Pretibial Edema Research Articles

Puffy hand syndrome

A 45-year-old man presented to the rheumatology outpatient unit with bilateral swelling of the hands from the proximal segments of the fi ngers to the wrist that developed gradually over the past 3 years (fi gure). The oedema was non-pitting and was not aff ected by raising the hands. Function of the hands and fi ngers was not impaired. He had no generalised or pretibial oedema. The patient reported drinking 1–1·5 L of wine per day; medical history was otherwise unremarkable. Blood tests and an ultrasound scan confi rmed hepatitis (alanine aminotransferase [ALT] 175 IU/L, aspartate amino transferase [AST] 170 IU/L, albumin 4·68 mg/dL) with a positive antibody test for hepatitis C virus; hepatitis B virus and HIV tests were negative. Rheumatoid factor was 29 IU/mL (normal <14 IU/mL); anti-nuclear antibodies, anticitrullinated peptide antibodies, complement, protein electrophoresis, and total bilirubin were normal. On further questioning he admitted that he had been injecting high-dose sublingual buprenorphine for more than 5 years, preferentially in the wrist either into or around the veins, three to four times a day. Puff y hand syndrome is a complication of intravenous drug misuse. Users themselves are often aware of the risk, particularly from hand injections, but most physicians, including addiction specialists and general practitioners, rarely encounter this presentation and might not be familiar with it. The frequency of puff y hand syndrome is unknown. The pathogenesis of the oedema probably includes venous and lymphatic insuffi ciency, and the direct toxicity of injected drugs. Biopsy samples of skin and subcutaneous tissue and lymphangiograms can show destruction of the lymphatics that leads to fi brosis of the subcutaneous tissue, probably due to soluble compounds of the drugs that damage lymphatic vessels. Treatment with lowstretch bandaging and the wearing of elastic garments help to decrease the volume in puff y hand syndrome.

Clinical Characteristics of Overhydration in Patients with Idiopathic Edema

Background: Idiopathic edema (IE) is a common clinical syndrome. Designing treatment plans for IE is problematic because of the difficulty in assessing volume status. We aimed to evaluate volume status, measured by bioimpedance spectroscopy (BIS), and investigated clinical parameters associated with volume overload (VO) in patients with IE. Methods: Patients with IE were defined as those with symptomatic edema and without abnormal renal function or any other apparent cause of edema. A total of 124 patients were included. Overhydration (OH) and extracellular water (ECW) were calculated using BIS. Relative hydration status (ΔHS) was defined as OH/ECW. Patients were classified into 2 groups: overhydrated group (OG; ΔHS ≥7%) and non-OG (NOG; ΔHS <7). Simple and multiple logistic regression analyses were used to assess the influence of several variables on the incidence of VO. Results: Of 124 patients, 37 (29.8%) were in the OG. The proportion of men in the OG was higher than that in the NOG (p = 0.020). Patients in the OG showed more frequent pretibial pitting edema (PTPE, p < 0.001) and had lower hemoglobin (p = 0.008) and serum albumin levels (p < 0.001). The multivariate analysis showed that the presence of PTPE (OR 10.62, 95% CI 1.98-57.1), low serum albumin level (OR 0.01, 95% CI 0.00-0.25) and lower fat tissue index (OR 0.78, 95% CI 0.63-0.97) were independent risk factors for the presence of VO. Conclusions: BIS helps to identify volume status and body composition in patients with IE.

Hepatic Artery Pseudoaneurysm: A Life-Threatening Complication of Liver Transplantation.

Hepatic artery pseudoaneurysm is a rare but serious complication following liver transplantation. A 50-year-old male patient with ulcerative colitis, sclerosing cholangitis, and end-stage liver disease underwent right lobe transplantation from a living donor. The patient was hospitalized because of impairment in liver function tests and massive pretibial edema three months after surgery. In color Doppler ultrasound and multidetector computed tomography, a pseudoaneurysm with peripheral large thrombus was detected at the anastomosis site extending anterior to the hepatic artery. The patient died as a result of unstable hemodynamic conditions.

Pseudoaldosteronism induced by Yokukansan in an elderly Japanese type 2 diabetic patient with Alzheimer's disease.

