Lymphocytic Interstitial Pneumonitis Research Articles

Histophatological Damage to Heart and Lungs on Canine Dirofilariosis in Panama

Latin America and countries with hot climates have long suffered with vector-borne diseases, be they fleas, mosquitoes or ticks, among others. Canine Dirofilariasis is a vector disease whose etiological agent in America is Dirofilaria immitis, however, with little information on its real damage to canines and no information on its pathogenesis in humans in this country. Five anatomical pieces made up of heart and lungs, preserved in 10% formaldehyde, were evaluated histopathologically to define the damage caused by the nematode. The most common lesion found in the lungs was pulmonary emphysema and lymphocytic interstitial pneumonitis. Pseudo papillary hyperplasia of the endothelium was observed in one of the cases. The most common lesions found in the heart were endocarditis and pericarditis. We can conclude that the damage caused by D. immitis to the heart and lungs tissues of dogs is evident and that further studies are necessary to better understand this disease.

Interstitial Lung Disease in Immunocompromised Children.

The range of pulmonary complications beyond infections in pediatric immunocompromised patients is broad but not well characterized. Our goal was to assess the spectrum of disorders with a focus on interstitial lung diseases (ILD) in immunodeficient patients. We reviewed 217 immunocompromised children attending a specialized pneumology service during a period of 23 years. We assigned molecular diagnoses where possible and categorized the underlying immunological conditions into inborn errors of immunity or secondary immunodeficiencies according to the IUIS and the pulmonary conditions according to the chILD-EU classification system. Among a wide array of conditions, opportunistic and chronic infections were the most frequent. ILD had a 40% prevalence. Of these children, 89% had a CT available, and 66% had a lung biopsy, which supported the diagnosis of ILD in 95% of cases. Histology was often lymphocyte predominant with the histo-pattern of granulomatous and lymphocytic interstitial lung disease (GLILD), follicular bronchiolitis or lymphocytic interstitial pneumonitis. Of interest, DIP, PAP and NSIP were also diagnosed. ILD was detected in several immunological disorders not yet associated with ILD. Specialized pneumological expertise is necessary to manage the full spectrum of respiratory complications in pediatric immunocompromised patients.

CYSTIC LUNG DISEASE IN A YOUNG MALE WITH SYSTEMIC LUPUS ERYTHEMATOSUS

CYSTIC LUNG DISEASE IN A YOUNG MALE WITH SYSTEMIC LUPUS ERYTHEMATOSUS

O25 Catastrophic antiphospholipid crisis triggered by anticoagulant switch

O25 Catastrophic antiphospholipid crisis triggered by anticoagulant switch

Early onset acute lymphocytic interstitial pneumonitis (ALIP) in COVID-19 pathophysiology: preliminary lung autopsy findings

Sri Lanka Journal of Medicine is the official journal of the Kandy Society of Medicine. It is a peer-reviewed journal currently published biannually. Original articles, reviews, brief reports, case reports, points of view, and letters to the editor, in all fields of medical science and practice are accepted for publication.The Sri Lanka Journal of Medicine is now indexed in DOAJ

Opportunistic Illnesses in Children With HIV Infection in the United States, 1997-2016.

Among children with HIV infection, opportunistic illness (OI) rates decreased after introduction of highly active antiretroviral therapy (ART) in 1997. We evaluated whether such decreases have continued. Data from the Centers for Disease Control and Prevention's National HIV Surveillance System for children with HIV living in the US during 1997-2016 was used to enumerate infants experiencing the first OI by birth year and OIs among all children <13 years of age (stratified by natality). We calculated the time to first OI among infants using Kaplan-Meier methods. Among infants born during 1997-2016, 711 first OIs were diagnosed. The percentage of the first OIs diagnosed in successive 5-year birth periods was: 60.0% (1997-2001), 24.6% (2002-2006), 11.3% (2007-2011), and 3.4% (2012-2016). For every OI, the number of first cases decreased nearly annually. Time to first OI increased in successive birth periods. Among children <13 years of age, 2083 OI were diagnosed, including Pneumocystis jiroveci pneumonia, candidiasis, recurrent bacterial infection, wasting syndrome, cytomegalovirus, lymphocytic interstitial pneumonitis, tuberculosis, nontuberculous mycobacteriosis and herpes simplex virus. The rate (#/1000 person-years) decreased overall (60-7.2) and for all individual OIs. Earlier during 1997-2016, rates for all OIs were higher among foreign-born than US-born children but later became similar for all OIs except tuberculosis. Among children with HIV in the US, numbers and rates of all OIs decreased during 1997-2016. Earlier, OI rates were highest among non-US-born children but were later comparable with those among US-born children for all OIs except tuberculosis.

