Having noted symptomatic osteoporotic vertebral collapse in young adult survivors of childhood malignancy, bone mineral density (BMD) was examined at three sites by dual‐energy X‐ray absorptiometry in 64 patients treated in childhood for intracranial malignancy (group 1; n = 21) or acute leukaemia (group 2; n = 43). Patients in group 1 were selected for growth hormone deficiency (GHD) by auxological and biochemical criteria before the end of puberty (Tanner stage V). Seven patients (six men; mean (± SEM) age at study, 28.0 ± 2.9 years; mean age at diagnosis, 8.7 ± 1.5 years) in this group had been treated with human pituitary growth hormone (GH) for 1–12 years; and 14 patients (nine men; mean age at study, 26.8 ± 1.0 years; mean age at diagnosis, 10.7 ± 1.4 years) had not received GH. Bone densities in group 1 were normal in the GH‐treated patients at the femoral neck (98.4 ± 3.8% of control), lumbar spine (100.4 ± 6.1% of control) and Ward's triangle (101.0 ± 6.1% of control) but markedly reduced in the untreated group (femoral neck, 81.2 ± 2.6% of control (p= 0.002); lumbar spine, 79.1 ± 4.1% of control (p= 0.04); Ward's triangle, 80.1 ± 3.6% of control (p= 0.01)). The majority of patients in group 2 had been treated for acute lymphoblastic leukaemia (ALL) and were in three subgroups. Fifteen (ten men; mean age at study, 22.1 ± 0.8 years; mean age at diagnosis, 5.7 ± 0.8 years) had no auxological evidence of GHD, ten (six men; mean age at study, 18.8 ± 0.7 years; mean age at diagnosis, 6.6 ± 1.2 years) received GH therapy for a mean of 2.6 years (range, 0.5–5.0 years), while 14 patients (three men; mean age at study, 20.9 ± 0.4 years; mean age at diagnosis, 5.1 ± 0.8 years) had GHD but did not receive GH. A small group of four patients (three men; mean age at study, 23.2 ± 2.1 years; mean age at diagnosis, 8.0 ± 2.3 years) who had been treated for acute myeloid leukaemia (AML) in childhood was also studied. The patients with AML had normal bone densities at all three sites (femoral neck, 106 ± 6.1% of control; lumbar spine, 96.5 ± 3.0% of control; Ward's triangle, 110.8 ± 9.3% of control), as did the patients with ALL who did not have GHD (femoral neck, 102.3 ± 2.9% of control; lumbar spine, 98.6 ± 1.7% of control; Ward's triangle, 108.3 ± 3.2% of control). The patients with ALL and GHD not treated with GH had markedly reduced BMD at all three sites (femoral neck, 90.5 ± 2.6% of control; lumbar spine, 88.4 ± 2.5% of control; Ward's triangle, 94.5 ± 3.7% of control), but those treated with GH had a BMD no different from control (femoral neck, 100.6 ± 3.3% of control; lumbar spine, 95.7 ± 4.6% of control; Ward's triangle, 106.2 ± 4.9% of control). It is concluded that GHD during childhood and adolescence predisposes to osteopenia.

A case of enteropathy associated T cell lymphoma is reported in a 45 year old woman, presenting with isolated disease in the CNS, three years after diagnosis of coeliac disease. Initial staging showed no evidence of gastrointestinal tract lymphoma. A presumptive diagnosis of T cell primary cerebral lymphoma was made and the patient was treated with combination chemotherapy and craniospinal radiotherapy. The patient relapsed, seven months after treatment, with small bowel lymphoma. The inmunophenotype and T cell receptor polymerase chain reaction analysis confirmed the same tumour as in the CNS. Retrospective polymerase chain reaction analysis of intraepithelial lymphocytes in the duodenal biopsy sample, taken at the time of diagnosis of coeliac disease, failed to show evidence of a clonal T cell proliferation. (Gut 1997; 40: 801-803) Enteropathy associated T cell lymphoma usually presents as extranodal intestinal disease. Nodal involvement with associated lesions in the lung, thyroid, skin, and Waldeyer's ring have been described. Isolated lymphoma has also been reported in the lung, thyroid, skin, and Waldeyer's ring alone.5'6We report a case of coeliac associated T cell lymphoma, presenting as isolated CNS disease mimicking primary CNS lymphoma, and the presumed course of the lymphoma based on gene rearrangement studies.Case report A 45 year old woman presented in 1992 with intermittent diarrhoea, abdominal discomfort, skin rash, and a haematological picture consistent with malabsorption. A distal duodenal biopsy specimen showed subvillous atrophy and intraepithelial lymphocytosis consistent with coeliac disease. A gluten free diet was started with rapid resolution of the symptoms. Duodenal biopsy was not repeated. She remained on a gluten free diet.In 1995 she developed lethargy, confusion, short term memory impairment, and bitemporal headache. Brain computed tomography (CT) scan showed a low attenuation mass adjacent to and compressing the anterior horn of the right lateral ventricle, with considerable surrounding oedema and enhancement with intravenous contrast (Figure). The appearances were suggestive of primary cerebral lymphoma. A stereotactic biopsy specimen showed a necrotic tumour composed of pleomorphic lymphoid cells with immunophenotype CD45+ CD45RO+ CD3+ CD30+ CD20-EMA-. Polymerase chain reaction analysis for T cell receptor and immunoglobulin heavy chains was performed using three primer pairs.7 This demonstrated a clonal rearrangement of T cell receptor ,B and y chain genes of 80 bp and 70 bp respectively. The histological diagnosis was of a T cell variant of large cell anaplastic lymphoma.Staging investigations, which included full blood count, erythrocyte sedimentation rate, lactate dehydrogenase, bone marrow aspirate, and

OBJECTIVE Finerenone significantly improved cardiorenal outcomes in patients with chronic kidney disease (CKD) and type 2 diabetes (T2D) in the Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease trial. We explored whether baseline HbA1c level and insulin treatment influenced outcomes. RESEARCH DESIGN AND METHODS Patients with T2D, urine albumin-to-creatinine ratio (UACR) of 30–5,000 mg/g, estimated glomerular filtration rate (eGFR) of 25 to <75 mL/min/1.73 m2, and treated with optimized renin–angiotensin system blockade were randomly assigned to receive finerenone or placebo. Efficacy outcomes included kidney (kidney failure, sustained decrease ≥40% in eGFR from baseline, or renal death) and cardiovascular (cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure) composite endpoints. Patients were analyzed by baseline insulin use and by baseline HbA1c <7.5% (58 mmol/mol) or ≥7.5%. RESULTS Of 5,674 patients, 3,637 (64.1%) received insulin at baseline. Overall, 5,663 patients were included in the analysis for HbA1c; 2,794 (49.3%) had baseline HbA1c <7.5% (58 mmol/mol). Finerenone significantly reduced risk of the kidney composite outcome independent of baseline HbA1c level and insulin use (Pinteraction = 0.41 and 0.56, respectively). Cardiovascular composite outcome incidence was reduced with finerenone irrespective of baseline HbA1c level and insulin use (Pinteraction = 0.70 and 0.33, respectively). Although baseline HbA1c level did not affect kidney event risk, cardiovascular risk increased with higher HbA1c level. UACR reduction was consistent across subgroups. Adverse events were similar between groups regardless of baseline HbA1c level and insulin use; few finerenone-treated patients discontinued treatment because of hyperkalemia. CONCLUSIONS Finerenone reduces kidney and cardiovascular outcome risk in patients with CKD and T2D, and risks appear consistent irrespective of HbA1c levels or insulin use.