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Background Patients with hypopituitarism can have a complete or partial deficiency of pituitary hormones. If not treated adequately, it can result in episodes of myxedema coma or adrenal crisis. Our patient was unique with findings of both myxedema coma and adrenal crisis together on initial presentation. Clinical Case A 35-year-old female with a medical history of Sheehan's Syndrome, transient diabetes insipidus and lyme carditis presented to the emergency department with dizziness, lethargy, and generalized weakness for 1 day. EMS found her blood glucose level to be 21. The patient was given oral glucose. In the ED, her blood glucose level was found to be 34. She confessed she had been noncompliant with her medications for a month. She had no other complaints or possible precipitating factors including illness/trauma/stress. On admission, she was found to be hypothermic to 91.3 deg F, bradycardic to 40-50s, and hypotensive (Systolic 80s-90s/diastolic 50s-60s). On physical examination, she was thin and lethargic but oriented. No gross focal neurological deficits were noted. In addition to the initial hypoglycemia, her laboratory findings were significant for a TSH level of 0.52, T3 level of Conclusion This is an interesting case presentation of myxedema coma and adrenal crisis in a patient with a history of Sheehan's Syndrome. It is important to consider the unique and similar presentations of both myxedema coma and adrenal crisis such as hypotension, bradycardia, hypothermia, hypoglycemia, and lethargy. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m., Monday, June 13, 2022 12:51 p.m. - 12:56 p.m.

Pheochromocytoma is a tumor arising from chromaffin cells of the medulla of adrenal gland and secretes excessive amounts of catecholamines: epinephrine and norepinephrine. It can also arise from sympathetic ganglia when it is referred to as catecholamine-secreting paragangliomas or extra-adrenal pheochromocytoma. Pheochromocytoma has been referred to as "the masquerader" for its numerous atypical presentations, which makes its diagnosis medically challenging. Here, we present a case of a 66-year-old female, presenting with high-grade fever for two weeks associated with generalized body aches. She had an extensive infectious, rheumatological and hematological workup. Ultimately, she was diagnosed with pheochromocytoma. After adrenalectomy, her fever and body ache resolved.

Metformin is the first-line therapy for patients with type 2 diabetes, and its most common adverse effects are gastrointestinal. Lactic acidosis associated with metformin use is rare. Here, we report the case of a 77-year-old man with a medical history of diabetes (treated with metformin), hypertension, chronic alcohol abuse, and prostate and bladder cancer, who presented with abdominal pain, nausea, vomiting, and diarrhea for five days. He was admitted with severe metabolic acidosis due to metformin toxicity (metformin-associated lactic acidosis) with metformin level 23 mcg/mL (therapeutic range approximately 1-2 mcg/mL) in the setting of acute kidney failure due to acute pancreatitis and sepsis secondary to aspiration pneumonia. He was intubated, required pressor support, and received daily hemodialysis. Despite aggressive management, his hospital course became complicated with acute respiratory distress syndrome, myocardial infarction, acute hepatic failure, and ischemic and metabolic encephalopathy. In the end, the family decided to withdraw care and the patient was terminally extubated.

Hypercortisolism is a multisystem disorder that results from inappropriate and excessive glucocorticoid secretion and loss of normal feedback mechanisms of the hypothalamic-pituitary axis. It is broadly divided into adrenocorticotropic hormone (ACTH) dependent and ACTH-independent categories. Primary bilateral macronodular adrenal hyperplasia (PBMAH) is a rare cause of ACTH-independent hypercortisolism, accounting for less than 2% of cases. It usually presents as hypertension, metabolic abnormalities, thromboembolic, cardiovascular, or endocrine disorders but rarely as a neuropsychiatric illness. Therefore, a delay in the diagnosis and management of cognitive illnesses substantially increases morbidity in these patients. Herein, we report a case of severe psychosis due to Cushing's syndrome with PBMAH. A 49-year-old male with a past medical history of diabetes and hypertension presented with acute onset of confusion. The patient’s uncontrolled hypertension, hypokalemia, metabolic alkalosis, and resistant psychosis to various psychotropic medications raised the suspicion of an underlying metabolic disorder. Further workup revealed an inappropriate suppression of morning (AM) cortisol after administration of dexamethasone and elevated values of serum AM cortisol and 24-hour urinary cortisol, in addition to low ACTH. Computed tomography (CT) of the abdomen and pelvis with intravenous (IV) contrast was performed to evaluate the adrenal gland which showed multiple nonspecific adrenal nodules bilaterally measuring between 3.5 cm - 4.5 cm. The patient was hence diagnosed with hypercortisolism secondary to PBMAH. The patient was treated with ketoconazole after he refused surgery as a treatment option and was noted to have significant improvement in his psychosis within a week, along with improvement of his hypertension, electrolyte abnormalities, and a significant decrease in the 24-hour urine cortisol level. Neuropsychiatric illness is a rare manifestation and an unusual initial presenting symptom of Cushing’s syndrome secondary to primary bilateral macronodular adrenal hyperplasia. A delay in diagnosis often subjects these patients to unnecessary psychotropic medications and prolonged psychiatric hospitalizations. Hence, clinicians must be cognizant of this rare entity when making a diagnostic evaluation to prevent subsequent morbidity and mortality.