EP33 Sjögren’s and lymphoproliferative disorders

Case report - IntroductionSjögren’s syndrome (SS) is a chronic autoimmune inflammatory condition characterised by lymphocytic infiltration of predominantly exocrine glands as well as other organs involving more commonly in skin, lungs, and neurological system. It is associated with increased risk of both benign and malignant lymphoproliferative disorders.Case report - Case descriptionA 29-year-old woman with 5-year history of Primary SS (ANA, Ro/La positive) was reviewed in a routine follow up. She has mild dry eyes, intermittent vasculitic rash around the ankles, occasional pleuritic chest pain but no cough or dyspnoea initially. She used artificial tears but took no regular mediations. Oxygen saturation at rest was 99% and BP 127/70. Heart sounds were normal, and chest was clear.Blood results showed alanine transaminase (ALT) had risen from 50 (normal 5-45) to 145 over 6 months. Viral screen (hepatitis, HIV, CMV, EBV) and liver ANA panel were negative. C4 was low 0.09 (n 0.15-0.55), C3 normal and DsDNA antibodies 1 (n 0-15.1). Ig G was high, fluctuating between 27 - 33 (n 7.67-15.9). ESR had been mildly elevated at 26 (n 0-19). CRP had always been within normal limits. Ultrasound abdomen showed enlarged spleen (15 cm). CT chest abdomen and pelvis showed multifocal groundless opacification affecting mid to upper zones, bilateral cyst formation, solid nodularity, and mild septal thickening with no pleural effusion. There were multiple prominent bilateral axillary and mediastinal lymph nodes measuring upto15 mm. The spleen measured 15.4 cm. Six months later, she developed mild dyspnoea on exertion. Examination revealed fine basal crackles. Oxygen saturation remained 99% at rest. TLco was mildly reduced and Kco in lower limit of normal. Echocardiogram was normal. Ultrasound guided core biopsy of axillary lymph node showed benign reactive features with follicular hyperplasia and plasmacytosis.The diagnosis of lymphocytic interstitial pneumonitis was made. She was started on a reducing dose of Prednisolone 30 mg and Mycophenolate stepwise increment to 1 gm BD. Chest pain resolved shortly after starting glucocorticoid therapy and exercise tolerance improved.Liver enzyme normalised. Case report - DiscussionThe diagnosis of lymphocytic interstitial pneumonia (LIP) in this patient was incidental from the retrospective investigation of the persistently abnormal unexplained liver function test. Splenomegaly is a recognised manifestation of active systemic SS. The main differential diagnoses are lymphoma and other types of interstitial lung diseases (ILD). Her presentation was insidious and there were no constitutional symptoms. Her ANA, Ro, La and Rheumatoid factor were strongly positive. She has hypergammaglobulinemia which is commonly associated with LIP. Histological findings were typical reactive changes with characteristic polymorphic plasmacytosis. In the absence of malignant lymphoid cells and radiological features of ground glass changes and bilateral cysts formation suggested that the most likely diagnosis was LIP secondary to primary SS.The management strategies vary for different types of ILD based on their etiological conditions. There are no specific guidelines for the treatment of LIP. For initial acute stage, glucocorticoid therapy is usually prescribed for symptomatic improvement. For later stages and cysts, immunosuppressants are used and depending on the severity, azathioprine, cyclosporin, rituximab and cyclophosphamide have been used.Median survival for LIP is 11.2 years. Increased risk of secondary infection because of immunosuppressive therapy is common and there are recommendations for atypical chest infection prophylaxis.Case report - Key learning pointsInterstitial lung disease is commonly associated with SS and predicts a higher mortality rate.Glucocorticoid is the main stay of treatment for ILD acute stage with active inflammatory changes.For refractory cases and chronic cystic stages on radiological findings, further immunosuppression therapy may be required.Standardised treatment guidelines are not available.Secondary chest infections may be seen in those with cystic disease and on immunosuppression.Close monitoring and MDT approach is required in the management of LIP.LIP may transform into lymphoma or co-present with lymphoma associated with SS.

