Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection primarily affects the respiratory tract, but gastrointestinal (GI) symptoms may obscure a secondary diagnosis. GI symptoms similar to the ones presented in acute pancreatitis (AP) have been reported. SARS-CoV-2 binds to angiotensin-converting enzyme 2 receptors, which have been identified in the lungs and pancreas. It has been discussed that systemic response to the infection prompts dysregulation in the affected organs. Hyperglycemia is an independent risk factor for increased mortality and thus a detailed assessment must be performed. A 47 year-old man with dyslipidemia arrived at the ER due to a severe constant epigastric pain of 1 day of evolution with back radiation associated with nauseas, emesis, and hyporexia. Upon examination he was tachycardic and in distress due to pain. Laboratories revealed normocytosis, normal hemoglobin, mild thrombocytopenia, hyperglycemia (150 mg/dL), corrected hyponatremia (130 mmol/L), and corrected hypocalcemia (7.4 mg/dL). Amylase (2,332 U/L) and lipase (2,990 U/L) were elevated. Triglycerides were 6,256 mg/dL and glycated hemoglobin was 6.1%. Abdominal CT scan revealed pancreatitis. He was admitted to the ICU due to severe AP due to hypertriglyceridemia with IV hydration and IV insulin infusion. During the first day of admission, he developed respiratory distress requiring intubation, marked abdominal distension, hemodynamic instability, and oliguria. Intra-abdominal pressure yielded 24 mmHg leading to the diagnosis of abdominal compartment syndrome. He underwent emergent abdominal decompressive laparotomy with Bogota Bag placement. COVID-19 PCR test was performed and reported positive. 72 hours later, triglycerides improved and IV insulin was discontinued, but hyperglycemic state prompted subcutaneous basal and correction boluses. Insulin requirement progressively decreased and was discontinued after 14 days. He continued to show clinical improvement and by day 40, the patient was successfully extubated and discharged after physical rehabilitation. SARS-CoV-2 infection has shown a complex multisystem involvement leading to variable presentations which can be fatal if not identified and addressed properly. Albeit, AP is a rare manifestation of COVID-19, clinicians should be aware and pay attention to the related complications. Proposed mechanisms for hyperglycemia and AP include β-cell damage. The pathogenetic role of COVID-19 in hypertriglyceridemia is unclear. Little attention has been paid to the extent of pancreatic injury caused by this virus. To our knowledge this is the second case presenting with hyperglycemia, hypertriglyceridemia, and AP in COVID-19 infection. As the global pandemic is still growing, elucidation of key pathways and mechanisms underlying these associations would aid in the treatment of patients with COVID-19 worldwide.
The coexistence of diabetic ketoacidosis (DKA), hypertriglyceridemia and acute pancreatitis (AP) represent a complex phenomenon described as the enigmatic triad. The exact initial culprit and pathophysiologic mechanism of this chain of events are still unclear posing a challenge in management. DKA may lead to glucose and lipid metabolism dysregulation which can result in hypertriglyceridemia leading to AP. On the other hand, hypertriglyceridemia may induce AP which may decompensate diabetes and lead to DKA. In both scenarios, this triad results in an uncommon clinical presentation with up to 80% mortality rate. Most frequently reported in children, this entity accounts for only a handful of cases reported in the literature. Case of an obese, non alcoholic 57 year old male without history of systemic illness who visits the emergency room due to mid-upper abdominal pain for the past day. Pain radiates to the back, worsens upon laying flat, and is associated with bloating and nausea. He denies previous similar episodes, vomiting, fever or bowel habit changes. Laboratory workup revealed lipidemic sample with hyperglycemia, metabolic acidosis, positive serum ketones, and normal amylase and lipase. Lipid panel revealed hypertriglyceridemia at 6,260 mg/dL (35-150). Glycated hemoglobin at 14.7%. Abdominal computed tomography showed peripancreatic inflammation consistent with pancreatitis. Given clinical and imaging criteria the diagnosis of severe hypertriglyceridemia induced AP and DKA were made. The patient was admitted to ICU and treated with intravenous insulin drip and supportive management. Resolution of DKA and successful decrease in triglycerides to less than 500 mg/dL was achieved by the third day of admission. After six days, the patient was discharged home with insulin and lipid lowering regimens. This case demonstrates an extremely rare initial presentation of diabetes mellitus. This triad is the result of a toxic chain of events that may be lethal if not promptly identified. This case makes an exemplary lesson as to always take under consideration atypical etiologies to potentially life threatening conditions and also remarks that while uncommon, pancreatitis with normal pancreatic enzymes is a possible phenomenon. Even though false negative amylase has been associated with hypertriglyceridemia induced AP, only a few cases with negative lipase have been described. While no definite explanation has been yet discovered, negative lipase may be explained by early acinar cell apoptosis in AP. More research efforts are necessary in order to improve early diagnosis, treatment, and mortality rate for this rare but potentially deadly triad and to better understand the mechanisms underlying AP and the role that digestive enzymes play.