A 54-year-old Caucasian postmenopausal woman presented to an endocrinologist with increasing fatigue and worsening virilising symptoms mainly male type of baldness, increasing facial hair and deepe...

Over the past several decades, improved technologies used in the care of hospitalized and outpatient pediatric populations have resulted in a decreased but still significant number of iatrogenic injuries. Children at the highest risk for cutaneous injury include those with the most immature skin barriers, such as neonates younger than 32 weeks of gestational age. Additional risk factors include low birth weight, increased length of hospital stay, and indwelling instrumentation. Also at risk are older children with compromised skin barriers owing to infectious disease (staphylococcal scalded skin syndrome), inflammatory disease (atopic dermatitis), drug eruptions, and inherited or acquired blistering disorders. This review highlights the presentation, course, and management of iatrogenic skin injury events in children.

The successful use of venovenous bypass (VVB) in orthotopic liver transplantation (OLT) was first reported by Shaw in 1984.1 Subsequently the technique was generally adopted as a de facto standard, with the vast majority of transplant centers in the United States and Europe using VVB routinely during OLT. It was felt that the use of VVB was associated with improved hemodynamic stability and reduced blood loss, and that it allowed less experienced surgeons more time during the anhepatic phase. Despite these perceived advantages, many clinicians have questioned the reported benefits of VVB in OLT. There are also increasing concerns about the morbidity and even mortality that can be associated with its use. This is reflected in the fact that in the mid 1990s, many centers in the United States were slowly moving to a more selective use of VVB, with less than 50% using it routinely. However there is still enormous variability between centers, both in the frequency of use and the indications for bypass.2,3 In 2003, a survey of the transplant centers in the United Kingdom found that 2 centers used VVB routinely, 3 used it selectively (10-30% patients), and 2 centers used it rarely, if ever. This difference is despite 5 of the centers routinely using caval preservation techniques (unpublished data). The marked differences between transplant centers both in terms of the use of and indications for VVB is somewhat perplexing and has stimulated this review. A literature search for venovenous bypass/liver transplantation, renal failure/liver transplantation, reperfusion syndrome/liver transplantation was performed using Medline, PubMed, Embase, Cinahl, journals@ovid. These searches revealed 84 studies, of which 34 were relevant to the topic. Further references were obtained from these papers and by hand search of relevant transplant journals. In total 47 studies were identified, of which only 2 were randomized controlled trials. Only 1 study showed improved outcomes with the use of bypass; however, this was not a randomized controlled trial.1

Increased circulating free fatty acids (FFAs) inhibit both hepatic and peripheral insulin action. Because the loss of effectiveness of glucose to suppress endogenous glucose production and stimulate glucose uptake contributes importantly to fasting hyperglycemia in type 2 diabetes, we examined whether the approximate twofold elevations in FFA characteristic of poorly controlled type 2 diabetes contribute to this defect. Glucose levels were raised from 5 to 10 mmol/l while maintaining fixed hormonal conditions by infusing somatostatin with basal insulin, glucagon, and growth hormone. Each individual was studied at two FFA levels: with (NA+) and without (NA−) infusion of nicotinic acid in nine individuals with poorly controlled type 2 diabetes (HbA1c = 10.1 ± 0.7%) and with (LIP+) and without (LIP−) infusion of lipid emulsion in nine nondiabetic individuals. Elevating FFA to ∼500 μmol/l blunted the ability of glucose to suppress endogenous glucose production (LIP− = −48% vs. LIP+ = −28%; P < 0.01) and increased glucose uptake (LIP− = 97% vs. LIP+ = 51%; P < 0.01) in nondiabetic individuals. Raising FFA also blunted the endogenous glucose production response in 10 individuals with type 2 diabetes in good control (HbA1c = 6.3 ± 0.3%). Conversely, normalizing FFA nearly restored the endogenous glucose production (NA− = −7% vs. NA+ = −41%; P < 0.001) and glucose uptake (NA− = 26% vs. NA+ = 64%; P < 0.001) responses to hyperglycemia in individuals with poorly controlled type 2 diabetes. Thus, increased FFA levels contribute substantially to the loss of glucose effectiveness in poorly controlled type 2 diabetes.