The impact of health programmes to prevent vertical transmission of HIV. Advances, emerging health challenges and research priorities for children exposed to or living with HIV: Perspectives from South Africa.

Over the past three decades, tremendous global progress in preventing and treating paediatric HIV infection has been achieved. This paper highlights the emerging health challenges of HIV-exposed uninfected (HEU) children and the ageing population of children living with HIV (CLHIV), summarises programmatic opportunities for care, and highlights currently conducted research and remaining research priorities in high HIV-prevalence settings such as South Africa. Emerging health challenges amongst HEU children and CLHIV include preterm delivery, suboptimal growth, neurodevelopmental delay, mental health challenges, infectious disease morbidity and mortality, and acute and chronic respiratory illnesses including tuberculosis, pneumonia, bronchiectasis and lymphocytic interstitial pneumonitis. CLHIV and HEU children require three different categories of care: (i) optimal routine child health services applicable to all children; (ii) routine care currently provided to all HEU children and CLHIV, such as HIV testing or viral load monitoring, respectively, and (iii) additional care for CLHIV and HEU children who may have growth, neurodevelopmental, behavioural, cognitive or other deficits such as chronic lung disease, and require varying degrees of specialised care. However, the translation thereof into practice has been hampered by various systemic challenges, including shortages of trained healthcare staff, suboptimal use of the patient-held child's Road to Health book for screening and referral purposes, inadequate numbers and distribution of therapeutic staff, and shortages of assistive/diagnostic devices, where required. Additionally, in low-middle-income high HIV-prevalence settings, there is a lack of evidence-based solutions/models of care to optimise health amongst HEU and CLHIV. Current research priorities include understanding the mechanisms of preterm birth in women living with HIV to optimise preventive interventions; establishing pregnancy pharmacovigilance systems to understand the short-, medium- and long-term impact of in utero ART and HIV exposure; understanding the role of preconception maternal ART on HEU child infectious morbidity and long-term growth and neurodevelopmental trajectories in HEU children and CLHIV, understanding mental health outcomes and support required in HEU children and CLHIV through childhood and adolescence; monitoring HEU child morbidity and mortality compared with HIV-unexposed children; monitoring outcomes of CLHIV who initiated ART very early in life, sometimes with suboptimal ART regimens owing to medication formulation and registration issues; and testing sustainable models of care for HEU children and CLHIV including later reproductive care and support.

28. Acute pulmonary arterial hypertension in primary Sjögren’s syndrome with known cryptogenic organising pneumonia

28. Acute pulmonary arterial hypertension in primary Sjögren’s syndrome with known cryptogenic organising pneumonia

Diagnostic challenge between placental transmogrification and low-grade endometrial stromal sarcoma metastases in a patient with cavitary pulmonary nodules

Cystic lung lesions have limited differential diagnosis, which includes pulmonary Langerhans cell histiocytosis (LCH), lymphangioleiomyomatosis (LAM), lymphocytic interstitial pneumonitis (LIP), tracheobronchial papillomatosis, and Birt-Hogg-Dube syndrome. However, a few rare entities such as pulmonary placental transmogrification (PPT) and metastatic endometrial stromal cell sarcoma (ESS) also can present as cystic lung lesions and pose diagnostic challenges to both radiologists and pathologists. Clinical history is the key in such situations. Since the first description in the literature of these both entities, there have been very few cases reported. We present our case in a middle-aged female who was known to have cystic lung disease but treated as LAM and had a recurrent pneumothorax. Surgical pathology ruled out LAM and other interstitial cystic lung diseases and provided a diagnosis of PPT on wedge resection. Subsequent recurrence of cystic lung nodules led to the re-examination of histopathology and immunohistochemistry, concluding a diagnosis of metastasis from remote but undiagnosed low-grade stromal cell sarcoma. We will discuss the clinical, imaging and pathologic features of both of the diagnoses in this report. Institutional review board approval was not required since it was a single patient report.

