Patient: Female, 34Final Diagnosis: Refractory thrombotic thrombocytopenic purpuraSymptoms: FatigueMedication: —Clinical Procedure: Plasma exchangeSpecialty: Rheumatology • Hematology and Critical CareObjective:Rare co-existance of disease or pathologyBackground:Thrombotic thrombocytopenic purpura (TTP) is one of the thrombotic microangiopathic (TMA) syndromes, caused by severely reduced activity of the vWF-cleaving protease ADAMTS13. Systemic lupus erythematosus (SLE), on the other hand, is an autoimmune disease that affects various organs in the body, including the hematopoietic system. SLE can present with TMA, and differentiating between SLE and TTP in those cases can be very challenging, particularly in patients with no prior history of SLE. Furthermore, an association between these 2 diseases has been described in the literature, with most of the TTP cases occurring after the diagnosis of SLE. In rare cases, TTP may precede the diagnosis of SLE or occur concurrently.Case Report:We present a case of a previously healthy 34-year-old female who presented with dizziness and flu-like symptoms and was found to have thrombocytopenia, hemolytic anemia, and schistocytes in the peripheral smear. She was subsequently diagnosed with TTP and started on plasmapheresis and high-dose steroids, but without a sustained response. A diagnosis of refractory TTP was made, and she was transferred to our facility for further management. Initially, the patient was started on rituximab, but her condition continued to deteriorate, with worsening thrombocytopenia. Later, she also fulfilled the Systemic Lupus International Collaborating Clinics (SLICC) criteria for diagnosis of SLE. Treatment of TTP in SLE patients is generally similar to that in the general population, but in refractory cases there are few reports in the literature that show the efficacy of cyclophosphamide. We started our patient on cyclophosphamide and noticed a sustained improvement in the platelet count in the following weeks.Conclusions:Thrombotic thrombocytopenic purpura is a life-threatening hematological emergency which must be diagnosed and treated in a timely manner. Refractory cases of TTP have been described in the literature, but without clear evidence-based guidelines for its management, and is solely based on expert opinion and previous case reports. Further studies are needed to establish guidelines for its management. We present this case to highlight the role that cyclophosphamide might carry in those cases and to be a foundation for these future studies.
In spite of developments with novel insulin preparations, novel modes of insulin delivery with insulin infusion pumps, and the facility of continuous glucose monitoring, only 20% of patients with type 1 diabetes are under adequate control. The need for innovation is clear, and, therefore, the use of adjunct therapies with other pharmacological agents currently in use for type 2 diabetes, has been tried. Currently, pramlintide is the only agent licensed for use in this condition in addition to insulin. Global trials have been conducted with liraglutide, a glucagon‐like peptide 1 receptor agonist (GLP‐1RA), dapagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor, and sotagliflozin, an inhibitor of both SGLT1 and SGLT2 transporters. While dapagliflozin and sotagliflozin have now been licensed for clinical use in this condition in Europe and Japan, they have hitherto not been licensed in the United States due to a small increase in the risk of diabetic ketoacidosis. However, these agents reduce glycosylated hemoglobin (HbA1c) by 0.4%, reduce glycemic oscillations, and do not increase the risk of hypoglycemia. Liraglutide, on the other hand, induced a smaller reduction in HbA1c and thus was not considered for a license. However, further trials are currently being conducted with a combination of semaglutide, the most potent GLP‐1RA, and dapagliflozin to determine whether this approach would yield better outcomes.
Patient: Male, 35Final Diagnosis: RhabdomyolysisSymptoms: Muscle pain • nauseaMedication: —Clinical Procedure: Intravenous fluidsSpecialty: Family MedicineObjective:Unusual or unexpected effect of treatmentBackground:Rhabdomyolysis is a syndrome characterized by skeletal muscle breakdown, that involves the release of intracellular contents into the circulation, including creatine kinase (CK), myoglobin, electrolytes, organic acids, and purines. Causes of rhabdomyolysis include trauma, exertion, drugs, and toxins (including alcohol), and electrolyte abnormalities. The treatment of rhabdomyolysis is to remove the cause and use intravenous (IV) fluids. When this treatment strategy fails to work, high-dose IV steroids may be used.Case Report:We present a case of rhabdomyolysis following the use of 3,4-methylenedioxy-methamphetamine (MDMA) or ‘ecstasy’ with hypophosphatemia, which was found to be refractory to intravenous hydration. In this case, pulsed dosing of steroid therapy was found to be effective.Conclusions:Rhabdomyolysis that is refractory to treatment with IV fluids may respond to a short-term, high-dose course of IV steroids.