The superlative therapeutic response of cancer immunotherapy is activation of the immune system against cancer cells. Currently, one of the most considered immune system enhancer are the immunomodulatory antibodies well known as checkpoint inhibitor therapy. Among this type of treatment, programed cell death-1 receptor blocker, is one of the most sought-after therapies on demand now a day. Notwithstanding the important clinical benefits of this therapeutic modality, serial autoimmune adverse effects and variety of atypical presentations of life-threatening endocrinopathies are expected to occur. We present a case of a 78-year-old man with dyslipidemia and lung CA who was referred to our clinic after developing electrolyte disturbances with associated dizziness and fatigue one month after Pembrolizumab therapy initiation. Physical exam was unremarkable. Laboratory data was consistent with mild hyponatremia, hyperkalemia and adequate fasting blood sugar levels. Aldosterone levels were extremely low, ACTH levels were extremely high with inappropriate low total cortisol response and negative 21-Hydroxylase antibodies. Diagnosis of primary adrenal insufficiency was established and Fludrocortisone 0.05 mg PO daily therapy was started with further resolution of hyponatremia and initial symptoms. In addition, concurrent primary hyperthyroidism along with thyroid RAIU-Scan results were consistent with thyroiditis, but TSI and TPO’s antibody levels were unexpectedly negative. Eventually, a suspicious thyroid nodule was identified requiring biopsy. Initial FNA results showed a follicular lesion of undetermined significance followed by a benign finding when repeated after six months. During follow up, patient’s primary hyperthyroidism converted to severe primary hypothyroidism without any intervention for her prior hyperthyroidism. Patient’s TPO’s levels remain undetectable and his current status is post-thyroiditis with residual primary hypothyroidism. Primary adrenal insufficiency also persist and its antibodies have not yet been identified either. It is known that autoimmunity can predispose to the development of primary adrenal and thyroid disorders in patients undergoing PD-1 receptor blockers therapy against cancer. Both disorders are increasingly recognized and reported as one of the most common adverse effects presenting in patients treated with these agents. However, to our knowledge, cases of non-immune related adverse effects are barely documented. This case of uncommon endocrine manifestations related to checkpoint inhibitors therapy is meritorious of being reported since it should raise awareness in the medical community for prompt identification of signs and symptoms, as well as to offer adequate management, accurate treatment and provide a better standard of care.
Background Thyroid T-cell lymphoma is an unusual diagnosis, responsible for less than 2% of all thyroid malignancies and all extra-nodal lymphomas. Hashimoto’s thyroiditis may predispose patients to its development, but only half of the cases reported were associated with it. We present a case of a 42 years old man with generalized skin rash with subsequent development of a rapidly growing anterior neck mass arising from the thyroid gland without TFT impairments. Ultimately, an excisional cervical node biopsy disclosed immune-pathological characteristics of Angioimmunoblastic T-cell lymphoma. Clinical Course A 42 y/o Hispanic male patient without past medical history, presents for the first time complaining of a generalized intense pruritic-excoriated skin rash of 3-week duration. Rest of physical examination and biochemical test were unremarkable. Five weeks later, he reports worsening skin rash and rapid enlargement of a painless anterior neck mass. Review of systems was non contributory. An enormous, not previously palpated, left thyroid mass and a cervical lymphadenopathy was found. Laboratory data reported leukocytosis with lymphocytic predominance, microcytic hypochromic anemia and mild hypercalcemia. Analysis of ANA test, HIV test, Hepatitis profile and VDRL were negative. TFT within normal reference, and negative TPO-antibodies. Auxiliary laboratory test as CRP, ESR and LDH were elevated. A thyroid ultrasound showed multiple cervical lymph nodes with intense hilar vascularity and a large isoechoic nodularity involving upper, lower and interpolar left thyroid region, measuring 7.4cm-CC x 3.9 cm-AP x 5.3 cm-TRV. FNA biopsy reported unspecific lymphoma. Supplemental excisional lymph node biopsy disclosed pathological diagnosis of a T-cell lymphoma with immunophenotype of Angioimmunoblastic type. Further PET CT and CT scans of head, neck and abdominopelvic area, suggested a large enhancing posteriorly extended neck mass, intimately associated and originating from the left thyroid gland. The diagnosis of a Primary Thyroid Angioimmunoblastic T-cell Lymphoma was established and patient was referred to an Oncology evaluation for staging and management considerations. Discussion Angioimmunoblastic T-cell Lymphoma is a rare form of non-Hodgkin lymphoma arising from the lymphatic system not from the thyroid gland. In addition, a metastatic process in our patient was ruled out, following the definition of primary thyroid lymphoma which exclude direct malignant invasion to the thyroid gland. According to our literature revision, no cases of such pathology have yet been reported. We consider that our case poses a unique etiological manifestation with extraordinary clinical significance worthy to be the first one communicated in order to diversify diagnostic approach of unexpected manifestations of a thyroid diseases.
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