm in diameter by sonography). Laboratory tests showed hypergammaglobulinaemia (50 g/l, 53%), increased WBC count, as well as decreased haemoglobin concentration and platelet count (900 WBC/microliter, Hb 10.9 g/l, 146,000 platelets/microliter). Bone marrow puncture unexpectedly revealed a large number of Leishmania donovani. Five-valent antimony was administered (sodium stibogluconate 20 mg/kg daily intravenously as bolus for 14 days). She has been free of symptoms since then (follow-up period of one year). Visceral leishmaniasis is a rare disease in Europe. Incubation periods of several years have been reported and the infection can be easily mistaken for other chronic liver disease, in this case for an autoimmune hepatitis. Leishmaniasis should be included in the differential diagnosis of unclear liver disease if there is a suggestive history (country of origin or journey into an endemic area).

HIV Nephropathy -- Evaluation

Currently, combination antiretroviral therapy (cART) induced nephropathy is a far more common disease than HIVAN. Differentiating patients with HIVAN versus cART induced nephropathy is important, as management is different. Besides history and physical examination findings, patients with HIVAN present with CD4 count <200 cells/mm, viral load >400 copies/mL, a rapid decline in renal function, proteinuria >300 mg/24h, hyaline or proteinaceous casts on urinalysis, and large-sized kidneys with intense cortical echogenicity. In contrast, cART induced nephropathy presents in patients with CD4 count >200 cells/mm, viral load <400 copies/mL, proteinuria <30 mg/24h, an indolent decline in renal function, hematuria or leukocyturia, needle or rod-like crystals on urine microscopy and unremarkable ultrasound findings. [13] [14]

Disseminated histoplasmosis presenting as pyoderma gangrenosum-like lesions in a patient with acquired immunodeficiency syndrome.

A 33-year-old Hispanic woman with newly diagnosed human immunodeficiency virus (HIV) infection, a CD4 T-lymphocyte count of 2, viral load of 730,000 copies/mL, candidal esophagitis, seizure disorder, a history of bacterial pneumonia, and recent weight loss was admitted with tonic clonic seizure. On admission, her vital signs were: pulse of 88, respiration rate of 18, temperature of 37.7 degrees C, and blood pressure of 126/76. Her only medication was phenytoin. On examination, the patient was found to have multiple umbilicated papules on her face, as well as painful, erythematous, large, punched-out ulcers on the nose, face, trunk, and extremities of 3 months' duration (Fig. 1). The borders of the ulcers were irregular, raised, boggy, and undermined, while the base contained hemorrhagic exudate partially covered with necrotic eschar. The largest ulcer on the left mandible was 4 cm in diameter. The oral cavity was clear. Because of her subtherapeutic phenytoin level, the medication dose was adjusted, and she was empirically treated with Unasyn for presumptive bacterial infection. Chest radiograph and head computed tomography (CT) scan were within normal limits. Sputum for acid-fast bacilli (AFB) smear was negative. Serologic studies, including Histoplasma antibodies, toxoplasmosis immunoglobulin M (IgM), rapid plasma reagin (RPR), hepatitis C virus (HCV), and hepatitis B virus (HBV) antibodies were all negative. Examination of the cerebrospinal fluid was within normal limits without the presence of cryptococcal antigen. Blood and cerebrospinal cultures for bacteria, mycobacteria, and fungi were all negative. Viral culture from one of the lesions was also negative. The analysis of her complete blood count showed: white blood count, 2300/microl; hemoglobin, 8.5 g/dL; hematocrit, 25.7%; and platelets, 114,000/microl. Two days after admission, the dermatology service was asked to evaluate the patient. Although the umbilicated papules on the patient's face resembled lesions of molluscum contagiosum, other infectious processes considered in the differential diagnosis included histoplasmosis, cryptococcosis, and Penicillium marnefei. In addition, the morphology of the ulcers, particularly that on the left mandible, resembled lesions of pyoderma gangrenosum. A skin biopsy was performed on an ulcer on the chest. Histopathologic examination revealed granulomatous dermatitis with multiple budding yeast forms, predominantly within histiocytes, with few organisms residing extracellularly. Methenamine silver stain confirmed the presence of 2-4 microm fungal spores suggestive of Histoplasma capsulatum (Fig. 2). Because of the patient's deteriorating condition, intravenous amphotericin B was initiated after tissue culture was obtained. Within the first week of treatment, the skin lesions started to resolve. Histoplasma capsulatum was later isolated by culture, confirming the diagnosis. The patient was continued on amphotericin B for a total of 10 weeks, and was started on lamivudine, stavudine, and nelfinavir for her HIV infection during hospitalization. After amphotericin B therapy, the patient was placed on life-long suppressive therapy with itraconazole. Follow-up at 9 months after the initial presentation revealed no evidence of relapse of histoplasmosis.

[The usefulness of the bone marrow examination in the etiological diagnosis of prolonged fever in patients with HIV infection].

To analyze the usefulness of bone marrow (BM) study in the diagnosis of fever of unknown origin (FUO) in patients infected by the human immunodeficiency virus (HIV) in a single center during a period of 42 months. 182 episodes of FUO in 162 patients p3th HIV infection were studied. Age, sex, risk factor for HIV infection, hemoglobin level, counts of leucocytes, neutrophils, lymphocytes, CD4 positive lymphocytes, platelets and levels of hepatic enzymes, albumin and beta 2-microglobulin were studied. BM aspirate was performed in all episodes for cytologic and microbiologic examination, and BM biopsy was done in 43. Analysis of factors related with the probability of diagnosis by BM examination was carried out. The median age was 33 years (range, 22-70), and 123 were males. Drug abuse was the most frequent risk factor for HIV infection (63%). One hundred thirty patients had previous AIDS diagnosis before they were evaluated for unexplained fever. A specific diagnosis was achieved in 161 episodes (88%) and the most frequent diagnoses were Mycobacterium spp. (55%) and Leishmania spp. (14%) infections. Fifty-four episodes (30%) were diagnosed by BM examination, and in 36 (20%) BM study was the only diagnostic tool. Examination of the BM aspirate yielded the diagnosis in 40 out of the 178 episodes (13%), whereas BM biopsy was a diagnostic tool in 8 (19%); in 9 additional cases (21%) granulomas were observed. Microbiologic study of BM smears for mycobacterial infections was positive in 28 of the 143 episodes (19%), and the culture for Leishmania was positive in 2 out of the 42 cases. The presence of thrombocytopenia (< 75 x 10(9)/l) and elevated serum levels of aspartate-aminotransferase (AST) (> 100 U/l) were the factors associated with a high probability to obtain the diagnosis through BM study. In patients infected by the HIV and unexplained fever, BM examination is an useful procedure for the diagnosis, particularly in areas where infections by Mycobacterium spp. and Leishmania are prevalent. So that, in our setting, systematic use of this procedure is justified for diagnosis of FUO in those patients.