Systemic lupus erythematosus (SLE) is an autoimmune multisystem disease that is characterized by various antibodies to nuclear and cytoplasmic antigens and diagnosed by either fulfilling the 2012 Systemic Lupus International Collaborating Clinics (SLICC) criteria, American College of Rheumatology (ACR) criteria or by Renal Biopsy. Renal involvement is common in SLE and is primarily related to anti-double-stranded DNA antibodies. However, small group of SLE nephritis patients have shown negative anti-dsDNA and ANA. We present a case of 25-year-old female who presented with proteinuria and negative serum antibodies except anti-Ro/SSA. Renal biopsy was performed and was consistent with class IV lupus nephritis (LN). In this report, we highlight the possible role of antiRo antibodies in the pathogenesis and the prognosis of LN, although the mechanism is yet to be understood. Anti-Ro/SSA antibodies might play an important role in the pathogenesis and prognosis in LN. However, further studies are required to understand the exact mechanism.
Thyroid tuberculosis (TT) is a rare disease and can be a diagnostic challenge. Here we highlight a case of TT following COVID-19 infection. A 38-year Myanmar immigrant female presented with nocturnal fever, fatigue, nausea, sore throat, appetite and weight loss for 1 week with dysphagia, neck swelling, dyspnea, and watery diarrhea. Medical history included renal transplant due to ESRD from IgA nephropathy, DM and treated latent TB with no prior or family history of thyroid disease. She had COVID 7 months ago, complicated by allograft rejection. She was tachycardic, febrile but not in acute distress. Neck exam revealed diffuse thyromegaly with tenderness on right lobe without bruit, palpable cervical lymphadenopathy nor tremors. Labs showed WBC 12.8x109/L (4.8-10), and ESR 50 ml/hr (20-40). On admission, she developed AKI and immunosuppressant meds were discontinued. She was started on broad-spectrum antibiotic. CT chest reported moderate loculated right pleural effusion with mid and lower lobe consolidation. Blood and urine culture, pleural fluid, sputum culture for acid-fast bacilli (AFB) and QuantiFERON-TB were negative. Upon persistent fever, RIPE therapy (rifampin, isoniazid, pyrazinamide, ethambutol) was started and stopped after 10 days due to transaminitis and negative TB PCR. Further labs showed TSH 0.04 mIU/ml (0.27-4.2), FT4 2.81 ng/dl (0.93-1.7), TT3 127 ng/dl (80-200), negative TPO and TSI. Endocrinology was consulted for thyroiditis. Ibuprofen and Propranolol were initiated with continuation of prednisone. Repeat thyroid labs normalized in 4 days. US thyroid noted diffuse, heterogenous thyromegaly without hypervascularity or abscess. CT neck showed diffuse thyromegaly 4.2x7.2x7.5 cm in size; right thyroid lobe extended to posterior clavicle with enhanced capsule, without discrete lymph node or vascularity changes, suggestive of thyroiditis. Fine needle aspiration (FNA) of left thyroid lobe drained 3 ml purulent fluid and AFB were seen on direct smear. She was diagnosed as TT, but unable to restart RIPE therapy due to worsening liver function. She expired after cardiac arrest due to intracranial bleeding and brain abscess. Thyroid tuberculosis is a rarely reported clinical entity. This is the first reported case of secondary TB (TT) in post-COVID infected patient from reactivation of latent TB. In our case, follicular destruction caused initial hyperthyroidism with later recovery. It can be difficult to distinguish subacute from suppurative thyroiditis due to TB. Imaging may not always show clear abscess formation. FNA is crucial for diagnosis, and drainage of any abscess. Anti-TB meds can be given, surgery is rarely required. TT should be considered in any immunocompromised patient with fever and neck pain. Imaging should also include evaluation for any CNS spread of TB. Early detection and treatment will help reduce significant morbidity and mortality.
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