Objective To assess the effect of an immediately available hemoglobin A1c (HbA1c) result on glycemic control and physician decisions about pharmacologic therapy in an office practice. Methods In a 1-year retrospective review of medical records, HbA1c results were analyzed in 115 patients beyond the age of 65 years, who had type 2 diabetes and were referred for the first time to a private endocrinology practice between April 1, 1997, and March 31, 1998. These patients were classified into two groups: group A (N = 93, insured by standard Medicare) had immediate HbA1c results (during the patient encounter) and group B (N = 22, insured by Medicare health maintenance organization [HMO]) had commercial laboratory HbA1c results available within 2 to 3 days. We reviewed the changes in the HbA1c level during the 12-month period and the presence or absence of a change in therapy at each visit. HbA1c levels were measured by ion-exchange low-pressure liquid chromatography in group A and by one of three capitated commercial laboratories (depending on HMO contracts) in group B. Results At the end of the 12 months, the mean HbA1c decrease was 1.03 ± 0.33% in group A and 0.33 ± 0.83% in group B. During the first visit, 52% of the patients in group A had pharmacologic treatment interventions, whereas only 27% in group B had such interventions. Conclusion Rapid availability of the HbA1c results during the clinical encounter improves the ability of the physician to make appropriate therapeutic decisions and results in improved glycemic control. (Endocr Pract. 2001;7:85-88)

The aim of the literature review was to compile and compare similar cases of massive haemoperitoneum in an asymptomatic woman where the bleeding was from the right uterine artery, which had been eroded by pelvic endometriosis. To our knowledge this is the second case reported in the literature. Case reports of other sources of bleeding leading to haemoperitoneum were studied, comparisons were made, and the results compiled. Although several cases of massive haemoperitoneum have been reported, spontaneous bleeding from uterine artery erosion is a rare occurrence. The abdominal surgeon should be vigilant and alert to localise rare sites of bleeding. This literature review emphasises that endometriosis can present in many ways and a high level of clinical suspicion is necessary.

The evaluation of skin findings is critical in identifying many types of injury, whether self- inflicted or accidentally or intentionally inflicted. Specific causes of injury include homicide, abuse, neglect, assault, self-inflicted injury, suicide, torture, poisoning, and bioterrorism. Forensic findings in hair and nails are also discussed. This overview of dermatologic findings in forensic pathology highlights the significance of the cutaneous manifestations of injury.

Examination of the skin and adnexae is a critical part of the forensic examination. Little information on forensic sciences has been published in the dermatologic literature. Correct forensic terminology and documentation of dermatologic findings is of critical importance in forensic investigations. The skin may reveal clues to the identity of an individual and the time and method of death or injury. Normal postmortem changes in the skin are described along with pseudopathology and damage from postmortem animal activity. The forensic classification of types of injuries is introduced in this first of a two-part paper on forensics in dermatology.

Purpose: Melanoma is a solid tumor that is notoriously resistant to chemotherapy, and its incidence is rapidly increasing. Recently, several signaling pathways have been shown to contribute to melanoma tumorigenesis, including constitutive activation of mitogen-activated protein kinase, Akt, and Stat-3. The activation of multiple pathways may account in part for the difficulty in treatment of melanoma. In a recent screen of compounds, we found that an organopalladium compound, Tris (dibenzylideneacetone) dipalladium (Tris DBA), showed significant antiproliferative activity against melanoma cells. Studies were carried out to determine the mechanism of action of Tris DBA.Experimental Design: Tris DBA was tested on efficacy on proliferation of human and murine melanoma cells. To find the mechanism of action of Tris DBA, we did Western blot and gene array analyses. The ability of Tris DBA to block tumor growth in vivo was assessed.Results: Tris DBA has activity against B16 murine and A375 human melanoma in vivo. Tris DBA inhibits several signaling pathways including activation of mitogen-activated protein kinase, Akt, Stat-3, and S6 kinase activation, suggesting an upstream target. Tris DBA was found to be a potent inhibitor of N-myristoyltransferase-1, which is required for optimal activity of membrane-based signaling molecules. Tris DBA showed potent antitumor activity in vivo against melanoma.Conclusion: Tris DBA is thus a novel inhibitor of N-myristoyltransferase-1 with significant antitumor activity and is well tolerated in vivo. Further preclinical evaluation of Tris DBA and related complexes is warranted.