Adenopathy -- Introduction -- Algorithmic Analysis of Lymphadenopath y

Although there is no "cookbook" for the laboratory evaluation of generalized unexplained lymphadenopathy, the initial steps are to obtain a complete blood count (CBC) with a manual differential and EBV serology. If non-diagnostic, the next steps would be PPD placement, RPR, chest x-ray, ANA, hepatitis B surface antigen, and HIV test. Again if any of the above are positive, appropriate treatment can be initiated. In the presence of negative serological examinations and radiological examinations, and or significant symptomology, a biopsy of the abnormal node is the gold standard for diagnosis. [9] [10] [11] [12] Statistics concerning lymphadenopathy are not accurate as the great majority of lymphadenopathy is caused by a non-reportable illness and thus not reported or taken into account. This results in a statistical bias, or skew, toward the reportable causes of lymphadenopathy:  malignancies, HIV, tuberculosis, and sexually transmitted infections (STIs). Citations in the recent literature for general medical practice indicate that less than 1% of people with lymphadenopathy have malignant disease most often due to leukemia and younger children Hodgkin disease in adolescence non-Hodgkin disease and chronic lymphocytic leukemia (CLL) in adults. It has been reported the general prevalence of malignancy is 0.4% in patients under 40 years and around 4% in those older than 40 years of age seen in a primary care setting. It is reported that the prevalence rate of neoplastic disease rises to near 20% in referral centers and rises to 50% or more in patients with initial risk factors. [13]

Simultaneous pancreas-kidney transplantation in a human immunodeficiency virus-positive recipient: a case report.

After the development of highly active antiretroviral therapy (HAART) for patients with human immunodeficiency virus (HIV), there has been increased interest in organ transplantation for this selected population. There is a lack of reports about pancreas transplant in HIV+ recipients. We report the case of a 43-year-old HIV+ man who presented with type 1 diabetes for 25 years and end-stage-renal disease. He underwent dialysis therapy for the prior 3 years. His CD4 count was 830 cells/mL and a negative viral load was achieved after 3 months of antiretroviral therapy. His nutritional status was favorable; no opportunistic infections had occurred. A simultaneous pancreas-kidney transplantation (SPKT) was performed from a 19-year-old deceased trauma victim. Pancreas implantation was enteric-portal drainage. No induction immunosuppression was used, but rather tacrolimus, sodium mycophenolate, and steroids. In the postoperative period, there was a delayed kidney graft function requiring hemodialysis for 14 days. On postoperative day 11, a kidney biopsy specimen showed mild rejection, which was successfully treated with steroids. The patient was discharged after 22 days; he was normoglycemic and insulin-independent with a serum creatinine value of 1.9 mg/dL. Currently, his outcome has been uneventful, without a readmission or opportunistic infections. After 5 months postoperation, the viral load is negative and the CD4 count is 460 cells/mL. The current serum creatinine level is 1.1 mg/dL; no insulin has been required. HIV has been considered to be an absolute contraindication to organ transplantation, because of the infection risk due to severe immunosuppression, to interactions between antiretroviral and immunosuppressive drugs, and to reluctance to offer an organ to a terminal patient. However, transplants in HIV+ patients have shown good results, when a patient has an acceptable CD4 level, a low viral load, and minimal antiretroviral therapy.

[The natural history and laboratory parameters of HIV infection].

Since 1983 the morbidity and mortality rates as well as results of haematological, immunological and (later) HIV serological tests were recorded prospectively for 497 HIV-positive patients during 1837 clinic visits at least twice within at most six months for a median period of observation of 18 months (range 6-64 months). The rate of progression to a higher stage was calculated according to the method of Kaplan-Meier. The rate for asymptomatic patients was 16% after one and 33% after two years; for patients with persisting generalized lymphadenopathy it was 13% and 21%, respectively, for those with AIDS-related complex 28% and 47%, respectively, and for those with AIDS 33% and 82%, respectively. As for results of laboratory tests, patients with progressive disease had significantly lower titres of anti-HIV nuclear antibodies, as well as a higher incidence of HIV-p24 antigen. Haemoglobin levels, platelet and lymphocyte counts and number of CD-4-positive lymphocytes were significantly lower, Neopterin and beta 2-microglobulins higher (P less than 0.01).

Is there a role for the use of IFN-α in primary myelofibrosis?