P69: BIOLOGIC THERAPY‐INDUCED PSORIASIS: AN ILLUSTRATIVE CASE

Introduction Psoriasis is a T‐cell driven, chronic inflammatory skin disease. In recent literature, biologics and small molecule therapies have been reported to induce psoriasis de novo, including tumour necrosis factor inhibitors, rituximab, abatacept and anti‐programmed cell death 1 inhibitors. Case A 52‐year‐old female was diagnosed with lung biopsy‐confirmed lymphocytic interstitial pneumonitis in 2012, after Sjogren's syndrome was diagnosed in 2011. Therapies trialled to halt her decline in respiratory function included cyclosporine, cyclophosphamide, mycophenolate, belimumab, tacrolimus, abatacept and rituximab. In February 2018 dry, scaly, hyperkeratotic plaques developed on her hands, extensor surfaces of her elbows and neck. She was diagnosed clinically with psoriasis. She had no personal or family history of psoriasis. Her psoriasis was suspected to be drug‐induced, and responded to standard topical therapies. Discussion Psoriasis is driven by T‐cell‐mediated cytokine production, resulting in proliferation of keratinocytes and angiogenesis. Activation of the T‐helper 1 (Th1) axis and abnormalities of T‐helper 17 (Th17) and T‐regulatory cell (Treg) balance are characteristic. Biologic‐induced psoriasis is a more recently described phenomenon. Onset of psoriasis from medication initiation varies, has varied morphology, and may persist after drug discontinuation. Cases of abatacept and rituximab‐induced psoriasis have been reported. Abatacept downregulates T‐cell proliferation, and may interfere with CTLA‐4 signalling in Tregs, resulting in exacerbated Th17 immunity and initiation of a pro‐inflammatory feedback loop. B‐cell depletion from rituximab leading to psoriasis suggests B‐cell regulation of T‐cells plays an unknown role in pathogenesis of psoriasis. Abatacept and rituximab may have induced psoriasis in our patient, with onset two and three years after initiation of these therapies, respectively. Conclusion Biologic‐induced psoriasis is increasingly reported, but mechanisms are not well understood. Onset from initiation of medication varies, with diverse morphology. This case illustrates how biologics can inadvertently cause adverse effects through T‐cell dysregulation, manifesting as psoriasis in this instance.

Cystic Lung Disease from Protein Deposition: Pathogenesis and Associated Conditions

We explicate the development of cystic lung disease from the deposition of protein in the lung. The protein may be in the form of amyloid or non-amyloid (typically immunoglobulin-associated light chains) and is usually seen in the context of three entities: idiopathic light-chain deposition disease, Sjogren’s syndrome, and clonal lymphoplasmacytic proliferative disorders. A commonly observed and distinctive feature of the circumscribed cystic spaces is the presence of internal tissue septations. The traditional causal association of lung cysts and the pathologic entity of lymphocytic interstitial pneumonitis is untenable. Instead, the development of cysts as a consequence of the degradation of lung extracellular matrix by metalloproteinases, the process initiated with the accumulation of macrophages around deposited protein, is a compelling alternative explanation. Lung cysts may be a consequence of parenchymal protein deposition. When internal septations are present, this particular pathogenesis should explicitly be considered, and the presence of associated clinical disorders further pursued.

