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• W2008379144 abstract "Disseminated Mycobacterium genavense infection accounts for 4–13% of nontuberculous mycobacteria infections in patients infected with HIV [1,2]. Those with poorly controlled HIV infection and CD4+ cell counts below 100/mm3 are currently at the highest risk of acquiring this disease [3]. The clinical presentation is similar to that of infection by Mycobacterium avium complex (MAC) [4], although M. genavense has a greater affinity for the gastrointestinal tract [5]. New clinical conditions involving the gastrointestinal tract in HIV are emerging, such as retractile mesenteritis, described in 2013 [3], but there are no reports of intestinal lymphangiectasia due to M. genavense in HIV patients. Cases caused by MAC infection have been described [6,7], but they are uncommon since the introduction of highly active antiretroviral therapy (HAART) [8]. Furthermore, there are no reported cases of protein-losing enteropathy associated with nontuberculous mycobacteria infection in pediatric HIV patients. We present the case of a 13-year-old boy diagnosed with HIV infection in 2008 after consulting for persistent diarrhea, weight loss, and abdominal and mediastinal lymphadenopathy due to disseminated M. genavense infection. At the time of the diagnosis, CD4+ lymphocyte count was 1/mm3 and viral load was 47 000 copies/ml. The patient was simultaneously started on primary prophylaxis against Pneumocystis jirovecii with trimetoprim-sulfametoxazol, A antiretroviral therapy (ART) with abacavir, lamivudine, and efavirenz, and mycobacteriosis treatment with azithromycin, ethambutol, and rifabutin. At 8 months, failure of mycobacteriosis treatment was evidenced by persistent diarrhea, and treatment was changed to levofloxacin, ethambutol, rifabutin, and amikacin. This regimen was maintained for 22 months (amikacin for 10 weeks) and at completion, secondary levofloxacin prophylaxis was started, with a satisfactory clinical and radiologic response. At the same time, the patient experienced virologic failure (viral load, 8100 copies/ml) and the ART components were changed to ritonavir-boosted didanosine, zidovudine, and lopinavir, with a good response. Since the start of that regimen to the time of writing, viral load has been undetectable (<50 copies/ml) and CD4+ lymphocyte count always above 300/mm3. In September 2011, severe hypogammaglobulinemia [immunoglobulin G (IgG) 167 mg/dl, IgA 145 mg/dl, and IgM 20 mg/dl] and moderate hypoalbuminemia (2.8 g/dl) were detected on routine 3-month follow-up testing. Three months later, the patient presented facial and lower limb edema, viral load was undetectable, and CD4+ lymphocyte count was 1007/mm3. Proteinuria was ruled out, and an alfa-1-antitripsin level of 4.76 mg/g in stool samples (later confirmed) established the diagnosis of protein-losing enteropathy. Abdominal MRI showed signs consistent with intestinal lymphangiectasia: dilation of lymphatic vessels, small intestinal wall thickening, and ascites, as well as retroperitoneal and mesenteric adenopathy. Video capsule endoscopy and intestinal biopsy confirmed the diagnosis (Fig. 1). Smear microscopy findings and mycobacteria detection by molecular biology techniques were negative in biopsied tissue. Scintigraphy with 99mTc-labeled albumin showed no abnormalities. In March 2012, a low-fat diet with medium chain triglyceride supplementation and high-protein shakes was established. Periodic intravenous infusion of nonspecific serum albumin and gamma globulin was also started. Despite a progressive decrease in fecal α-1 antitrypsin values on serial monitoring (currently 1.29 mg/g), the patient continued to experience intermittent edema and gastrointestinal discomfort, whereas adherence to ART and immunovirologic control were both good.Fig. 1: Accumulations of PAS-positive histiocytes. Edematous villi with mild lymphangiectasia.We present the first reported case of intestinal lymphangiectasia due to M. genavense in a pediatric patient with HIV infection. The parallel pathogenesis and symptoms of this condition with those of MAC suggest that the mesenteric and retroperitoneal lymphadenopathy is related to chronic obstruction of lymphatic flow to the intestinal territory, which would lead to a loss of substances due to excessive pressure in the intestinal lumen [9]. Other studies have provided 99mTc-labeled albumin scintigraphy findings to support this idea [9,10], but this test yielded normal results in our patient. Management of this entity is difficult because the disruption of lymphatic vessels is currently irreversible and the treatments attempted (somatostatin analogues) have not been effective [6]. Dietary supplementation with medium chain triglyceride may attenuate the symptoms [7] because they avoid the lymphatic system, thereby reducing pressure in the lymphatic vessels. Replacement therapy by periodic infusion of nonspecific serum albumin and gamma globulin is the only option at this time [6,7,9,10]. To date, there are no data regarding a possible association of M. genavense with intestinal lymphangiectasia; hence, the approach used was extrapolated from the treatment for MAC. We believe it is important to make this association known so that suspicion will be raised when hypoproteinuria occurs in an HIV-infected pediatric patient with previous intestinal mycobacteriosis, despite resolution of this condition and good immunovirologic control. Acknowledgements Conflicts of interest There are no conflicts of interest." @default.
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• W2008379144 modified "2023-10-09" @default.
• W2008379144 title "Protein-losing enteropathy in an HIV-infected pediatric patient with previous disseminated Mycobacterium genavense infection" @default.
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