A 62-year-old man with a history of diabetes and hypertension is referred to your hematology clinic for an incidental discovery of anemia. He does not have any constitutional symptoms and previous blood counts have been within the normal range. He has hepatosplenomegaly with a palpable spleen of 6 cm below the left costal margin and a liver size of 2.5 cm below the right costal margin. Laboratory evaluation shows a WBC count of 12.8 K/μL, hemoglobin of 11.0 g/dL, and platelets of 202 K/μL, with a mean corpuscular volume of 85.7, 72% neutrophils, 13% lymphocytes, 4% monocytes, 5% eosinophils, 1% basophils, 1% promyelocytes, 4% myelocytes, and lactate dehydrogenase of 447 U/L (upper limit of normal is < 340 U/L). Peripheral blood smear shows 2+ teardrop-shaped RBCs, large hypogranular platelets, and rare nucleated RBCs. Bone marrow (BM) biopsy exhibits a hypercellular BM with atypical megakaryocytes and increased reticulin fibrosis (MF-1). BCR-ABL gene rearrangement by FISH was negative and JAK2 V617F mutation was 95% positive. He was diagnosed with primary myelofibrosis considered low risk (risk score of 0) by the International Prognostic Scoring System.(1) Because he is low risk and asymptomatic, he does not need treatment at this time.(2) However, he has read about the possible clinical benefits of IFN-α and its potential reduction of BM fibrosis and wonders whether this would be an appropriate treatment.

[Visceral leishmaniasis: a comparative study of patients with and without human immunodeficiency virus infection].

The changes that HIV coinfection can induce in clinical symptoms, response to treatment and prognosis of visceral Leishmaniasis (VL) are not well known. We retrospectively describe the characteristics of VL in patients with and without HIV infection, between 1988-1998. Fifty episodes of VL were diagnosed in 40 patients. Nineteen (47.5%) were HIV coinfected, 57.8% of them have had an aids defining illness, and the median of CD4+ lymphocytes was 50/mm3. Clinical and laboratory data were similar to patients non HIV infected, except for lower levels of LDH (437 vs 578 U/ml; p = 0.02) and total lymphocytes (665 vs 1.500/mm3; p = 0.004) and higher levels of hemoglobin (9.8 vs 8.7 gr/dl; p = 0.01) and ESR (85 vs 44 mm; p = 0.01). The first episode of VL was diagnosed in 87.5% patients through bone marrow aspirate, and the other cases were diagnosed by biopsies of gum (2), lymph node (1) or liver (1). One patient was diagnosed clinically: he had a positive serology and a good response to antileishmanial therapy. Treatment failed in nine patients (22.5%), 7 HIV-coinfected. Eight patients died (20%), 6 HIV-coinfected. Five deaths were directly attributed to VL. Six coinfected patients (31.5%) relapsed and only one (4.7%) in the other group. We did not find major differences in clinical manifestations or laboratory data between the two groups. Biopsies of several tissues can be particularly helpful for diagnosis in immunocompromised patients with negative bone marrow aspirates. Failures, mortality and relapses are more common in HIV infected patients. VL coinfection usually affects HIV infected patients when they develop severe immunodepression.

Subcutaneous panniculitis-like T-cell lymphoma with hemophagocytic syndrome successfully treated with cyclosporin A.

A 17-year-old girl previously in good health presented with a 2-month history of recurrent, high-grade fever; general fatigue; anorexia; a 10-kg weight loss; and multiple, painful, reddish skin lesions on the lower abdomen. Some lesions were ulcerated, with an oily yellowish brown discharge. A systemic review was unremarkable other than bleeding from the nose. Her medical and family histories were unremarkable. On examination, the patient was pale, jaundiced, and febrile (temperature of 39 degrees C). She had enlarged lymph nodes in the axillary and inguinal areas. There was moderate hepatosplenomegaly. Local skin examination revealed multiple erythematous, tender, and firm subcutaneous nodules of variable size (1-2 cm) on the lower abdomen. Some nodules were ulcerated, with oily yellowish brown discharge and overlying ecchymosis (Figures 1 and 2). Mucous membranes were free of lesions. Laboratory investigations showed pancytopenia, an elevated erythrocyte sedimentation rate (>80 mm/h), normal renal function tests, abnormal hepatic function tests (alanine aminotransferase 172 U/L, aspartate aminotransferase 229 U/L, alkaline phosphatase 725 U/L, and total bilirubin 100 mmol/L [normal range 0-18 mmol/L]), conjugated bilirubin 45 mmol/L (normal range 0-5 mmol/L), and high triglycerides 855 mg/dL (normal range 20-200 mg/dL). Prolonged prothrombin time, 26 seconds (normal range 13-16 seconds); prolonged activated partial thromboplastin time, 61 seconds (normal range 26-38 seconds); positive disseminated intravascular coagulation studies evidenced by low fibrinogen, 74 mg/dL (normal range 160-350 mg/dL); and positive fibrinogen degradation products were also noted. Throat, midstream urine, and blood culture results were negative. Serologic tests for syphilis, HIV, and hepatitis B and C viruses were negative. Epstein-Barr virus and cytomegalovirus serologic values revealed evidence of past infection. Tuberculin and Coombs tests were negative. The alpha1-antitrypsin level was normal. Antinuclear and anti-smith antibodies, rheumatoid factor, and cryoglobulins were negative. CT showed enlarged lymph nodes in the axillary and inguinal areas, bilateral small pleural effusion, moderate hepatosplenomegaly, severe fatty infiltration of the liver, and thickening of lower abdominal subcutaneous tissue. A liver biopsy showed steatohepatitis. Bone marrow aspirate and trephine were normal. A deep punch biopsy of a nodule from the right lower abdomen revealed lobular panniculitis with atypical lymphocytes and large macrophages with cytophagocytosis ("beanbag" cells) (Figures 3 and 4). Immunohistochemistry showed that these atypical cells were positive for CD3, CD8, granzyme B, and perforin, and negative for CD56. T-cell gene rearrangement studies on skin lesions revealed a monoclonal T-cell receptor (gamma-chain) gene rearrangement, supporting the diagnosis of subcutaneous panniculitis-like T-cell lymphoma. On presentation, the initial treatment included 6 U of fresh frozen plasma, 2 U of packed red blood cells, and 2 g IV fibrinogen for 3 consecutive days. The patient was started on prednisolone 60 mg orally once daily and cyclosporine A 5 mg/kg/d orally in two divided doses. The fever and other systemic symptoms and skin lesions resolved within 2 weeks after the treatment. The prednisolone dose was tapered gradually, and a maintenance dose of cyclosporine A was continued. The patient's condition remained in remission at 12-month follow-up; there was no evidence of clinical relapse.

