High serum zinc and serum testosterone levels were associated with excessive erythrocytosis in men at high altitudes

Chronic mountain sickness (CMS), a lack of adaptation to altitude characterized by excessive erythrocytosis (EE), is a health problem associated with life at high altitude. The erythropoietic process is regulated by both erythropoietin and testosterone. Zinc (Zn) is known to be related with testosterone and hemoglobin levels; meanwhile, nitric oxide was also associated with adaptation to high altitude. The aim of this study was to determine the relationship of hemoglobin and CMS score with serum levels of zinc, total testosterone (TT), calculated free testosterone (cFT), bioavailable testosterone (BAT), hemoglobin, and nitric oxide in men at high altitude with or without EE. Men residing in Lima (150?m) and Cerro de Pasco (4,340?m), Peru, were divided into three groups: (1) low altitude, (2) high altitude without EE (hemoglobin?相似文献   

Distinct increase in hematocrit associated with paroxysm of atrial fibrillation

In a previous study we found that hemoconcentration, which was identified by an increase in hematocrit, occured during a paroxysm of atrial fibrillation. In the present study we investigated the changes in hematocrit from sinus rhythm to paroxysm in 10 patients who had multiple paroxysms of atrial fibrillation in order to assess the ranges of the changes in hematocrit among the paroxysms. In these patients hematocrit was measured simultaneously with electrocardiographic recording during 3 or more paroxysms and sinus rhythm just before each paroxysm. The changes in hematocrit varied among the paroxysms. The maximum increase in hematocrit in each patient ranged from 3.5 to 8.0 points with an average of 5.1 points. Such a distinct increase in hematocrit which abruptly develops with a paroxysm of atrial fibrillation may be a potential risk for thrombus formation.     

Spontaneous increase in erythropoietin and hematocrit value associated with transient liver enzyme abnormalities in an anephric patient undergoing hemodialysis

An anephric patient undergoing hemodialysis experienced an increase in his hematocrit value (19 ± 1 per cent to 31 ± 1 per cent) as a result of increased erythropoiesis (reticulocyte count 1.8 per cent to 7.4 per cent). This increase occurred in concert with an elevation of the patient's liver enzyme levels and was maintained for four months. The hematocrit value returned to its base line only after the liver function tests showed improvement. During the period when the hematocrit value was increasing, the circulating level of erythropoietin was elavated to 71.0 mU/ml—a level higher than that seen in either anephric or nephric patients undergoing dialysis. When the hematocrit value and liver enzyme levels had returned to their base line values, the erythropoietin level was 4.3 mU/ml—a level in the range seen in anephric patients undergoing dialysis. The observations in this patient suggest that under certain circumstances, the liver can produce erythropoietin in the anephric patient; and, more importantly, that the bone marrow of at least some uremic patients is capable of responding to the endogenous erythropoietin.     

A patient with intravascular lymphoma presenting with cerebral infarction and a high serum MPO-ANCA level

A 74-year-old woman presented with multiple brain infarctions, an inflammatory reaction, and a high serum titer (414 U/ml) of myeloperoxidase-specific antineutrophil cytoplasmic antibody (MPO-ANCA) with no hematological abnormalities. After the inflammation and ANCA titers were resolved with steroid therapy for suspected microscopic polyangiitis, hemophagocytic syndrome developed. Biopsies revealed non-Hodgkin’s intravascular lymphoma (IVL). The flare of IVL with negative serum ANCA suggested that the initial high serum MPO-ANCA had not originated from tumor cells.     

A patient with intravascular lymphoma presenting with cerebral infarction and a high serum MPO-ANCA level

Abstract

A 74-year-old woman presented with multiple brain infarctions, an inflammatory reaction, and a high serum titer (414 U/ml) of myeloperoxidase-specific antineutrophil cytoplasmic antibody (MPO-ANCA) with no hematological abnormalities. After the inflammation and ANCA titers were resolved with steroid therapy for suspected microscopic polyangiitis, hemophagocytic syndrome developed. Biopsies revealed non-Hodgkin’s intravascular lymphoma (IVL). The flare of IVL with negative serum ANCA suggested that the initial high serum MPO-ANCA had not originated from tumor cells.     