Incidental Finding to Diagnostic Dilemma

SESSION TITLE: Pulmonary Manifestations of Systemic Disease 2 SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Lymphocytic Interstitial Pneumonitis (LIP) is a common manifestation of lung disease associated with Sjogren’s disease. We present a case fraught with diagnostic challenges. CASE PRESENTATION: A 59 year old man with history of Sjogren’s syndrome and asthma was referred to pulmonology after incidental X-ray finding of right lower lobe infiltrate. Review of systems revealed dry eyes, dry cough and dyspnea on exertion. He had a 25 pack-year smoking history. Medications were notable for saline eye drops and Albuterol inhaler. Physical examination revealed temperature 37 degrees Celsius; blood pressure 145/77; pulse 61; oxygen saturation 96% on room air. He was obese, with no lymphadenopathy and chest clear to auscultation. Initial Lab work was unremarkable. Serology was positive for antinuclear antibodies (ANA), anti Anti-Sjögren’s- syndrome-related antigen A and antigen B (SSa/SSb) antibodies. Pulmonary function tests revealed a mildly restrictive pattern. Initial CT scan showed right upper lobe infiltrate which worsened on 3 month follow up CT. Bronchoscopy with bronchoalveolar lavage (BAL) showed normal cell count and cytology, cultures grew beta streptococcus group B. After 2 weeks of antibiotics he developed night sweats and dyspnea on mild exertion. A third CT scan demonstrated dense right lower lobe consolidation, bilateral ground-glass opacities and enlarged sub-pleural nodules. Repeat BAL grew Cryptococcus. He received 7 weeks of fluconazole without improvement. Needle biopsy for sub-pleural nodule revealed multiple dense lymphoplasmacytic infiltrates. Ultimately, wedge biopsy confirmed dense lymphoplasmacytic infiltrate, lymphoid follicles, intra-alveolar macrophages and histiocytes. B-cell polyclonality was confirmed by PCR. He was diagnosed with focal lymphoid hyperplasia and lymphocytic interstitial pneumonia. Treatment with corticosteroids yielded transient resolution. Dramatic resolution was achieved with Rituximab (with azathioprine for maintenance). DISCUSSION: The pathogenesis of LIP is thought to be abnormal proliferation of indigenous cell lines and lung parenchymal infiltration with lymphoid cells. It may be a focal or diffuse, benign (monoclonal) or potentially malignant (polyclonal). It is most commonly seen in women in their 50s and is associated with autoimmune disease. Frequently, LIP presents with cough, chest pain and hemoptysis. There may be a restrictive ventilatory defect on PFTs. Imaging is variable and a lung biopsy required for diagnosis. CONCLUSIONS: Timely recognition of LIP prevents misdiagnosis. Treatment usually is with high dose corticosteroids. Alternative to steroid use may be immunosuppressant agents such as rituximab and azathioprine, however literature to support use of such agents is limited to case reports. Reference #1: Lymphocytic Interstitial Pneumonia, Tanmay S. Panchabhai MD, Carol Farver MD, Kristin B. Highland MD, MSCR Clinics in Chest Medicine, 2016-09-01 DISCLOSURE: The following authors have nothing to disclose: Reema Qureshi, Saira Imran No Product/Research Disclosure Information

International, evidence-based consensus diagnostic criteria for HHV-8–negative/idiopathic multicentric Castleman disease