[Evolution of biochemical and hematological parameters in patients living with HIV/AIDS treated with antiretroviral therapy at the Aboubacar Sangoulé Lamizana General Camp Medical Center].

This study aimed to evaluate the impact of treatment on biochemical and hematological parameters in HIV-positive patients followed up at the Aboubacar Sangoulé Lamizana General Camp Medical Center in Burkina Faso. We conducted a retrospective study over the period January 2010-September 2015. The study only included HIV-positive patients treated with ART having undergone laboratory tests at treatment initiation (M0), at sixth month (M6), and at twelfth month (M12). Sex-ratio was 0.88 and the most affected age group was 45-55 years. The most prescribed treatments were triple combination therapies based on 2INTI + 1INNTI (74,5%), 2INTI+1 IP (14,9%). Viral load test was little requested. The rate of patients with normal laboratory tests showed a statistically significant regression between M0 (70%), and M6 (13%) (p<0.05). Severely immunocompromised patients showed a significant increase in average TCD4 lymphocytes value, ranging from 79,22 at M0 to 227.95 cells/mm<sup3</sup at M12 (p<0.05). Anaemic patients showed a significant increase in the rate of mean haemoglobin levels from 10.5 g/dl at M0 to 12.53 g/dl at M12 (p<0.05). The analysis of biochemical parameters could not be performed because of a lack of data. The increase in the rate of TCD4 lymphocytes and in the rate of hemoglobin levels gives an indication of ART effectiveness and of patient's tolerance to treatment. Viral load test accessibility and an improvement in laboratory testing monitoring are essential.

Virological failure

Virological failure is defined as the failure to meet a specific target of antiviral drug treatment, namely the non-attainment or non-maintenance of undetectable viral load, particularly in the treatment of HIV. As antiretroviral therapy is evaluated by detecting the amount of copies of the virus in blood samples, the concept of virological failure gives a way to modify treatment of this disease. Virological failure in HIV is characterized by a confirmed viral load above 400 copies / ml after 24 weeks or above 50 copies / ml after 48 weeks of treatment or, even for individuals who have reached complete viral suppression, by confirmed rebound of viral load above 400 copies / ml. Non-adherence of HIV antiretroviral therapy increases the risk of drug suppression and resistance (Bangsberg, D. R., Moss, A. R., & Deeks, S. G. (2004)).

[Efficiency of bone marrow aspirate for diagnosis of opportunistic infections in HIV infected patients].

AIDS is the first cause of opportunistic infections. The objective of the present study was the evaluation of the efficiency of bone marrow aspirate (BMA) for diagnosis of opportunistic infections in HIV infected patients with prolonged fever. Charts from 92 patients with BMA from 1992 to 1994 were reviewed. Diagnosis was achieved in 14.1% of cases. Diagnosis cannot be made by other methods in six leishmaniasis and in two disseminated tuberculosis. The sensibility was of 33.3% for mycobacterial infections, the sensibility of hemoculture was of 50%. The hemoglobin level was lower for patients with diagnostic BMA than for patients with not diagnostic BMA (77 g/l vs 97 g/l, p < 0.0004). The WBC counts was not different in both groups of patients, and platelets counts was greater in patients with BMA diagnostic (165 x 10(9)/l vs 102 x 10(9)/l, p < 0.001). In the patients with hemoglobin lower than 100 g/l the diagnostic efficiency was 18.6% (11 of 59 cases). The BMA was unprofitable in HIV infected patients with prolonged fever without hemocytopenias. Profitability increase in patients with hemoglobin lower than 100 g/l. The BMA in useful for leishmania identification. The hemoculture has greater sensitivity than BMA for the diagnosis of mycobacterial disseminated infection.

Case of haemophagocytic lymphohistiocytosis following Epstein-Barr virus infection.

Haemophagocytic lymphohistiocytosis (HLH) is a rare diagnosis that carries a high degree of mortality. We present this case of a previously healthy 22-year-old woman, who was admitted acutely ill to the hospital. One week prior, she had been seen by her primary care physician for fatigue and malaise. At that time, she was noted to have anterior and posterior cervical lymphadenopathy. She was referred to the emergency room and was diagnosed with acute Epstein-Barr virus (EBV) mononucleosis based on her clinical symptoms and positive heterophile antibody test. She was discharged after an uneventful 48-hour stay on the wards. She represented 7 days after discharge with cough, fatigue, nausea, vomiting, epigastric abdominal pain, diarrhoea, weight loss and subjective fevers. She had also reported haematemesis, epistaxis and melaena. Vital signs included temperature 36.9°C, blood pressure 90/50 mm Hg, heart rate 130 beats per minute and respiratory rate 32 breaths per minute. Physical examination was notable for an acutely ill appearing woman with scleral icterus, hepatosplenomegaly and palpable cervical and axillary lymphadenopathy. Complete blood count showed pancytopaenia with haemoglobin 59 g/L (normal 120-160 g/L), white blood cell count 2.7×10<sup9</sup/L (normal 4-10.5×10<sup9</sup/L) and platelet count 50×10<sup9</sup/L (normal 150-450×10<sup9</sup/L). The white blood cell count differential included 58% neutrophils (normal 38%-77%) with immature neutrophils in band form elevated at 45% (normal <14%), 16% lymphocytes (normal 20%-48%), 7% monocytes (normal <12%) and no eosinophils (normal <6%). Blood smear revealed anisocytosis, poikilocytosis and hypochromia. Coagulation panel showed elevated levels of d-dimer level at 1.39 µg/mL (normal <0.45 µg/mL), prolonged prothrombin time at 34.4 s (normal 11-15 s), prolonged activated partial thromboplastin time of 55.6 s (normal 25-34 s), prolonged international normalised ratio at 3.31 (normal <1.1) and low fibrinogen 60 mg/dL (normal >200 mg/dL). Lipid panel showed cholesterol at 114 mg/dL (normal 125-200 mg/dL), triglycerides 207 mg/dL (normal 30-150 mg/dL), high-density lipoprotein cholesterol 10 mg/dL (normal 40-60 mg/dL) and low-density lipoprotein cholesterol 63 mg/dL (normal <100 mg/dL). Other lab abnormalities included elevated ferritin of 6513 ng/mL (normal 10-150 ng/mL) and elevated lactate dehydrogenase of 1071 unit/L (normal 95-240 unit/L). Soluble interleukin-2 receptor alpha level was elevated at 60 727 units/mL (normal 223-710 units/mL). Fluorodeoxyglucose-positron emission tomography (FDG-PET) scan showed abnormal tracer localisation within the paratracheal, hilar, pelvic, abdominal and subcarinal lymph nodes, along with FDG-PET positive hepatosplenomegaly. A bone marrow biopsy showed hypercellular marrow (95% cellularity) with trilineage haematopoiesis, haemophagocytic cells, polytypic plasmacytosis and T-cell lymphocytosis, along with positive latent membrane protein-1 immunohistochemical staining for EBV. EBV quantitative DNA PCR showed >1 million copies. These findings were consistent with a diagnosis of HLH secondary to EBV infection. Despite intense therapy with the HLH-94 protocol, the patient expired from her illness after a prolonged hospital course.