Antiplatelet therapy with aspirin and clopidogrel is known to confer protection against ischemic events. Increasing numbers of patients are presenting for surgery while taking these drugs. This may lead to an increase in perioperative blood loss, particularly in those who have a heightened response to the drugs. Identifying these patients preoperatively would allow us to plan appropriate management.The antiplatelet effect of aspirin and/or clopidogrel was measured using two point-of-care monitors: the platelet function analyzer (PFA-100; Dade, Miami, FL) and the modified thromboelastograph (mTEG; Haemoscope Corp., Niles, IL). This was compared with optical light transmission aggregometry.All people taking aspirin displayed a definitive aspirin effect on aggregometry (n = 20). Ninety percent of these were identified by modified thromboelastography (n = 18). Seventy percent were identified by the platelet function analyzer (n = 14). Fifty percent of people taking clopidogrel displayed a definitive response to the drug on aggregometry. Seventy percent of these were identified on modified thromboelastography (n = 7). None were identified by the platelet function analyzer. There was good agreement between the results of the aggregometry and modified thromboelastography in clopidogrel patients (kappa = 0.81).The search for a point-of-care monitor of platelet function has been the focus of much research. This study has shown that the modified thromboelastograph can be used for monitoring the effect of clopidogrel as well as aspirin. It potentially has a wide scope to be used for the monitoring of effectiveness of therapy as well as a possible predictor of perioperative bleeding.

Impaired effectiveness of glucose to suppress endogenous glucose production (EGP) is an important cause of worsening hyperglycemia in type 2 diabetes. Elevated free fatty acids (FFAs) may impair glucose effectiveness via several mechanisms, including rapid changes in metabolic fluxes and/or more gradual changes in gene expression of key enzymes or other proteins. Thus, we examined the magnitude and time course of effects of FFAs on glucose effectiveness in type 2 diabetes and whether glucose effectiveness can be restored by lowering FFAs. Glucose fluxes ([3-3H]-glucose) were measured during 6-h pancreatic clamp studies, at euglycemia (5 mmol/l glucose, t = 0–240 min), and hyperglycemia (10 mmol/l, t = 240–360 min). We studied 19 poorly controlled subjects with type 2 diabetes (HbA1c 10.9 ± 0.4%, age 50 ± 3 years, BMI 30 ± 2 kg/m2) on at least two occasions with saline (NA− group) or nicotinic acid (NA group) infusions for 3, 6, or 16 h (NA3h, NA6h, and NA16h groups, respectively) to lower FFAs to nondiabetic levels. As a reference group, glucose effectiveness was also assessed in 15 nondiabetic subjects. There was rapid improvement in hepatic glucose effectiveness following only 3 h of NA infusion (NA3h = 31 ± 6% suppression of EGP with hyperglycemia vs. NA− = 8 ± 7%; P < 0.01) and complete restoration of glucose effectiveness after 6 h of NA (NA6h = 41 ± 8% suppression of EGP; P = NS vs. nondiabetic subjects). Importantly, the loss of hepatic glucose effectiveness in type 2 diabetes is completely reversible upon correcting the increased FFA concentrations. A longer duration of FFA lowering may be required to overcome the chronic effects of increased FFAs on hepatic glucose effectiveness.