The number of patients with Alzheimer's disease (AD), and/or behavioral and psychological symptoms of dementia (BPSD) has been markedly increasing all over the world, and has become a social and health problem. Furthermore, it has been recently established that the diabetic condition is a major risk factor for the development of dementia1. Second-generation antipsychotics have been used, but some cases are refractory2. Yokukansan is a licorice-containing Chinese medicine, and has been very often used for the treatment of such disease3. A previous report showed that Yokukansan exerts beneficial effects and can be used very safely3. It is known that a large amount of licorice could induce pseudoaldosteronism, but Yokukansan contains only a small amount of licorice. Therefore, it has been thought that the use of Yokukansan does not lead to the onset of pseudoaldosteronism. However, here we report a case of pseudaldosteronism that developed after starting Yokukansan in an elderly Japanese diabetic patient with AD and BPSD. In February 2013, a 77-year-old Japanese man with type 2 diabetes was admitted to the Kawasaki Medical School, Kurashiki, Japan, because of hypokalemia and weight gain. He had been taking Yokukansan for 5 months (7.5 g/day containing 1.5 g of licorice). He frequently felt general fatigue, and his bodyweight was increased by 7 kg. On admission, his bodyweight was 64.3 kg and height 160.5 cm. He did not have vomiting or diarrhea and did not use any diuretics. Physical examination revealed mild systolic hypertension. Marked pretibial pitting edema was observed in the bilateral lower extremities. Table​Table11 shows the laboratory findings on admission. Serum potassium was 3.0 mEq/L with mild renal dysfunction. The low-renin and low-aldosterone state was observed with concomitant metabolic alkalosis. In addition, the transtubular potassium gradient (TTKG) was very high (11.0). Given these findings, we made the diagnosis of Yokukansan-induced pseudoaldsteronism, and stopped this drug. After commencement of oral potassium replacement, potassium level was increased (3.8 mEq/L at day 10) and TTKG was decreased to 3.5. Pitting edema disappeared with 6-kg weight reduction. On day 20, he was discharged from the hospital. Table 1 Laboratory findings on admission Recently, Yokukansan has been very often used for dementia, and its sales amount has been drastically increasing. It has been thought that Yokukansan can be used very safely3. To the best of our knowledge, this is the first report showing that Yokukansan induced pseudoaldosteronism in diabetic patients. The mechanism of how licorice causes pseudoaldosteronism is likely through the inhibition of renal enzyme 11-hydroxysteroid dehydrogenase type 2. Cortisol, as well as aldosterone, can bind to the mineralocorticoid receptor (MR), but, 11-hydroxysteroid dehydrogenase type 2 converts cortisol to cortisone that does not work on MR. As a result, aldosterone dominantly binds to MR4. However, licorice inactivates 11-hydroxysteroid dehydrogenase type 2 and increases the cortisol binding to MR, which explains the mechanism for licorice-induced pseudoaldosteronism. It is known that the onset of pseudoaldosteronism depends on the dose of licorice, but the present case developed pseudoaldosteronism with a very low dose of licorice (1.5 g/day). In fact, a similar frail and elderly female case of Yokukansan-induced pseudoaldosteronism with severe hypokalemia was reported by Nishiya et al.5 Thereby, we should pay careful attention when using Yokukansan, even with a low-dose component of licorice. Taken together, we should consider the possibility of pseudoaldosteronism when we use Yokukansan for dementia, and careful monitoring of electrolytes, especially potassium, is necessary.

