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To the Editor: Progressive disseminated histoplasmosis (PDH) of infancy occurs most commonly in previously healthy infants 1 of the genes required for perforin-dependent lymphocyte cytotoxicity; secondary HLH occurs in a person who does not have genetic risk factors (3). Both forms can be triggered by infection or malignancy (3). Diagnosis of HLH is based on clinical assessment (Table); no definitive diagnostic test exists (6). Initial treatment of HLH involves the use of corticosteroids, etoposide, or other drugs to block the hyperinflammatory response and specific therapy for the inciting infection if available (7). In some cases, in which a treatable inciting infection is identified, antimicrobial drug therapy alone might be sufficient. However, concurrent immunosuppressive therapy is usually recommended, especially for patients who are critically ill or whose condition is clinically deteriorating (3). Table Diagnostic criteria for HLH* Many clinical manifestations of disseminated histoplasmosis, including prolonged fever, hepatosplenomegaly, pancytopenia, and coagulopathy, overlap with those of HLH. Because of the similarity in manifestations, differentiating these 2 conditions is challenging without specialized testing. Furthermore, laboratory tests specific for HLH, such as measuring soluble interleukin-2 receptor, have not been investigated in patients with isolated PDH, so whether they distinguish between the 2 conditions is unclear. To add further complexity, coexisting histoplasmosis and HLH has been described in several adult patients (5,8–10). However, whether HLH identification and adjunctive immunosuppressive therapy leads to improved outcomes in this situation is unknown. On the basis of our investigation of this infant with HLH and PDH, we recommend that all infants exhibiting HLH in Histoplasma-endemic regions be assessed for histoplasmosis. In addition, the similarity with the clinical features of PDH and the difficulty in diagnosis of HLH without specialized testing raise the question of whether a large number of infants with PDH would also meet the diagnostic criteria for HLH. If so, currently poor outcomes of PDH might be related to co-existing HLH with failure to control the inflammatory response, and the outcomes could be improved by diagnosis and simultaneous treatment of both conditions. Further research is needed to investigate this phenomenon. Technical Appendix: Wright-Giemsa stain of the bone marrow biopsy specimen of a 6-month-old girl with hemophagocytic lymphohistiocytosis and progressive disseminated histoplasmosis. Click here to view.(174K, pdf)

Non-penetrating ocular injuries from badminton shuttlecocks can result in severe damage and life-long complications. This case series highlights the morbidity of such injuries, particularly in regard to post-traumatic glaucoma.This is a retrospective case series of 12 patients with shuttlecock-related blunt eye injuries sustained during badminton play without eye protection. By approaching colleagues through conference presentations and networking, the authors have attempted to gather all known cases of shuttlecock ocular injury managed in tertiary ocular emergency departments or private ophthalmological clinics in Victoria and New South Wales, Australia in 2015.This is the first multicentre case series to describe badminton-related ocular injuries in Australia. Our case series demonstrates, in particular, long-term glaucoma-related morbidity for patients over a large age range (16 to 77 years), with one patient requiring ongoing management 26 years following their initial injury. The cases reported further add to the literature promoting awareness of badminton-related ocular injury.We encourage player education and advocacy on badminton-related eye injuries and appropriate use of eye protection to reduce associated morbidity.

Background: The human kallikrein gene family has contributed the best prostatic biomarkers currently available, including prostate-specific antigen (PSA) and human glandular kallikrein 2 (hK2). Recently, new members of the human kallikrein gene family have been identified. One new member is the KLK6 gene, encoding for human kallikrein 6 (hK6), which is also known as zyme/protease M/neurosin. In this paper, we describe development of antibodies and a sensitive immunofluorometric procedure for hK6 protein. Methods: Recombinant hK6 protein was used as immunogen to develop polyclonal antibodies in rabbits and mice. These antibodies were used to develop a sandwich-type time-resolved immunofluorometric procedure for hK6. Results: The newly developed hK6 immunofluorometric assay has a detection limit of 0.5 μg/L and upper concentration range of 200 μg/L. The assay is highly specific (no detectable cross-reactivity from PSA and hK2) and was used to quantify hK6 protein in various biologic fluids. Highest concentrations of hK6 were found in milk of lactating women, cerebral spinal fluid, nipple aspirate fluid, and breast cyst fluid. hK6 was also detected in male and female serum, in the majority of seminal plasmas and in a small fraction of amniotic fluids and breast tumor cytosols. hK6 was not detectable in urine. Chromatographic studies indicated that hK6 is present in these biologic fluids in its free, 30-kDa form. Conclusions: This is the first reported sensitive immunofluorometric procedure for quantifying hK6 protein. hK6 is a secreted proteolytic enzyme that is found at high levels in cerebrospinal fluid and all breast secretions. This assay will facilitate further studies to examine the possible application of hK6 in diagnostics, including cancer and neurodegenerative disorders.