Immune checkpoint inhibitors are widely used in the treatment of cancers. They are known to cause multisystem immune related adverse effects, including endocrinopathies. Primary thyroid dysfunction has been documented as an adverse effect of immunotherapy. We report a case of primary hypothyroidism detected in a patient after treatment with anti -PD-L1 agent, Atezolizumab. The patient presented with altered mental status 6 months after the initiation of immunotherapy. TSH was measured as part of the workup for encephalopathy, revealing TSH >20 with undetectable free T3, free T4. Anti TPO antibodies were elevated to >7500 IU/ml with anti thyroglobulin antibodies elevated to about 50U/ml. Thyroid ultrasound showed a diffusely heterogeneous gland with no other abnormalities. Patient was detected to have metastatic disease to the brain and spinal cord likely causing her change in mental status and was treated with steroids and radiation after which she improved. She was started on Levothyroxine 50mcg daily and discharged on the same dose. This case illustrates the need for measurement of TSH in all patients prior to the initiation of immunotherapy given the possibility of development of primary thyroid dysfunction mediated by inflammatory thyroiditis in these settings.
Objective The COVID-19 pandemic altered health outcomes in populations through a host of downstream social, economic, and psychological changes, especially among those with chronic non-communicable diseases (NCDs). Some studies reveal worsened glycemic control and weight gain, while others indicate improved glycemic control and weight loss. Thus, evidence demonstrates conflicting results in this context. We aimed to conduct a study to explore changes in these metrics in an outpatient setting providing for an underserved population. Methods We conducted a single-site observational study at a Federally Qualified Health Center (FQHC) in New York City to compare glycemic control and body weight, measured by Hemoglobin A1c (HbA1c) and body mass index (BMI) respectively, before and after the onset of the COVID-19 pandemic. Results After the pandemic, there was a 103% increase in the annual change in average HbA1c from the years prior to the pandemic versus from early 2020 to 2021 (p < 0.005). Mean BMI increased during the pandemic, although this was not statistically significant. The slope for the change in BMI over five years prior to the pandemic is -0.09, while the slope of change in BMI before and after the onset of COVID-19 is 0.31. The difference between the two slopes is 0.48 (p = 0.37). Discussion/Conclusion Our study reveals that the COVID-19 pandemic could have contributed to a worsening in the status of metabolic disorders due to decreased physical activity, worsened dietary habits, psychosocial stressors, and reduced access to healthcare, emphasizing the need for enhanced medical, pharmaceutical and emotional support. Concurrently, many individuals adopted healthier practices through dietary and activity modifications, with a resulting improvement in cardio-metabolic parameters.
Hypophosphatemia is a less known complication of parenteral iron use, particularly after the use of certain iron formulations. We report the case of a young male with inflammatory bowel disease and iron deficiency anemia, who developed severe symptomatic hypophosphatemia after his third exposure to iron carboxymaltose with no evidence of the same occurring upon prior exposures to the compound. Investigations revealed serum phosphorous levels of 0.7 mg/dl, corrected serum calcium of 8–9.5 mg/dl, alkaline phosphatase of 50 U/L (38–126), 25 hydroxy vitamin D level of 40.2 ng/ml, and intact PTH elevated to 207 pg/ml. Urine studies indicated renal phosphate wasting. Presentation was not in keeping with refeeding syndrome. Intact fibroblast growth factor 23 level, measured after the initiation of treatment was within the normal range at 179 RU/mL (44–215). 1,25 dihydroxy vitamin D level, also measured after the initiation of treatment, was normal at 26.3 pg/ml (19.9–79.3). The patient was treated with calcitriol and aggressive oral and intravenous phosphorous repletion. Symptoms then resolved and the patient was discharged on an oral regimen. This phenomenon is postulated to occur due to an increase in the level and activity of FGF23 and decreased cleavage of the same, due to anemia as well as use of specific iron formulations. This is the first instance, in our literature review, of this complication known to occur, not after initial exposure to an implicated iron formulation but occurring on subsequent exposure.
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A 53 year old male with history of HTLV-1 infection associated myelopathy but with unknown mode of transmission, presented with acute on chronic bilateral lower extremity weakness and numbness with no other deficits. Examination revealed decreased strength (grade 1/5) in lower extremities with normal bulk, tone and sensations. Initial blood work revealed hypercalcemia with corrected Calcium of 16.2mg/dl(8.5-11.5), Phosphorus of 2.7mg/dl (2.5- 4.5) and Alkaline Phosphatase of 126mg/dl(20-140). Workup for hypercalcemia revealed Parathyroid hormone (PTH) level of 14pg/ml (10-65), 25 hydroxy vitamin D at 19.6 ng/ml(30-100), 1,25 dihydroxy vitamin D at 6.7pg/ml(19.9-79.3) and TSH of 1.265 microIU/ml(0.5-5). The Parathyroid hormone related protein(PTHrP) level was low at < 2pmol/L while Lactate Dehydrogenase (LDH) was 433U/L(100-220). Urine calcium creatinine ratio was 0.388. Reverse Transcriptase PCR was positive for HTLV-1 but negative for HTLV-2. Smudge cells and atypical lymphocytes were noted on peripheral smear. Imaging revealed generalized lymphadenopathy with splenomegaly but no spinal cord compression. Flow cytometry showed 7.8% atypical helper T cells, positive for CD3, CD4, CD5 and CD45. Clonal T cell receptor gene rearrangements were found, suggesting an underlying T cell neoplasm. Lymph node biopsy confirmed ATLL. He received treatment with fluids, Calcitonin and Denosumab after which serum Calcium levels fell (nadir 7.7mg/dl) and then normalized. He developed another episode of hypercalcemia 5 weeks later which was treated similarly. Discussion Human T cell Lymphotropic Virus-1 (HTLV-1) is a retrovirus causing asymptomatic infections, symptomatic systemic disorders and adult T cell Leukemia and lymphoma(ATLL). HTLV-1 infections, whether in asymptomatic or symptomatic patients, and ATLL are rare but important causes of hypercalcemia and hypercalcemic crises. Individuals with ATLL have the highest incidence of hypercalcemia(50-70%) among all hematologic malignancies. Hypercalcemia is a poor prognostic factor and predicts lower overall survival. It is caused by increased bone resorption, mediated by various factors with the largest role being played by Receptor Activator of Nuclear Factor Kappa B ligand (RANKL), followed by PTHrP, Interleukins, Macrophage Inflammatory Protein 1 alpha and gp 46. RANKL expression is increased upon transactivation by the viral TAX gene product and mediates conversion of osteoclast precursors to mature osteoclasts engaging in bone resorption. PTHrP expression is variable among patients, relating to levels of the TAX gene product that transactivates the PTHrP gene promoter. Thus, a low level, like in our patient, does not rule out HTLV infection as the cause of hypercalcemia. Management of hypercalcemia is in keeping with guidelines for management of other causes of hypercalcemia but may be better responsive to monoclonal antibodies against RANKL than bisphosphonates given the role of the ligand in mediating hypercalcemia in these cases. It can also be used in the setting of poor renal function, which is commonly encountered in hypercalcemic patients. Presentation: No date and time listed
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