Severe Pancreatitis Exacerbation in a Perinatal Patient with Severe Preeclampsia

<h2>Poster Presentation</h2><h3>Background</h3> Pancreatitis in pregnancy is rare, and when complicated, mortality may exceed 10%. The subject of this case report also had severe preeclampsia, which stimulated discussion of the new guidelines from the Task Force on Hypertension in Pregnancy. This poster presentation will provide education about a rare condition and also review important points in the hypertension guidelines. <h3>Case</h3> The woman presented at 39 weeks gestation with abdominal pain, nausea, and vomiting but no scotoma or headache. Her blood pressure was 180–190/110–120. Labs were unremarkable, except for lipase, which was >4000 (normal 20–300). Prior to pregnancy her lipase was 9500, and pancreatectomy and islet cell transplantation were recommended, but she did not follow up. Instead, the woman had been using narcotics daily at home via a peripherally inserted central catheter (PICC). She was treated for preeclampsia with antihypertensives and magnesium sulfate. Consults were ordered with pain management, surgery, gastroenterology, maternal‐fetal medicine (MFM), and neonatology. The attending physician on call wanted to perform an emergency cesarean, but MFM recommended stabilization, and the surgery consult concurred. A male was born with a tight nuchal cord, was intubated, and was transported to the neonatal intensive care unit (NICU). The woman's postpartum course consisted primarily of nutrition support and pain management, but on postpartum Day 3 she needed a transfusion due to hemoglobin of 6.1. On Day 6, creatinine levels rose to 1.7 and her blood pressure became elevated again, so a nephrology consult was added. On Day 7, she developed a headache and 3+ pretibial edema, so magnesium sulfate was restarted. The newborn underwent body cooling due to hypoxic ischemic encephalopathy but was discharged at 12 days of life in stable condition. The woman was finally discharged on postpartum Day 15, with oral analgesics and on total parenteral nutrition. She was to follow up with the same specialists who recommended the pancreatectomy. <h3>Conclusion</h3> Pancreatitis is an inflammatory state that can cause respiratory failure, renal failure, and cardiac complications due to the pancreatic enzymes being released into the circulation. Treatment is to alleviate the inflammation and symptoms. Perinatal nurses need to know that a more typically seen condition in pregnancy‐gallbladder disease can precipitate pancreatitis. Two points that stood out in this scenario were the insistence on stabilization of the woman prior to cesarean, which is always recommended in the literature but not always practiced. Second, magnesium sulfate was restarted because of an earnest attempt at our institution to follow the taskforce guidelines.

Predictors of lower-extremity amputation in patients with an infected diabetic foot ulcer.

Infection commonly complicates diabetic foot ulcers and is associated with a poor outcome. In a cohort of individuals with an infected diabetic foot ulcer, we aimed to determine independent predictors of lower-extremity amputation and the predictive value for amputation of the International Working Group on the Diabetic Foot (IWGDF) classification system and to develop a risk score for predicting amputation. We prospectively studied 575 patients with an infected diabetic foot ulcer presenting to 1 of 14 diabetic foot clinics in 10 European countries. Among these patients, 159 (28%) underwent an amputation. Independent risk factors for amputation were as follows: periwound edema, foul smell, (non)purulent exudate, deep ulcer, positive probe-to-bone test, pretibial edema, fever, and elevated C-reactive protein. Increasing IWGDF severity of infection also independently predicted amputation. We developed a risk score for any amputation and for amputations excluding the lesser toes (including the variables sex, pain on palpation, periwound edema, ulcer size, ulcer depth, and peripheral arterial disease) that predicted amputation better than the IWGDF system (area under the ROC curves 0.80, 0.78, and 0.67, respectively). For individuals with an infected diabetic foot ulcer, we identified independent predictors of amputation, validated the prognostic value of the IWGDF classification system, and developed a new risk score for amputation that can be readily used in daily clinical practice. Our risk score may have better prognostic accuracy than the IWGDF system, the only currently available system, but our findings need to be validated in other cohorts.

Huge Intravascular Tumor Extending to the Heart: Leiomyomatosis.

Intravenous leiomyomatosis (IVL) is a rare neoplasm characterized by histologically benign-looking smooth muscle cell tumor mass, which is growing within the intrauterine and extrauterine venous system. In this report we aimed to present an unusual case of IVL, which is originating from iliac vein and extended throughout to right cardiac chambers. A 49-year-old female patient, who was treated with warfarin sodium due to right iliac vein thrombosis, was admitted to our department with intermittent dyspnea, palpitation, and dizziness. Physical examination was almost normal except bilateral pretibial edema. On magnetic resonance venography, there was an intravenous mass, which is originated from right internal iliac vein and extended into the inferior vena cava. Transthoracic echocardiography and transesophageal echocardiography revealed a huge mass extending from the inferior vena cava through the right atrium, with obvious venous occlusion. Thoracic, abdominal, and pelvic MR showed an intravascular mass, which is concordant with leiomyomatosis. Surgery was performed through median sternotomy. A huge mass with 25-cm length and 186-gr weight was excised through right atrial oblique incision, on beating heart with cardiopulmonary bypass. Histopathologic assessment was compatible with IVL. Exact strategy for the surgical treatment of IVL is still controversial. We used one-stage approach, with complete resection of a huge IVL extending from right atrium to right iliac vein. In such cases, high recurrence rate is a significant problem; therefore it should be kept in mind.