Objectives: The Thromboelastogram (TEG; Haemoscope Corporation, Niles, IL) and the ROTEM thromboelastometry analyzer (Pentapharm GmbH, Munich, Germany) are coagulation monitors that measure the viscoelastic changes accompanying whole-blood coagulation generation and lysis. It is not clear whether TEG and ROTEM transfusion algorithms suggest similar blood component intervention. This study aims to report the extent to which administration of platelets, fresh frozen plasma, and cryoprecipitate would be indicated using protocol-dictated interventions by the Rotem, TEG, and conventional coagulation screens during orthotopic liver transplantation (OLT).Design: Prospective observational study.Setting: University hospital.Participants: Twenty patients undergoing orthotopic liver transplantation.Interventions: Coagulation was managed with native TEG protocols. Additional samples for kaolin TEG, kaolin heparinase TEG, Rotem in-TEM, Rotem hep-TEM, Rotem fib-TEM, full blood count, prothrombin time, and Clauss fibrinogen assays were taken at 5 fixed operative stages.Measurements and Main Results: Results were reviewed and protocol-indicated interventions recorded. There was moderate agreement between Clauss fibrinogen and Rotem fib-TEM assays about fulfilling fibrinogen transfusion criteria (kappa = 0.42, p

Background Epstein–Barr virus (EBV) is associated with the malignant transformation of B, T, and NK lymphocytes in humans, especially in immunosuppressed individuals. Objective We describe an unusual case confined to the skin in a 39-year-old African American female following a renal transplant. Methods Morphologically and immunophenotypically, the tumor was best classified as a plasmablastic lymphoma; however, the neoplastic population revealed rearrangements of both immunoglobulin heavy chain (IgG) and T cell receptor gamma (TCR-γ). In situ hybridization demonstrated the presence of Epstein–Barr early RNA species (EBER) in the lymphoma cells, consistent with EBV infection. Results We have previously demonstrated that EBV-induced reactive oxygen is associated with hypermethylation of the tumor suppressor gene p16 in Burkitt lymphoma, and that p16 hypermethylation is nearly always associated with EBV infection in Burkitt lymphoma. Limitations Further studies are needed to determine whether p16 is widely suppressed in immunosuppression-induced lymphoma. Conclusion In this study, we demonstrated high levels of hypermethylation of the tumor suppressor gene p16, thus supporting the role of EBV as a carcinogen in post-transplant lymphoproliferative disease.

Glucose effectiveness is impaired in type 2 diabetes. We hypothesize that chronic hyperglycemia and hyperlipidemia contribute importantly to this defect. To test this hypothesis, we compared the effect of acute hyperglycemia on glucose turnover in type 2 diabetic subjects in good control (GC) (n = 14, age 51.7 +/- 3.7 years, BMI 28.4 +/- 1.0 kg/ m(2), HbA(1c) 5.9 +/- 0.2%) and poor control (PC) (n = 10, age 50.0 +/- 2.5 years, BMI 27.9 +/- 1.5 kg/m(2), HbA(1c) 9.9 +/- 0.6%) with age- and weight-matched nondiabetic subjects (ND) (n = 11, age 47.0 +/- 4.4 years, BMI 28.5 +/- 1.0 kg/m(2), HbA(1c) 5.1 +/- 0.2%). Fixed hormonal conditions were attained by infusing somatostatin for 6 h with replacement of basal insulin, glucagon, and growth hormone. Glucose fluxes ([3-(3)H]glucose) were compared during euglycemic (5 mmol/l, t = 180-240 min) and hyperglycemic (Hy) (10 mmol/l, t = 300-360 min, variable glucose infusion) clamp intervals. Acute hyperglycemia suppressed hepatic glucose production (GP) by 43% and increased peripheral glucose uptake (GU) by 86% in the ND subjects. Conversely, GP failed to suppress (-7%) and GU was suboptimally increased (+34%) in response to Hy in the PC group. However, optimal glycemic control was associated with normal glucose effectiveness in GC subjects (GP -38%, GU +72%; P > 0.05 for GC vs. ND). To determine whether short-term correction of hyperglycemia and/or hyperlipidemia is sufficient to reverse the impairment in glucose effectiveness, five PC subjects were restudied after 72 h of normoglycemia ( approximately 100 mg/dl; variable insulin infusions). These subjects regained normal effectiveness of glucose to suppress GP and stimulate GU and in response to Hy (GP -47%, GU + 71%; P > 0.05 vs. baseline studies). Thus, chronic hyperglycemia and/or hyperlipidemia contribute to impaired effectiveness of glucose in regulating glucose fluxes in type 2 diabetes and hence to worsening of the overall metabolic condition. Short-term normalization of plasma glucose might break the vicious cycle of impaired glucose effectiveness in type 2 diabetes.