Surgical management of extensive hypertrophic scarring of the halluces secondary to a decade of untreated onychocryptosis: An illustrative case report

Extensive hypertrophic scarring of the halluces secondary to chronic onychocryptosis is a rare condition, which causes significant physical and psychosocial effects. In this case, a 31-year-old male developed large lesions on both great toes after he delayed treatment of chronic hallucal onychocryptosis for over a decade. Current treatment options for hypertrophic and keloid lesions in the foot and ankle vary considerably and differentiation is critical for appropriate treatment planning. In this case, surgical excision with total matrixectomy (modified Zadik–Syme) was considered optimal management. Histopathology testing confirmed the diagnosis of irritated hypertrophic scar secondary to onychocryptosis. The patient was monitored closely and at 3 months post-operatively, the incisional scars exhibited progressive maturation, and there was no recurrence of the lesions and no nail regrowth. Furthermore, the halluces were only marginally shorter providing good function and cosmesis. At the long-term follow-up consultation (5.5 years), the patient indicated complete satisfaction and had returned to regular footwear and social activities. Chronic onychocryptosis can trigger and facilitate proliferation of large benign keloid-like fibrous lesions; excision with total matrixectomy can provide an excellent long-term outcome

Hospital service utilisation of people previously hospitalised with different subtypes of psychotic disorder: A record linkage study

Objective: Little research has examined the physical and mental comorbidities, and health service use patterns, of people diagnosed with psychotic disorder subtypes other than schizophrenia spectrum disorders. This study aims to examine the physical and mental comorbidities, and subsequent hospital service use patterns, of individuals previously hospitalised with various psychotic disorder subtypes using linked health service data. Methods: We included individuals hospitalised with a psychotic disorder in New South Wales, Australia, between 1 July 2002 and 31 December 2014 (N = 63,110). We examined the demographic profile of the cohort and rates of subsequent acute hospital care and ambulatory mental health service use. We compared the rates of subsequent hospital admissions, emergency department presentations and ambulatory mental health treatment days of people hospitalised with different psychotic disorder subtypes to people hospitalised with schizophrenia spectrum disorders using Poisson regression. Results: People most recently hospitalised with mood/affective disorders and psychotic symptoms had a higher rate of subsequent hospital admissions than those most recently hospitalised with schizophrenia spectrum and delusional disorders (adjusted incident rate ratio = 1.06; 95% confidence interval = [1.02, 1.10]), while people most recently hospitalised with drug-induced and other organic (adjusted incident rate ratio = 1.19; 95% confidence interval = [1.12, 1.27]) and acute psychotic disorders (adjusted incident rate ratio = 1.10; 95% confidence interval = [1.03, 1.18]) had more subsequent emergency department presentations than those most recently hospitalised with schizophrenia spectrum and delusional disorders. All three groups had fewer subsequent mental health ambulatory days than those most recently hospitalised with schizophrenia spectrum and delusional disorders (adjusted incident rate ratios = 0.85–0.91). Conclusion: The health profiles and subsequent hospital service use patterns of people previously hospitalised with different psychotic disorder subtypes are heterogeneous, and research is needed to develop targeted health policies to meet their specific health needs

The health service contact patterns of people with psychotic and non-psychotic forms of severe mental illness in New South Wales, Australia: A record-linkage study

Objective: To describe and compare the health profiles and health service use of people hospitalised with severe mental illness, with and without psychotic symptoms. Methods: We conducted a historical cohort study using linked administrative datasets, including data on public hospital admissions, emergency department presentations and ambulatory mental health service contacts in New South Wales, Australia. The study cohort comprised 169,306 individuals aged 12 years and over who were hospitalised at least once with a mental health diagnosis between 1 July 2002 and 31 December 2014. Of these, 63,110 had a recorded psychotic illness and 106,196 did not. Outcome measures were rates of hospital, emergency department and mental health ambulatory service utilisation, analysed using Poisson regression. Results: People with psychotic illnesses had higher rates of hospital admission (adjusted incidence rate ratio (IRR) 1.26; 95% confidence interval [1.23, 1.30]), emergency department presentation (adjusted IRR 1.17; 95% confidence interval [1.13, 1.20]) and ambulatory mental health treatment days (adjusted IRR 2.90; 95% confidence interval [2.82, 2.98]) than people without psychotic illnesses. The higher rate of hospitalisation among people with psychotic illnesses was driven by mental health admissions; while people with psychosis had over twice the rate of mental health admissions, people with other severe mental illnesses without psychosis (e.g. mood/affective, anxiety and personality disorders) had higher rates of physical health admissions, including for circulatory, musculoskeletal, genitourinary and respiratory disorders. Factors that predicted greater health service utilisation included psychosis, intellectual disability, greater medical comorbidity and previous hospitalisation. Conclusion: Findings from this study support the need for (a) the development of processes to support the physical health of people with severe mental illness, including those without psychosis; (b) a focus in mental health policy and service provision on people with complex support needs, and (c) improved implementation and testing of integrated models of care to improve health outcomes for all people experiencing severe mental illness