A Rare Primary Liver Tumor That Responded to Sorafenib

A Rare Primary Liver Tumor That Responded to Sorafenib

Atypical Manifestation of Whipple’s Disease

Introduction: Whipple’s disease is a multi-system, chronic infectious disease with a classic presentation of recurrent arthralgias/arthritis, weight loss, and diarrhea. Diagnosis can be challenging in patients with atypical presentations. We share our experience of pulmonary manifestations as the presenting symptoms. A 59-year-old African American male with a history of seronegative inflammatory polyarthritis, chronic smoking, and remote alcohol dependence presented with nonproductive cough, chest pain, and shortness of breath for 3 weeks. The review of system revealed intermittent non-bloody diarrhea, leg swelling, abdominal pain at right upper and right lower abdomen, and a 10-pound weight loss. Exam was pertinent for no fever, mild tachycardia of 110 beats/minute, and no desaturation. He had bibasilar crackles and wheezing, abdominal tenderness without signs of peritoneal irritation, bilateral pretibial pitting edema, and bilateral inguinal lymphadenopathy. Labs showed new microcytic anemia (hemoglobin 10 g/dL, MCV 78 fl, low iron 28 mcg/dL, normal TIBC 283 mcg/dL, low iron saturation 10%, and ferritin 85 ng/mL) normal liver enzymes except mildly elevated alkaline phosphatase (174 U/L), and hypoalbuminemia (2.9 g/dL). Imaging studies showed a small pleural effusion, granuloma in the right upper lung field, diffuse anasarca, and generalized lymphadenopathy. Other investigations for a rheumatologic condition, chronic infection, and malignancy were all negative. He underwent upper endoscopy for the unexplained microcytic anemia and weight loss, which revealed marked chronic active gastritis with focal intestinal metaplasia in the antrum and prepyloric region, and a macroscopically normal duodenum. Ileo-colonoscopy showed only 2 3-5-mm tubular adenoma without dysplasia in the transverse and descending colon. Duodenal biopsies revealed focal collections of histiocytes within the superficial lamina propria with widening and flattening of the villi. Periodic acid-Schiff (PAS) was positive and immunohistochemical stains for Trepheryma whipplei were strongly positive. His pulmonary symptoms, diarrhea, weight loss, joint pain, and hypoalbuminemia were resolved at 3 weeks after initiation of antibiotics. Pulmonary involvement is an uncommon presentation of Whipple’s disease, and duodenal biopsies with PAS staining is indicated in suspected cases, even in the absence of profound gastrointestinal symptoms. Whipple’s disease can be fatal without treatment, but is responsive to a prolonged course of antibiotic treatment.

PO-0787 Congenital Nephrotic Syndrome Of The Finnish Type – A New Mutation Enters The Scene

Background Nephrin was first identified in 1998. The Congenital Nephrotic Syndrome of the Finnish type is an autosomal recessive transmitted disease caused by a mutation in the NPHS1 gene that codifies nephrin. The clinical manifestations appear in the first three months of life and progress to end stage renal failure. Clinical case A seven weeks-old boy with normal grow and psycho-motor development was admitted to the emergency room with vomiting, diarrhoea and mild bilateral pretibial oedema. Laboratory data revealed anaemia, thrombocytosis, normal serum creatinine and urea, normal Na + , K + , pH and HCO 3 - , hypoalbuminemia and proteinuria (263 mg/m 2 /day). The renal biopsy suggested a Congenital Nephrotic Syndrome of the Finnish type or mesangial sclerosis. The patient was treated with indomethacin and captopril for proteinuria without response. The genetic study confirmed the presence of the IVS9+4 (A >G) variant in homozygosity in the NPHS1 gene. His parents, first-degree cousins, had the same mutation in heterozygosity. The renal disease progressed to end stage renal failure at the age of four years-old. He was supported by continuous ambulatory peritoneal dialysis until the age of six, when he was successfully transplanted with a cadaveric kidney graft. Conclusions The role of nephrin in the glomerular filtration and stability of the podocytes is unequivocally established. The Congenital Nephrotic Syndrome of the Finnish type, initially found in Finnish families, is present in other areas of the world. The identification of a new mutation in the NPHS1 gene reflects the great variability in the mutations associated with the disease.