AbstractHuman herpesvirus-8 (HHV-8)–negative, idiopathic multicentric Castleman disease (iMCD) is a rare and life-threatening disorder involving systemic inflammatory symptoms, polyclonal lymphoproliferation, cytopenias, and multiple organ system dysfunction caused by a cytokine storm often including interleukin-6. iMCD accounts for one third to one half of all cases of MCD and can occur in individuals of any age. Accurate diagnosis is challenging, because no standard diagnostic criteria or diagnostic biomarkers currently exist, and there is significant overlap with malignant, autoimmune, and infectious disorders. An international working group comprising 34 pediatric and adult pathology and clinical experts in iMCD and related disorders from 8 countries, including 2 physicians that are also iMCD patients, was convened to establish iMCD diagnostic criteria. The working group reviewed data from 244 cases, met twice, and refined criteria over 15 months (June 2015 to September 2016). The proposed consensus criteria require both Major Criteria (characteristic lymph node histopathology and multicentric lymphadenopathy), at least 2 of 11 Minor Criteria with at least 1 laboratory abnormality, and exclusion of infectious, malignant, and autoimmune disorders that can mimic iMCD. Characteristic histopathologic features may include a constellation of regressed or hyperplastic germinal centers, follicular dendritic cell prominence, hypervascularization, and polytypic plasmacytosis. Laboratory and clinical Minor Criteria include elevated C-reactive protein or erythrocyte sedimentation rate, anemia, thrombocytopenia or thrombocytosis, hypoalbuminemia, renal dysfunction or proteinuria, polyclonal hypergammaglobulinemia, constitutional symptoms, hepatosplenomegaly, effusions or edema, eruptive cherry hemangiomatosis or violaceous papules, and lymphocytic interstitial pneumonitis. iMCD consensus diagnostic criteria will facilitate consistent diagnosis, appropriate treatment, and collaborative research.

Bronchiectasis and other chronic lung diseases in adolescents living with HIV.

The incidence of pulmonary infections has declined dramatically with improved access to antiretroviral therapy (ART) and cotrimoxazole prophylaxis, but chronic lung disease (CLD) is an increasingly recognized but poorly understood complication in adolescents with perinatally acquired HIV. There is a high prevalence of chronic respiratory symptoms, abnormal spirometry and chest radiographic abnormalities among HIV-infected adolescents in sub-Saharan Africa, wherein 90% of the world's HIV-infected children live. The incidence of lymphocytic interstitial pneumonitis, the most common cause of CLD in the pre-ART era, has declined with increased ART access. Small airways disease, particularly constrictive obliterative bronchiolitis and bronchiectasis, are emerging as leading causes of CLD among HIV-infected adolescents in low-income and middle-income countries. Asthma may be more common in high-income settings. Likely risk factors for CLD include recurrent pulmonary infections, air pollution, HIV-related immune dysfunction, and untreated HIV infection, particularly during critical stages of lung development. Globally, the importance of HIV-associated CLD as a cause of morbidity and mortality is increasing, especially as survival has improved dramatically with ART and growing numbers of children living with HIV enter adolescence. Further research is urgently needed to elucidate the natural history and pathogenesis of CLD, and to determine optimal screening, diagnostic and treatment strategies.

Sjögren Syndrome: Why Do Clinical Trials Fail?

Sjögren syndrome (SS) comprises glandular and extraglandular manifestations. Double-blind prospective trials of traditional disease-modifying antirheumatic drugs and biologics have failed because they have not improved benign symptoms, the major cause of lowered quality of life. Rituximab has proven effective in SS patients with associated mixed cryoglobulinemia, parotid gland swelling, lymphocytic interstitial pneumonitis, thrombocytopenia, and other manifestations. There were few of these SS patients in the trials required for FDA approval. Most patients had benign symptoms and did not show benefit, leading to failure of the study. This article examines the reasons for these failures and proposes future directions.

Pulmonary manifestations of Sjögren's syndrome.

In 9-20% of cases, Sjögren's syndrome is associated with various respiratory symptoms. The most typical manifestations are chronic interstitial lung disease (ILD) and tracheobronchial disease. The most common manifestation of ILD is nonspecific interstitial pneumonia in its fibrosing variant. Other types of ILD, such as organising pneumonia, usual interstitial pneumonia and lymphocytic interstitial pneumonitis, are rare. Their radiological presentation is less distinctive, and definitive diagnosis may require the use of transbronchial or surgical lung biopsy. Corticosteroid therapy is the mainstay of ILD treatment in Sjögren's syndrome, but the use of other immunosuppressive drugs needs to be determined. ILD is a significant cause of death in Sjögren's syndrome. Tracheobronchial disease is common in Sjögren's syndrome, characterised by diffuse lymphocytic infiltration of the airway. It is sometimes responsible for a crippling chronic cough. It can also present in the form of bronchial hyperresponsiveness, bronchiectasis, bronchiolitis or recurrent respiratory infections. The management of these manifestations may require treatment for dryness and/or inflammation of the airways. Airway disease has little effect on respiratory function and is rarely the cause of death in Sjögren's syndrome patients. Rare respiratory complications such as amyloidosis, lymphoma or pulmonary hypertension should not be disregarded in Sjögren's syndrome patients.