Case report of a patient with pseudohypoparathyroidism associated with slight increase in serum level of unconjugated bilirubin

We treated a 29-year-old male patient with pseudohypoparathyroidism type I, who showed a slight increase in serum indirect bilirubin without any signs of liver dysfunction. Serum levels of total, direct and indirect bilirubins were 2.4, 0.7 and 1.7mg/dl, respectively (normal ranges: 0.2-0.8, 0-0.2 and 0.2-0.6mg/dl, respectively). The cause of the increases in serum bilirubin levels was not clear; however, hemolytic anemia, hereditary unconjugated hyperbilirubinemia or ineffective erythropoiesis were ruled out as causes for the increase, since 1) his serum level of haptoglobin was normal, 2) increase in serum level of indirect bilirubin 120 minutes after the infusion of 50mg nicotinic acid was within the normal range, and 3) severe anemia was not observed. Osmotic fragility of his circulating red blood cells was also within normal range. Three other patients with pseudohypoparathyroidism visiting our clinic also showed slightly high levels of serum indirect bilirubin, although four outpatients with idiopathic hypoparathyroidism showed no such abnormality. Abnormality in the responsiveness to parathyroid hormone and/or to that in the cyclic AMP productivity in this disease may cause the increase in the circulating unconjugated bilirubin.     

Cerebral infarction in a patient with congenital complete heart block

Stokes-Adams attacks are fairly common in children with congenital complete heart block, but the occurrence of cerebral infarction is quite unusual. We present the case of a 13-year-old boy with congenital heart block and an embolic stroke involving the cerebral artery. Echocardiography revealed no valvular regurgitation, hypokinetic segments, mural thrombus, or myxoma. Electrocardiographic monitoring demonstrated good response of ventricular rate to exercise and no episodes of atrial or ventricular dysrhythmia. It is assumed that embolism occurred due to bradycardia.     

Multiple renal infarction associated with lupus anticoagulant in a patient with systemic lupus erythematosus]

We report a rare case with multiple renal infarction associated with lupus anticoagulant and SLE. A 20-year old woman presented with remitent fever, butterfly rash and, abdominal pain. Laboratory findings showed leukopenia, positive antinuclear and anti-DNA antibodies, and biological false positive for syphilis. Despite a therapy with prednisolone 25 mg/day, the patient showed hypocomplementemia, high titer of anti-DNA antibody and a development of proteinuria and an elevation of serum creatinine. Renal biopsy revealed no abnormalities. She presented abdominal pain with an elevation of serum LDH. Abdominal dynamic computed tomography demonstrated multiple perfusion defects in both kidneys indicating multiple renal infarction. Brain MRI showed multiple micro infarction in the anterior lobes. She was treated with 80 mg of aspirin and have been in remission for two years. Although there have been reported 18 cases with renal infarction associated with antiphospholipid syndrome, this is the first report in Japan. Renal infarction should be differentiated from renal involvement in patients with SLE who have antiphospholipid antibodies.     

A case of pneumonitis possibly due to isocyanate associated with high levels of serum KL-6]

A 47-year-old automobile painter developed dry cough, chills and dyspnea after four months of painting work. The spray contained isocyanates (HDI). A chest radiograph showed bilateral ground-glass shadows. The serum KL-6 level was very high: 11,100 U/ml. Marked lymphocytosis and a striking decrease in the CD4/CD8 ratio were observed in the bronchoalveolar lavage fluid. Transbronchial lung biopsy specimens showed alveolitis and bronchiolitis. Cessation of exposure to isocyanates improved the symptoms and laboratory data. We suspected that the patient was suffering from hypersensitivity pneumonitis induced by isocyanates. Specific IgG antibodies for TDI, MDI, and HDI were not demonstrated by enzyme-linked immunosorbent assay. Because abnormal shadows in the chest radiograph did not improve quickly after admission, we administered glucocorticoids which improved the symptoms, the chest radiograph findings, and the serum KL-6 level.     