PP-321 Right Ventricle Myocarditis due to Acute Cholecystitis

Inflammatory changes at the neighbouring tissues of heart can mimic cardiac pathologies. Acute cholecystitis, acute pancreatitisand pneumonia can make some electrocardiography (ECG) changes and most of the time the clinical course goes benign. Here, we present a case diagnosed with right ventricular myocarditis and right heart failure due to acute cholecystitis.Case ReportA 61 year old, male patient with a history of hypertension and coronary artery disease was preparing for elective cholecystectomy after a cholecystitis episode at general surgery clinic. He was consulted to cardiology for sudden onset, severe upper abdominal pain with ECG changes. ECG showed marked ST segment elevation in V 1-2 leads and right precordial leads (Figure 1). The patient underwent an urgent coronary angiography which revealed there was no obstructive coronary lesion. The echocardiography showed dilated right ventricle, moderate tricusbid regurgitation, mild pericardial effusion and normal left ventricular functions. Partial oxygen and carbondioxide pressures were normal at arterial blood gas, D-dimer level was at upper limit of normal values. Thorax CT angiography was performed to exclude pulmonary embolism and no thrombus formation detected. Cardiac markers (CKMB and troponin) were risen significantly and decreased at follow up that was supporting myocardial injury. At clinical follow up, symptomatic right heart failure developed (three positive pretibial oedema, hepatic congestion and jugular venous distension) and the patient treated for symptomatic right heart failure. At first month follow up, control echocardiography revealed impressive recovery of right ventricle functions and the patient had no symptom or complaint about right heart failure.Discussion Inflammatory changes at the neighbouring tissues of heart can mimic cardiac pathologies. Acute cholecystitis, acute pancreatitisand pneumonia can make some electrocardiography (ECG) changes and most of the time the clinical course goes benign. Here, we present a case diagnosed with right ventricular myocarditis and right heart failure due to acute cholecystitis. Case ReportA 61 year old, male patient with a history of hypertension and coronary artery disease was preparing for elective cholecystectomy after a cholecystitis episode at general surgery clinic. He was consulted to cardiology for sudden onset, severe upper abdominal pain with ECG changes. ECG showed marked ST segment elevation in V 1-2 leads and right precordial leads (Figure 1). The patient underwent an urgent coronary angiography which revealed there was no obstructive coronary lesion. The echocardiography showed dilated right ventricle, moderate tricusbid regurgitation, mild pericardial effusion and normal left ventricular functions. Partial oxygen and carbondioxide pressures were normal at arterial blood gas, D-dimer level was at upper limit of normal values. Thorax CT angiography was performed to exclude pulmonary embolism and no thrombus formation detected. Cardiac markers (CKMB and troponin) were risen significantly and decreased at follow up that was supporting myocardial injury. At clinical follow up, symptomatic right heart failure developed (three positive pretibial oedema, hepatic congestion and jugular venous distension) and the patient treated for symptomatic right heart failure. At first month follow up, control echocardiography revealed impressive recovery of right ventricle functions and the patient had no symptom or complaint about right heart failure. A 61 year old, male patient with a history of hypertension and coronary artery disease was preparing for elective cholecystectomy after a cholecystitis episode at general surgery clinic. He was consulted to cardiology for sudden onset, severe upper abdominal pain with ECG changes. ECG showed marked ST segment elevation in V 1-2 leads and right precordial leads (Figure 1). The patient underwent an urgent coronary angiography which revealed there was no obstructive coronary lesion. The echocardiography showed dilated right ventricle, moderate tricusbid regurgitation, mild pericardial effusion and normal left ventricular functions. Partial oxygen and carbondioxide pressures were normal at arterial blood gas, D-dimer level was at upper limit of normal values. Thorax CT angiography was performed to exclude pulmonary embolism and no thrombus formation detected. Cardiac markers (CKMB and troponin) were risen significantly and decreased at follow up that was supporting myocardial injury. At clinical follow up, symptomatic right heart failure developed (three positive pretibial oedema, hepatic congestion and jugular venous distension) and the patient treated for symptomatic right heart failure. At first month follow up, control echocardiography revealed impressive recovery of right ventricle functions and the patient had no symptom or complaint about right heart failure. Discussion