Lymphocytic Interstitial Pneumonitis: An Unusual Presentation of X-Linked Hyper Ig M Syndrome.

Lymphocytic Interstitial Pneumonitis: An Unusual Presentation of X-Linked Hyper Ig M Syndrome.

Clinical features and lung function in HIV-infected children with chronic lung disease

Background. Although chronic lung disease (CLD) is commonly seen in children with advanced HIV disease, it is poorly studied. Objectives. To report on the clinical manifestations and lung function tests in children with advanced HIV disease at a tertiary care centre, and determine clinical predictors of poor lung function. Methods. We undertook a cross-sectional study of children with advanced HIV disease in whom CLD was suspected. We undertook clinical evaluation and lung function tests, accompanied by a retrospective chart review. Results. In 56 children identified, the median age was 5 (interquartile range (IQR) 2 - 8) years with equal gender ratio. The majority (93%) had been previously treated for tuberculosis and/or pneumonia (71%). The most common CLD identified was lymphocytic interstitial pneumonitis (54%). The median nadir CD4 percentage was 13% (IQR 8.5 - 16%) and the median highest reported viral load was log5.8 (IQR log5.0 - log6.5). The median duration of antiretroviral therapy was 9.8 (IQR 1.1 - 19.5) months. Lung function tests were performed in 27 (48%) children. The median forced expiratory volume in 1 second (FEV 1 ) was 60% (IQR 45.3 - 86.3%) predicted. Previous hospitalisation, respiratory rate, digital clubbing, chest hyperinflation and hyperpigmented skin lesions were associated with a decreased FEV 1 in a univariate relationship. In a multiple linear regression analysis, hyperinflation, increased respiratory rate and hyperpigmented skin lesions were associated with poor lung function (percentage FEV 1 ). Conclusion. We identified useful clinical signs predictive of poor lung function in HIV-infected children with CLD, especially in resource-limited settings.

HIV associated Lymphocytic Interstitial Pneumonia: a clinical, histological and radiographic study from an HIV endemic resource-poor setting.

BackgroundThere is a paucity of clinical and histopathological data about HIV-associated lymphocytic interstitial pneumonitis (LIP) in adults from HIV endemic settings. The role of Ebstein-Barr virus (EBV) in the pathogenesis remains unclear.MethodsWe reviewed the clinical, radiographic and histopathological features of suspected adult LIP cases at the Groote Schuur Hospital, Cape Town South Africa, over a 6 year period. Archived tissue sections were stained for CD3, CD4, CD8, CD20 and LMP-1 antigen (an EBV marker).Results42 cases of suspected LIP(100% HIV-infected) were identified. 75% of patients were empirically treated for TB prior to being referred to the chest service for further investigation. Tissue samples were obtained using trans-bronchial biopsy. 13/42 were classified as definite LIP (lymphocytic infiltrate with no alternative diagnosis), 19/42 probable LIP (lymphocytic infiltrate but evidence of anthracosis or fibrosis) and 10 as non-LIP (alternative histological diagnosis). Those with definite LIP were predominantly young females (85%) with a median CD4 count of 194 (IQR 119–359). Clinical or radiological features had poor predictive value for LIP. Histologically, the lymphocytic infiltrate comprised mainly B cells and CD8 T cells. The frequency of positive EBV LMP-1 antigen staining was similar in definite and non- LIP patients [(2/13 (15%) vs. 3/10 (30%); p = 0.52].ConclusionsIn a HIV endemic setting adult HIV-associated LIP occurs predominantly in young women. The diagnosis can often be made on transbronchial biopsy and is characterized by a predominant CD8 T cell infiltrate. No association with EBV antigen was found.