[HIV/AIDS and pathology in blood count].

HIV/AIDS pandemy has hit the entire world. With the use of retroviral therapy the disease became chronic. The life prolongation often leads to complications in various organs. The aim of our work was to determine the frequency of blood count pathology at the time when the HIV infection was diagnosed, that means before any antiretroviral treatment was administered, and its relation to the disease stage. Out of 70 patients registered in AIDS centre in Brno University Hospital by 1st March 2006, we have complete blood count results including absolute number of CD4+ lymphocytes. Out of these 70 we evaluated a group of 64 HIV-positive individuals (17 women, 47 men), who were examined at the time the disease was diagnosed. Average and medians of all blood count parameters were within the reference range, only CD4+ lymphocytes in 1 mm(3) were out of range. Pathology in red blood cells count was found 26 times (41.9 % of examined patients), in white cell count 22 times (35.5 %). Thrombocyte number was affected 3 times, and only in one of these cases it was a separate finding. Blood count pathology is relative frequent in the HIV infected. Therefore HIV infection should be considered as one of the possible causes of unexplained blood count pathology.

[Agranulocytosis due to anti-tuberculosis drugs including isoniazid (INH) and rifampicin (RFP)--a report of four cases and review of the literature].

We experienced 4 cases of agranulocytosis due to anti-tuberculosis drugs (rifampicin [RFP], isoniazid [INH], ethambutol [EB], streptomycin [SM] or pyrazinamide [PZA]) among some 6,400 tuberculosis patients who underwent chemotherapy over the past 20 years from 1981 to 2002 in our hospital, and the incidence rate of agranulocytosis was estimated at 0.06%. The 4 cases of agranulocytosis were as follows. CASE 1: A 51-year-old woman with right chest pain and fever was admitted to our hospital on Jan 4, 2001. The white blood cell (WBC) count was 5,200/microliter. The tubercle bacilli were cultured in her sputum. The treatment with INH 0.3, RFP 0.45, EB 0.75, PZA 1.2 g/day, allopurinol and teprenone was started on Jan 13. Pyrazinamide and allopurinol were stopped because of hyper-uric acidemia on Feb 7. Agranulocytosis and eosinophilia (WBC 1,300 [Neut 1%, Ly 57%, Eos 35%]) developed on Feb 13. All drugs were withdrawn and G-CSF drug nartograstim 100 micrograms was injected subcutaneously for 3 days. The WBC recovered to normal level and she was thereafter treated with INH, EB and Levofloxacin (LVFX) without any further trouble. Agranulocytosis in this case was supposed to be due to RFP. CASE 2: A 66-year-old man who had had nephrotic syndrome and hypothyroidism and has been treated with prednisolone 10 mg/day was admitted to our hospital on Aug 9, 2000 because of miliary tuberculosis. The tubercle bacilli were cultured in his sputum and the treatment with INH 0.3, RFP 0.45, and EB 0.75 g/day were started on Aug 10, but it was withdrawn on Aug 17 because of general skin eruption. After re-starting treatment with EB and INH on Aug 24, RFP was added in small dosage (0.05 g) on Oct 12, but agranulomatosis (WBC 2,300/microliter [Neut 2%]) developed on Nov 21, and all drugs were withdrawn again. The G-CSF drug filgrastim was used once subcutaneously, and WBC recovered immediately. He was thereafter treated with INH, EB, LVFX successfully. Agranulocytosis was supposed to be due to RFP. CASE 3: A 60-year-old woman without symptoms had abnormal chest roentgenograph, and consulted with our hospital on Aug 26, 2002. The broncho-alveolar lavage fluid was smear and culture-negative, but PCR-TB positive, and the case was diagnosed as pulmonary tuberculosis. Treatment with INH 0.3, RFP 0.45, EB 0.75, PZA 1.2 g/day, alloprinol 300 mg and rebamipide 300 mg/day was started on Sept. 5, 2002. Late in September, she complained of appetite loss. The laboratory data on Oct 3 revealed WBC 900/microliter (Neut 1%, Ly 94%), aspartate aminotransferase (AST) 199 IU/l, and alanine aminotransferase (ALT) 253 IU/l, showing agranulocytosis and drug-induced hepatitis. The chemotherapy was immediately withdrawn and she was admitted to our hospital on the next day. Glycyrrhizin derivative (SNMC) 40 ml was injected for 5 days, and WBC recovered, and AST and ALT also became normal. CASE 4: A 60-year-old man was admitted to our hospital on March 11, 1981 because pulmonary tuberculosis had recurred. He had been treated with SM, PAS and INH in 1973 for pulmonary tuberculosis. On admission examination of blood count and blood chemistry were normal. Treatment with RFP, INH and SM was started on March 11. He stopped out from the hospital on April 17, but in a few days he returned back with sore throat, lower lip swelling and gingival bleeding. Blood cell count on April 24 showed pancytopenia with RBC 226, Hb 7.5, WBC 800 (Ly 96%, Eos 4%) and Plt 10,000/microliter. The bone-marrow showed NCC (nuceated cell count) of 5,500, and megakaryocyte 0. Thereafter ground glass appearance shadows were seen on the whole lung field, and he died May 26. Autopsy showed generalized aspergillosis. It was strongly suspected that either of RFP, INH or SM was responsible for his pancytopenia. We collected another 10 cases of agranulocytosis due to anti-tuberculosis drugs in the world wide literature, and found men/women ratio 5/8 (in one case gender was not known), the duration of chemotherapy before appearance of agranulocytosis 1-3 months, no change in the lymphocyte count of the peripheral blood, and the accompanying of another allergic signs such as skin eruption, blood eosinophilia or drug-induced hepatitis in some cases, and these findings suggest that the mechanism of agranulocytosis due to anti-tuberculosis drugs was allergic in nature.