Pregabalin in the therapy of Generalized Anxiety Disorder

Generalized Anxiety Disorder (GAD) is among the most common psychiatric disorders. World Psychiatric Biological Treatment of GAD, WFBS (2009) recommend SSRI (Serotonin Selective Reuptake Inhibitors), Selective Serotonin and Norepinephrine Reuptake inhibitors (SNRI) and pregabalin as first line treatment. Unfortunately, any psychopharmaceutical treatment option can demonstrate side effects. What are the treatment possibilities? Must adverse events always be the reason for discontinuation of a highly efficacious therapy? This is the case of female 39 year old patient. The patient was admitted to our psychiatric clinic and was hospitalized from March 1 to April 4 2013. Before hospitalization, she had been treated by a psychiatrist due to diagnosis of Generalized Anxiety Disorder, for three years. Her ain symptoms were nervousness, irrational fears, problems with concentration and dysfunctionality. In addition, her appetite and sleep were disturbed. Before hospitalization, the patient had been treated with sertraline, escitalopram and paroxetine, all at adequate therapeutic doses. Remission was incomplete, with a few residual symptoms (tension, lack of concentration). Four months before hospitalization, the patient complained of intolerable tension, she quivered with an indefinite fear that something bad would happened to her family. In this period, she could not sleep and lost 7 kg within a month. Two days before admission, she attempted suicide by hanging. During hospital admission, patient was tense, complained of nervousness and agitation. She stated that nothing made her happy. She had lachrymose, shivered and lacked appetite. In addition, the patient could not sleep at night, felt unlucky and had suicidal ideation. As therapy with SSRIs had not achieved complete remission, 75 mg of pregabalin was introduced into the treatment, along with sertraline, for three days; the dose was titrated up to 225 mg/day . Sertraline was gradually discontinued. After a week, the symptoms lessened. The patient did not complain of tension, she started to sleep well, her appetite improved and there was no fear or suicidal ideation. During the second week, the patient complained of more prominent pretibial edema which did not improve when the limb was elevated. Extensive diagnostics were performed and all the results were within normal ranges (blood glucose, liver enzymes, kidney function markers, abdominal and pelvic minor ultrasound, gynecological exam, Doppler exam of blood vessels in the legs). Gradually, the pregabalin dose was decreased to 75 mg, and sertraline was reintroduced into the treatment (100mg/day) . After this correct ion in pharmacotherapy, the swelling disappeared. The remission of the patient was sustained, so the patient was discharged as recovered. Pregabalin showed a satisfying therapeutic effect. Luckily, the peripheral edema adverse effect disappeared, when the dosage was reduced so that it still could be included in the pharmacotherapy. In this case, compliance was good and the result was a full remission, as the patient and the doctor both decided to continue with this successful pharmacotherapy.

A Case of Sarcoidosis Presenting as Cirrhosis and Portal Hypertension

Sarcoidosis is a systemic granulomatous disease of unknown etiology that can involve nearly all organs. Liver is the third most commonly affected organ following the lungs and the lymph nodes. Cases with liver sarcoidosis are usually silent clinically while a few can progress to cirrhosis and portal hypertension in less than 1% of the patients. A 56 year old female was referred for ecchymosis, protuberant abdomen, bilateral pretibial and ankle edema. Medical history did not reveal any previous disease. Ascites, hepatomegaly, splenomegaly, and facial telengiectasies were present on physical examination. Chest x-ray and CT were normal. Papules and plaques on the knees developed six days after admission. Skin biopsy revealed granulomatous dermatitis. Serum ACE was 250 IU/L. Liver biopsy showed non-caseiting granulomas, severe hepatitis and fibrosis. Sarcoidosis was confirmed based on high serum ACE, histopathologic findings of the skin and liver biopsy samples that revealed non-caseiting granulomas. We report a case of sarcoidosis complicated by cirrhosis as the initial manifestation of the disease without lung involvement. An extensive literature review of sarcoidosis, Case Study British Journal of Medicine & Medical Research, 4(25): 4272-4277, 2014 4273 focusing on case reports, which presented with cirrhosis and portal hypertension without lung involvement, was made.