Association Of Large Granular Lymphocytic Leukemia (LGL) With B-Cell Lymphoproliferative Disorders

Abstract Introduction Large granular lymphocytic (LGL) leukemia is an uncommon disease, characterized by a clonal proliferation of mature, post-thymic T-cells, typically CD3+, CD4-, CD8+, CD16+, CD57+ phenotype, representing constitutively active T-cells Less commonly, LGL leukemia is derived from CD3-, CD56+ natural killer (NK) cells. Clonal T-LGLs escape apoptosis by failure to respond to the Fas/Fas ligand (FasL) pathway. Activating mutations in the STAT3gene occur frequently in LGL leukemia, and may play a role in pathogenesis. Autoimmune disorders are frequently associated with LGL leukemia (∼1/3 present with rheumatoid arthritis). The association between LGL leukemia and B-cell lymphoproliferative disorders has been reported, often with low-grade histologies, but is deemed uncommon and the pathogenesis is not well established. We have analyzed a series of patients (pts) diagnosed with both LGL leukemia or expansion and clonal B-cell disorders. Patients and methods Pts with NK or T-LGL leukemia or expansion who were evaluated at Fox Chase Cancer Center or the Cleveland Clinic Taussig Cancer Institute were reviewed, after Institutional Review Board approval. Inclusion criteria were age ≥ 18 yrs and diagnosis of both LGL and B-cell lymphoproliferative disorder. Results One hundred and twenty six pts with a diagnosis of T-LGL leukemia, NK-LGL leukemia or T-LGL expansion were identified. Of these, 44 (34.9%) pts were diagnosed with a clonal B-cell disorder. Twenty-six pts (20.6%) were diagnosed with a clonal B-cell disorder concomitantly with or shortly after the LGL diagnosis, 15 of whom presented with monoclonal gammopathy of unknown significance (MGUS) as their B-cell disorder, 9 with monoclonal B-cell lymphocytosis (MBL), 5 of whom also had monoclonal gammopathy. Eighteen pts (14.2%) had a previous diagnosis of clonal B-cell disorder, including diffuse large B cell lymphoma (DLBCL) (N= 6), CLL (N = 3), mantle cell lymphoma (N=3), multiple myeloma (N = 2), Hodgkin lymphoma (N = 2), Burkitt lymphoma (N = 1) and hairy cell leukemia (N = 1). Fifteen pts (11.9%) received treatment prior to the diagnosis of LGL, 10 of them (7.9%) with regimens including rituximab. The median time from completion of last treatment with rituximab to diagnosis of LGL disorder was 33 months. An additional patient with prior DLBCL was diagnosed with LGL shortly after receiving an oral SYK inhibitor. Two illustrative patients had unexpectedly prolonged remissions of their B cell disorder. A 66 years old man with multiple myeloma who achieved complete remission (CR) after 8 months of bortezomib therapy was then diagnosed with T-LGL, and his myeloma is in ongoing remission now 5 years after T-LGL diagnosis without further therapy. A 66 years old woman with relapsed DLBCL treated with 2ndline immunochemotherapy (R-ICE) for 3 cycles developed lymphocytosis and was diagnosed with T-LGL. With no further therapy, DLBCL is in ongoing remission now 5 years after diagnosis of T-LGL. Discussion We report a large series of patients with both clonal B-cell disorders and LGL. Where diagnosis of B-cell disorder and LGL are concurrent, we hypothesize an underlying immune dysregulation leading to both B-cell and T-cell proliferations. Where B-cell disorder precedes LGL, we hypothesize that the underlying disease and/or its treatment creates the environment for LGL, either directly allowing LGL expansion or permitting persistence of antigens that drive LGL expansion. Most pts with antecedent B lymphoma received rituximab (R), with a median time from R-treatment to LGL diagnosis of 33 months. Late onset neutropenia (LON) has been linked to bone marrow expansion of LGL in patients treated with rituximab, suggesting a possible pathogenetic role in our cases as well. Further, in some pts primary B-cell malignancies unexpectedly entered prolonged remission after T-LGL developed, suggesting a possible anti-B cell immune component of LGL. Further studies are warranted. Disclosures: No relevant conflicts of interest to declare