A high serum level of interleukin-6 in a patient with aggressive multiple myeloma]

A 58-year-old female was admitted to our hospital because of anemia in March 1987. Monoclonal protein (IgA, kappa) was detected and a diagnosis of multiple myeloma was made. Partial remission was obtained after VAD therapy with alpha-interferon. In December 1989, she was readmitted because of a pathological fracture of the left humerus. A white blood cell count was 4400/microliters with 30% myeloma cells and the urine protein (Bence Jones protein) was 26 g/day. Systemic chemotherapy was not effective. She developed pleural and pericardial effusions, bone mass, disturbance of consciousness and died of respiratory failure only 3 months after readmission. The pleural and pericardial fluids contained many myeloma cells. c-myc gene rearrangement was detected in myeloma cells obtained from the pleural fluid using c-myc exon1 and exon2 probes. The levels of interleukin-6 (IL-6) measured by ELISA was 107.4 pg/ml in serum, 56.2 pg/ml in pleural fluid and 780.0 pg/ml in pericardial fluid. Because of the lack of any overt infectious focus, the level of IL-6 appears to have been related to aggressive proliferation of myeloma cells. It was of interest that C-reactive protein, induced by IL-6, was a good marker reflecting disease activity.     

Cerebral infarction and cerebral salt wasting syndrome in a patient with tuberculous meningoencephalitis

A 38-year old female with underlying systemic lupus erythematosus was admitted with tuberculous meningoencephalitis. After an initial good response to anti-tuberculous treatment, she developed cerebral infarction and profound hyponatremia. This was due to cerebral salt wasting syndrome, which has only previously been described in 2 cases. The difficulties in diagnosis and management of this case are discussed.     

JAK2 V617F mutation negative erythrocytosis (or how to more simply perform diagnosis and treat a patient with increased hematocrit)

SUMMARY: This case report focuses on a 71-year old patient affected by unknown dyspnea and erythrocytosis referred by his general practitioner to our center for specialist advice after a hematological examination had excluded polycythemia vera on grounds of negative test for JAK2 V617F/exon 12 mutation. An accurate clinical history and physical examination accompanied by respiratory function tests resulted in diagnosis of JAK2 V617F mutation negative erythrocytosis, and treatment could be started. The discussion examines decisional algorithms when a polyglobulic patient is referred for diagnosis.     

Pulmonary hypertension secondary to serum hyperviscosity in a patient with rheumatoid arthritis

A patient with rheumatoid arthritis who was evaluated for dyspnea of six months' duration is described. Although no primary cardiac or parenchymal lung disease was identified, right heart catheterization revealed marked pulmonary hypertension. The patient was presumed to have pulmonary arteritis. Evaluation of her hyperproteinemia, however, led to the discovery of a polyclonal gammopathy with a marked increase in plasma viscosity. Although the classic clinical findings of the hyperviscosity syndrome were minimal, the patient underwent plasmapheresis, resulting in a marked reduction of pulmonary artery pressures (from 53 +/- 4 mm Hg, mean +/- SD, to 30 +/- 3 mm Hg, p less than 0.05) and pulmonary vascular resistance (from 707 +/- 63 dynes/second/cm5 to 421 +/- 72 dynes/second/cm5, p less than 0.05) concomitant with a return to normal plasma viscosity. Her dyspnea completely resolved. This represents the first successful treatment of pulmonary hypertension by plasmapheresis. Protein evaluation revealed the presence of intermediate complexes of IgG rheumatoid factor. The hyperviscosity syndrome should be considered in the differential diagnosis of pulmonary hypertension in patients with rheumatoid arthritis and other disorders associated with a polyclonal or monoclonal gammopathy. Pulmonary hypertension secondary to the hyperviscosity syndrome is reversible by plasmapheresis. Immunosuppressive therapy that reduces immunoglobulin production may provide a means of long-term treatment.     

Splenic infarction associated with sorafenib use in a hepatocellular carcinoma patient

Sorafenib,a multitargeted tyrosine kinase inhibitor,has been shown to improve survival in patients with advanced hepatocellular carcinoma(HCC).As the clinical use of sorafenib increases,many adverse effects have been reported,such as hand-foot skin reaction,diarrhea,anorexia,asthenia,alopecia,weight loss,hypertension and arterial thromboembolism.However,there are no prior reports of splenic infarction as an adverse effect of sorafenib.Here,a case of splenic infarction in a patient with HCC who was treated w...