Pitting type of pretibial edema in a patient with silent thyroiditis successfully treated by angiotensin II receptor blockade

Patient: Female, 56Final Diagnosis: Thyroiditis – silentSymptoms: Palpitations • pretibial pitting edema • short of breath • sweatingMedication: —Clinical Procedure: —Specialty: Endocrinology and MetabolicObjective:Unknown etiologyBackground:Hyper- or hypothyroidism sometimes causes pretibial myxedema characterized by non-pitting infiltration of a proteinaceous ground substance. However, in those patients, the “pitting” type of pretibial edema as a result of increased sodium and fluid retention or vascular hyper-permeability rarely occurs, except in cases complicated by heart failures due to severe cardiomyopathy or pulmonary hypertension.Case Report:A 56-year-old woman developed bilateral pretibial pitting edema, followed by occasional sweating, palpitations, and shortness of breath, which persisted for more than 2 months. The diagnosis of hyperthyroidism due to silent thyroiditis was supported by elevated levels of free thyroxine (T4) and triiodothyronine (T3), with a marked decrease in thyroid-stimulating hormone (TSH), and the negative results for TSH receptor antibodies with typical findings of destructive thyrotoxicosis. Despite her “pitting” type of pretibial edema, a chest radio-graph demonstrated the absence of cardiomyopathy or congestive heart failure. Oral administration of angiotensin II receptor blocker (ARB) was initiated for her systolic hypertension, with a relatively higher elevation of plasma renin activity compared to that of the aldosterone level. Although the symptoms characteristic to hyperthyroidism, such as increased sweating, palpitations and shortness of breath, slowly improved with a spontaneous resolution of the disease, ARB quickly resolved the pretibial pitting edema shortly after the administration..Conclusions:In this case, increased activity of the renin-angiotensin-aldosterone system stimulated by thyroid hormone was likely responsible for the patient’s pitting type of edema. The pharmacological blockade of the renin-angiotensin-aldosterone system was thought to be effective for the quick resolution of the symptom.

Constrictive pericarditis in a young patient with very thick pericardium initially diagnosed as cirrhosis

Constrictive pericarditis (CP) is a disease of pericardium that restricts filling of the heart. Patients with CP generally present to hospitals with exercise-induced dyspnea, pretibial edema and abdominal ascites, and it is sometimes mistakenly diagnosed as liver or renal disease. Pericardial thickening, which is defined as more than 4 mm in diameter, is observed in nearly 80% of patients. In the present paper, we describe a case of CP with a pericardial thickness of 12 mm that was initially diagnosed as cirrhosis.

Tolvaptan was Effective to Dilated Cardiomyopathy with Amiodarone Lung Damage: A Case Report

A 40-year-old man with orthopnea visited our hospital. Physical examination revealed wheeze, pretibial edema. Chest X-rays showed cardiac enlargement and pulmonary congestion. The echocardiography showed the left ventricular dilatation with diffuse severe hypokinesis(EF 16%). Coronary angiography was normal. Myocardial biopsy showed the slight fibrosis. Laboratory data indicated no other secondary cardiomyopathy. Based on these findings, a diagnosis of idiopathic dilated cardiomyopathy was considered. Administrations of dobutamine and intravenous furosemide were started and weight was decreased and cardiac status was compensated. After administration of low dose bisoprolol with milrinone, nonsustained ventricular tachycardia was detected. Oral administration of amiodarone had started. After several days, dyspnea and oligouria was appeared and chest X-rays revealed congestion,again. We stopped bisoprolol because we considered that its negative inotropic effect induced congestion. We restarted dobutamine and intravenous furosemide, but the therapy was not effective in spite of no significant changing in blood pressure, cardiac function, renal function, and estimated intravascular volume. An administration of tolvaptan (15mg/day) was started,which induced the marked increase of urine volume and improvement of symptom, but X-ray findings were not completely reversed. Chest CT showed interstitial filtration and a diagnosis of amiodarone lung damage was considered. After steroid therapy, interstitial shadow began to disappeared and we could stop dobutamine and intravenous furosemide. We report a case about dilated cardiomyopathy with amiodarone lung damage, to which tolvaptan was effective.