InternalMed_Harrison

Fever ˜38.3° C (101° F) and illness lasting ˜3 weeks and no known immunocompromised state History and physical examination Stop antibiotic treatment and glucocorticoids Obligatory investigations: ESR and CRP, hemoglobin, platelet count, leukocyte count and differential, electrolytes, creatinine, total protein, protein electrophoresis, alkaline phosphatase, AST, ALT, LDH, creatine kinase, antinuclear antibodies, rheumatoid factor, urinalysis, blood cultures (n=3), urine culture, chest x-ray, abdominal ultrasonography, and tuberculin skin test

[Focal mycobacterial lymphadenitis after starting highly active antiretroviral therapy].

A 30-year-old man with a known HIV infection for 7 years presented for treatment with antiretroviral drugs. He was known to have had herpes zoster, oral hairy leukoplakia and recurrent Candida stomatitis, but was otherwise without symptoms. The CD4 lymphocyte count was 19 cells/mm3 and there were 41,000 HIV-RNA copies/ml. The HIV infection was in CDC stage B3, indicating the need for combined antiretroviral treatment. A week after starting stavudine, saquinavir and ritonavir he had to be admitted because of nausea and vomiting, colicky abdominal pain, diarrhea, fever up to 39 degrees C and a rise of C-reactive protein to 207 mg/dl. Bacteriological examination of feces and biopsy of an enlarged retroperitoneal lymph node revealed atypical mycobacteria. Antituberculosis treatment was started. The CD4 cell count rose to 56/mm3 and the viral count fell to 11,000/ml. Each time after initiating a different antiviral regimen the symptoms recurred. This case illustrates an atypical manifestation of on opportunistic infection: during combined antiviral treatment the CD4 cell count rose and thus precipitated an heretofore subclinical mycobacterial infection with focal lymphadenitis. If, on starting antiretroviral treatment at a late HIV stage, new symptoms develop within 1-3 weeks, one should consider drug-induced side effects or the onset of an opportunistic infection that has become manifest as the result of an improved immunological state.

[Discriminative value for AIDS case of erythrocyte sedimentation rate, immunoglobulins IgA and IgM, and beta 2-microglobulin in combination with the CD4+ lymphocyte count].

To establish the probability to discriminate the evolution to "AIDS case" in relation to the common laboratory parametres in the follow-up of the HIV infection. We have studied a cohort of 118 patients (1986-95) with HIV infection, 14 of them (12%) had clinical criteria for AIDS (CDC/93) during the follow-up. Clinical evaluations and CD4+ and CD8+ lymphocytes, beta 2M, IgG, IgA, IgM and E.S.R determinations were done. Multivariate analysis (RSIGMA) was done. with the initial laboratory values, according to the clinical diagnostic (AIDS and NO AIDS) done during the follow-up. By multiple logistic regression those laboratory variables with more predictor value for "AIDS CASE" were selected. With the initial value of these variables (E.S.R., beta 2M, IgA, IgM and CD4+ lymphocytes) and the clinical diagnostic of AIDS done during the follow-up, we did the linear discriminatory analysis between two groups (AIDS, NO AIDS) obtaining generalized distance between both groups of 3,4609 and a probability of classification error of 4%. A very significant difference (p < 0.001) was obtaining when we compare the variables' mean of each of the clinical groups. In the HIV infection the values of ESR, beta 2M, IgA and IgM in combination with the absolute value of the CD4+ lymphocytes allows to discriminate those patients who will develop AIDS with a probability of classifications error of 4%. This has clinical interest in absence of viral load and helps to take therapeutical decisions.

Long-term nonprogressor

Long-term nonprogressors (LTNPs), sometimes also called elite controllers, are individuals infected with HIV, who maintain a CD4 count greater than 500 without antiretroviral therapy with a detectable viral load. Many of these patients have been HIV positive for 30 years without progressing to the point of needing to take medication in order not to develop AIDS. They have been the subject of a great deal of research, since an understanding of their ability to control HIV infection may lead to the development of immune therapies or a therapeutic vaccine. The classification "Long-term non-progressor" is not permanent, because some patients in this category have gone on to develop AIDS. Long-term nonprogressors typically have viral loads under 10,000 copies /mL blood, do not take antiretrovirals, and have CD4+ counts within the normal range. Most people with HIV not on medication have viral loads which are much higher.

[Peripheral and bone marrow hematological modifications in infection by the human immunodeficiency virus (HIV) in central Africa. Diagnostic and prognostic significance].

From the 24 March 1988 to the 15 June 1989, we noticed the peripheric and medullar haematologic modifications of 46 patients infected by HIV, classified in the group IV of CDC. The haematologic modifications found are: a peripheric cytopenia with a constant anemia often serious, a leuconeutropenia, a mild or missing lymphopenia. In comparison: the bone marrow is often rich in the different lineage with more often a sharp lymphoplasmocytal reaction, sometime very characteristic on the cytological side. 2 myeloid leukemia were diagnosed by participation of the myelogram. At least, the proteinogram showed a major polyclonal hypergammaglobulinemy sometimes monoclonal.

Diffuse Large B-Cell Lymphoma -- Evaluation

A detailed clinical and physical examination and the laboratory and imaging studies are essential for the diagnosis of lymphoma. Laboratory data include Complete blood count with differential (CBC), comprehensive metabolic profile (CMP), lactate dehydrogenase (LDH), HIV and Hepatitis B and C serologies, and serum protein electrophoresis. CBC can show cellular atypia on smears as well as cytopenias. Patients with symptoms or at risk of central nervous system (CNS) involvement should have a lumbar puncture. HIV should be tested as B cell lymphomas can be an AIDS-defining illness. Besides, as the treatment involves significant immunosuppression, it requires consideration of the patient’s HIV and hepatitis status. Renal involvement can be seen by up to 14% of the patients. LDH is elevated in more than 50% of the cases. LDH is a predictor of survival. [15]

Initial assessment of patients infected with human immunodeficiency virus: the yield and cost of laboratory testing.

Our objective was to determine the yield and cost of standardized laboratory testing of HIV-infected patients entering medical care after testing positive for HIV. An HIV staging and referral clinic in a municipal public hospital was our site for a cross-sectional study, and 308 patients were evaluated in the clinic between February 1, 1990 and October 1, 1991. Patients underwent standardized laboratory testing, including hematologic studies, serum chemistries, infectious disease serologies, and chest radiographs. The percentage of abnormal results for each test was determined. Abnormal results were stratified as mild or severe. They were also examined with regard to whether injection drug users or other patient subgroups had higher percentages of abnormalities. Changes and Medicare reimbursements for the tests were also determined. There were substantial numbers of abnormalities in all types of laboratory testing. Only 3% of patients had normal CD4 lymphocyte counts; 85% had counts of < 500/mm3, and 35% were < 200/mm3. Forty-four percent of patients had at least one abnormal hematologic study; 8% were severe. Nearly 75% had abnormal liver function tests; 20% of these were severe abnormalities. Fifteen percent of patients were PPD-positive, and > 50% were anergic. Fourteen percent had a positive nonspecific test for syphilis, and 7% had a positive confirmatory test. Fourteen percent of patients had an abnormal chest radiograph.(ABSTRACT TRUNCATED AT 250 WORDS)

[Severe oral mucositis in a patient with HIV infection].

A 50-year-old man with HIV infection (first diagnosed > 20 years ago) presented at our hospital with fulminant oral mucositis. Antiretroviral therapy (tenofovir, emtricitabine, raltegravir) had been started 2 months ago. Previously he had no opportunistic infections and no other pre-existing illnesses. He had not travelled outside Europe but stayed in Spain for several weeks during summer. Physical examination revealed swelling of the lips and severe ulcerative mucositis of the gums and pharynx. The patient complained of painful swallowing. The blood-chemistry showed no abnormalities. The microscopical analysis of a smear and a biopsy of the buccal mucosa revealed amastigotes of leishmania. By means of PCR technique, Leishmania donovani complex was specified. The patient was treated with liposomal amphotericin B (1 mg/kg) for 21 days. Because of the immunosuppression he was put on maintenance therapy afterwards (liposomal amphotericin B every 3 weeks). However, 4 months later there was a clinical relapse of the mucositis and a new cultural and PCR detection of leishmania in a buccal biopsy. After another course of 21 days with liposomal amphotericin B (3 mg/kg) and miltefosine (150 mg/d), the mucositis subsided. Therapy with liposomal amphotericin B (3 mg/kg single dose every 3 weeks) has since been maintained. The antiretroviral therapy was changed meanwhile to lamivudin, abacavir and raltegravir because of kidney failure with elevated urea and creatinine. The patient has been clinically stable ever since without any other HIV-related problems. The latest CD4 count was 456/µl and the HIV load 340 copies/ml. Leishmaniasis is a severe infection in HIV-positive patients. Clinical manifestations can be atypical in immunosuppressed patients and the treatment is complicated with HIV coinfection. This is also due to a lifelong persistence of the parasite with potential reactivation especially in patients with suppressed CD4 cells. Therefore maintenance therapy after standard therapy of leishmaniasis is mandatory at least for a CD4 count below 350/µl. Especially in HIV patients with a leishmaniasis relapse lifelong maintenance therapy should be considered.

Prognostic value of some laboratory parameters in a group of intravenous drug users in the early stages of HIV infection.

During a 5 year follow-up we found significantly reduced survival for non-accidental deaths in 37 intravenous drug users (IVUDs) in the early stages of HIV infection when compared with 32 HIV-negative IVUDs (p = 0.017). Moreover, in HIV-positive subjects, survival was significantly reduced for those groups which at the beginning of the follow-up showed the following values: circulating CD4+ lymphocytes <250/mmc (p = 0.007), CD4+/CD8+ ratio < 0.5 (p = 0.027), serum albumin < 4.13 g/dl (p = 0.045), IgA > or = 2.5 g/l (p = 0.043), IgM < 1.8 g/L (p = 0.041) and platelet count < 130 x 1,000/mmc (p = 0.038). In HIV positive patients, the value of 250 units/mmc for the circulating CD4+ lymphocytes still remained the most predictive parameter of increased mortality for disease at 5 years, even following investigations conducted with other cut-offs. Relationships existing at the beginning of the follow-up between circulating CD4+ lymphocytes and other prognostic parameters suggest that IgA (r = -0.34; p = 0.04), serum albumin (r = 0.33; p = 0.05), and CD4+/CD8+ ratio (r = 0.72; p = 0.0001), but not IgM (r = 0.25; N.S.) and platelets (r = 0.07; N.S.), are dependent variables of shortened survival.