Constrictive Pericarditis After Renal Transplantation: Three Case Reports

IntroductionPericardial exposure can be see in chronic kidney disease, but constrictive pericarditis (CP) development, which is usually present with signs of right-sided heart failure is rare. In renal transplant recipients CP can lead to graft dysfunction and serious liver disease. We present herein 3 such CP patients. Patient 1A 37-year-old male patient with end-stage renal disease (ESRD) due to membranoproliferative glomerulonephritis was on chronic hemodialysis (HD). He underwent living donor kidney transplantation in 1995. In 2006 he was admitted with complaints of shortness of breath, weakness, and abdominal distention. Patient 2A 17-year-old male patient with ESRD due to vesicoureteral reflux had 6 months of HD and underwent living donor kidney transplantation in 2008. Six months after transplantation, he showed leg edema, massive ascites, hepatosplenomegaly, and pretibial edema. Patient 3A 52-year-old male patient was 21 years after HD initiation when cadaveric donor kidney transplantation was performed in August 2011. Four months after transplantation, he presented with a shortness of breath and fatigue. Echocardiography revealed 2–3 degree aortic regurgitation and increased pericardial brightness. ConclusionAll patients underwent right-sided heart catheterization, leading to a diagnosis of constrictive pericarditis, requiring total pericardiectom. Pathological examination of the pericardium showed typical diffuse fibrosis.

Mood‐dependent changes of serum lithium concentration in a rapid cycling patient maintained on stable doses of lithium carbonate

Serum lithium levels may be influenced by mood state. We report on a 58-year-old female patient suffering from rapid cycling bipolar disorder. Her serum lithium levels varied greatly, despite stable medication. The patient was observed over a one-year period. The patient received a stable medication of lithium carbonate (450 mg), valproate (1500 mg), and clozapine (200 mg). Investigating mood and serum lithium levels over one year revealed six manic and six depressive phases. The mean lithium serum level was 0.67 mmol/L in the depressive states, 0.39 mmol/L in the manic states (t = 4.11, p = 0.001 versus depression), and 0.40 mmol/L in the euthymic states (t = 3.58, p = 0.003 versus depression). Noncompliance was ruled out. The patient gained up to 8 kg during manic phases, accompanied by pretibial edema. Changes in serum lithium concentration are probably not caused by altered lithium, but by water metabolism. During mania, body water increases, leading to dilution and therefore a reduction in serum lithium levels. As there is no proof for any other known cause of hypervolemia, we propose the hypothesis that the increase in body water is due to a variant of idiopathic edema.

Comparative study of sitagliptin with pioglitazone in Japanese type 2 diabetic patients: the COMPASS randomized controlled trial

To compare the efficacy and safety of these two agents and the impact on surrogate markers related to diabetic complications in Japanese type 2 diabetic patients. In a multicenter, open-label trial, 130 patients whose diabetes had been inadequately controlled (HbA1c, 6.9-9.5%) with metformin and/or sulphonylurea were randomly assigned to a sitagliptin group (50 mg/day) or a pioglitazone group (15 mg/day) and were followed up for 24 weeks. At 16 weeks, if the patient's HbA1c level was ≥6.5%, the dose of sitagliptin or pioglitazone was increased up to 100 or 30 mg/day, respectively. Main outcome measure was the difference in the mean changes in the HbA1c level from baseline at 24 weeks between these two groups. Of the 130 patients who were enrolled, 115 subjects (sitagliptin group: 58 patients, pioglitazone group: 57 patients) completed this trial. At 0 weeks, the mean HbA1c level was 7.47 ± 0.66% in the sitagliptin group and 7.40 ± 0.61% in the pioglitazone group. At 24 weeks, the mean changes in the HbA1c level from baseline were -0.86 ± 0.63% versus -0.58 ± 0.68% (p = 0.024). Hypoglycaemia (2 patients, 3.4% vs. 2 patients, 3.5%), gastrointestinal symptoms (3 patients, 5.2% vs. 1 patient, 1.8%) and pretibial oedema (0 patients, 0% vs. 39 patients, 68.4%, p < 0.001) were observed for 24 weeks. Sitagliptin was not only more tolerable, but also more effective than pioglitazone in Japanese type 2 diabetic patients who had been treated with metformin and/or sulphonylurea.

Revisiting amlodipine induced pedal edema: a student's perspective

Amlodipine, a dihydropyridine, is used frequently used in the treatment of hypertension and angina pectoris. The drug acts by blocking the L-gated calcium channels which causes the blood vessels to relax. It's taken orally and excreted through the urine like many other drugs. Calcium channel blockers are usually well tolerated but as always exceptions always exist. Common side effects are constipation, dizziness, flushing, and pre-tibial edema. Pre-tibial edema has been a very common side effect that has lead the drug to be withdrawn in some patients therapy.