[Chronic hepatitis C in patients with HIV/HCV coinfection with high CD4+ lymphocytes count].

analysis of data characterizing HCV infection in patients infected with HIV. 37 persons (29 male and 8 female) aged 23-49 years (mediana 34), with HIV/HCV coinfection, treated (n=25) and untreated (n=12) with antiretroviral therapy. HAART was effective in treated patients; CD4+ count >350 cells/microl. Viral load of HIV and HCV, HCV genotypes, CD4/CD8, biochemical tests, histopathological examination were measured. Results were analyzed statistically. the majority of patients were former IVDUs (n=31.84%), 3 persons (8%)--MSM, 3 (8%)--route of infection unknown. Duration of HCV infection 1-10 years, mediana 5. All patients were in A1 or A2 stage of HIV infection. Among patients treated with HAART (n=25) mediana of CD4+ count before treatment was 263 (69-595) cells/micro, mediana of HIV viral load 75000 copies/ml (n=7); 2040-263414 copies/ml. 17 patients were currently treated with PI, 17 with NNRTI, and 2 patients with NRTI only. HCV genotype was determined in 32 patients: 3a--n=19 (59%), 1--n= 9 (28%) 4--n=4 (13%). HCV viral load: 2.4 x 10(5)-7.73 x 10(6) IU/ml, mediana 1.6 x 10(6). Levels of ALT: 21-358 IU/ml, mediana 102, AST: 20-195 IU/ml, mediana 62, GGTP--9-463 IU/ml, mediana 58. ALT level was significantly higher in HCV genotype 3a infection (p=0.0214). Fibrosis stage above 2 was revealed in 3 patients and in majority (62%) was below 2. None patient had liver cirrhosis. Fibrosis was significantly higher in patients with low CD4+ nadir (p=0.03). Progression of liver fibrosis is slow in patients coinfected with HIV/HCV with high CD4+ count. High percentage of HCV genotype 3 and mild fibrosis are good prognostic factors for effectiveness of HCV infection treatment in HIV infected persons.

Burkitt's lymphoma nodular cystic hepatosplenic, in HIV patient. Case report

Patients with human immunodeficiency virus (HIV) are more likely to develop cancer. Malignant lymphomas are the main cancer group seen in these patients. Diffuse large B-cell lymphoma including central nervous system lymphoma and Burkitt's lymphoma account for 90% of HIV-related non-Hodgkin's lymphomas. A 22-year-old man with fever up to 39 ° C, malaise, excessive tiredness and night sweats, loss of 8 kg of weight, abdominal pain in the right hypochondrium, all 5 months before hospitalization. Hemoglobin: 9.5 g/dL, leukocytes 5.13 x 103/mm3, platelets 124 000 cel/mm3; albumin 2.9 g/dL, alanine aminotransferase 28 IU/L, aspartate aminotransferase 105 IU/L; HIV reactive, beta 2 microglobulin: 20 000 ng/mL. Viral load for HIV 100 034 cp/mL, CD4: 76 cel/mcL (5%). It was performed abdominal ultrasound and denoted cysts in the liver and spleen. Abdominal-pelvic computed tomography with hepatosplenomegaly, retroperitoneal and inguinal adenopathies and free fluid in abdominal cavity. Splenectomy was performed and Burkitt's lymphoma was reported in the histopathological study. HIV predisposes patients to any type of cancer. Intra-abdominal findings should be a warning of lymphoma suspicious and may occur from infiltration of the small intestine, solid organ and soft tissues.

[A pediatric case of HIV who diagnosed by virtue of disseminated cryptococcus infection].

Cryptococcus neoformans is an important opportunistic pathogen that causes serious mortality and morbidity in AIDS patients. Although its incidence has decreased with proper antiretroviral treatment (ART), it is still a major concern in areas with low socioeconomic HIV endemic countries with poor sources of therapy. In our country, pediatric HIV infection and so, HIV-related opportunistic infections are very rare. In order to pay attention to this unusual collaboration; herein, we presented a pediatric case who was diagnosed with HIV and disseminated cryptococcus infection concomitantly. A 6.5-year-old previously healthy girl has admitted to our hospital with the complaints of prolonged fever, cough and hemoptysis. On her physical examination she had oral candidiasis, generalized lymphadenopathy and hepatosplenomegaly. Laboratory findings were as follows; white blood cell count: 3170 µL (neutrophil: 2720 µL, lymphocyte: 366 µL), hemoglobin level: 7.8 gr/dl, hematocrit: 25.5% platelets: 170.000 µL, CRP: 15.2 mg/L and serum IgG level: 1865 mg/dl. Her anti-HIV test yielde,d positive result and confirmed by Western blot assay, together with a high viral load (HIV-RNA: 3.442.000 copies/ml). She was started ART (lamivudine, zidovudine and lopinavir/ritonavir combination) with the diagnosis of stage 3 HIV infection (AIDS). Posteroanterior chest radiograph showed mediastinal extension and nodular parenchyma. Since the patient was suspected to have pulmonary tuberculosis based on the clinical and radiological findings, empirical antituberculosis therapy was started. Because of the insistance of fever, three different blood specimens, bone marrow and gastric aspirates were collected for culture, in which all of them yielded C.neoformans growth. She was then diagnosed as disseminated cryptococcosis and treated with liposomal amphotericin B and fluconazole successfully. Although pediatric HIV infection is usually diagnosed secondary to maternal disease, it can rarely be presented later in life with opportunistic infections. In the case of unusual infectious diseases, in addition to primary immune deficiency syndromes, HIV infection should also be kept in mind. Herein, we discussed a pediatric case with two rare infectious agents reported in our country and wanted to focus on secondary immune deficiency related with pediatric HIV infection.