Biomedical subjects
R Rahamimov
Publications and source records attributed to R Rahamimov.
Cavoatrial shunt: a graft salvage procedure for suprahepatic caval anastomosis obstruction after liver transplantation.
A liver transplant recipient developed the Budd-Chiari syndrome because of an obstruction of the suprahepatic inferior vena cava anastomosis. Percutaneous balloon dilatation angioplasty was not feasible. On exploration, dense retrohepatic fibrotic reaction was observed. The patient underwent successful retrohepatic cavoatrial shunt placement by means of a 16-mm, ring-enforced polytetrafluoroethylene graft. We conclude that this shunt should be considered an additional graft salvage procedure for this complication.
Where is the "inverting factor" in hormone secretion from parathyroid cells?
Secretion of hormones and transmitters in the body fall into two general categories. In the majority of the secreting cells, including the presynaptic terminals in the nervous system, an increase in the extracellular calcium causes an increase in secretion. There are two notable exceptions to this general rule: the parathyroid cells and the renal juxtaglomerular cells, where an increase in extracellular calcium leads to a decrease in secretion. Because these two cell types have a cardinal role in a wide variety of physiological and pathophysiological functions, it is of great importance to understand the regulation of their hormone secretion process. A key element to such an understanding is the identification of the location of the "inverting step," which makes the parathyroid cells behave in a fashion contrary to most other secretory cells. Whole cell imaging studies strongly suggested that the inversion factor is between the changes in intracellular calcium concentration ([Ca2+]i) and the secretion of the hormone. Surprisingly, confocal calcium imaging of the parathyroid cells did not support this dogma. It revealed that the interior of the parathyroid cell is a nonhomogeneous medium and that an increase in the extra-cellular calcium concentration produces changes in [Ca2+]i, in both the same and opposite directions, in different parts of the parathyroid cell.
Hepatitis C-associated cryoglobulinemia after liver transplantation.
Mixed cryoglobulinemia is well known to be associated with hepatitis C virus (HCV) infection. We report two cases in which cryoglobulinemia appeared or became grossly exacerbated after orthotopic liver transplantation. In both cases, there was co-appearance of cryoglobulinemia with the reinfection of the grafted liver with HCV. It is postulated that the cryoglobulinemia might be related to secondary HCV infection in these patients.
Parathyroid cell proliferation in normal and chronic renal failure rats. The effects of calcium, phosphate, and vitamin D.
Secondary hyperparathyroidism is characterized by an increase in parathyroid (PT) cell number, and parathyroid hormone (PTH) synthesis and secretion. It is still unknown as to what stimuli regulate PT cell proliferation and how they do this. We have studied rats with dietary-induced secondary hyper- and hypoparathyroidism, rats given 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and rats after 5/6 nephrectomy for the presence of PT cell proliferation and apoptosis. PT cell proliferation has been measured by staining for proliferating cell nuclear antigen (PCNA) and apoptosis by in situ detection of nuclear DNA fragmentation and correlated with serum biochemistry and PTH mRNA levels. A low calcium diet led to increased levels of PTH mRNA and a 10-fold increase in PT cell proliferation. A low phosphate diet led to decreased levels of PTH mRNA and the complete absence of PT cell proliferation. 1,25 (OH)2D3 (25 pmol/d x 3) led to a decrease in PTH mRNA levels and unlike the hypophosphatemic rats there was no decrease in cell proliferation. There were no cells undergoing apoptosis in any of the experimental conditions. The secondary hyperparathyroidism of 5/6 nephrectomized rats was characterized by an increase in PTH mRNA levels and PT cell proliferation which were both markedly decreased by a low phosphate diet. The number of PCNA positive cells was increased by a high phosphate diet. Therefore hypocalcemia, hyperphosphatemia and uremia lead to PT cell proliferation, and hypophosphatemia completely abolishes this effect. Injected 1,25 (OH)2D3 had no effect. These findings emphasize the importance of a normal phosphate and calcium in the prevention of PT cell hyperplasia.
Psoriasis is not a contraindication for alpha interferon treatment in patients with chronic hepatitis C.
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False ascites: fallopian tube pseudocyst imitating ascites.
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The molecular basis of secondary hyperparathyroidism in chronic renal failure.
Renal osteodystrophy is a debilitating complication of chronic renal failure and secondary hyperparathyroidism (2HPTH) is one of its central features. 2HPTH develops as a result of the low levels of serum calcium and 1,25-dihydroxyvitamin D [1,25(OH)2D3] and the high serum phosphate that occur in chronic renal failure. 1,25(OH)2D3 markedly decreases PTH gene transcription and its lack leads to 2HPTH. A low serum calcium increases PTH mRNA and iPTH levels while a high serum calcium has no effect on PTH gene expression. In experimental uremia there are increased levels of PTH mRNA. In chronic renal failure there is a shift in the calcium set-point to the right. This may be a function of a change in properties of the parathyroid cell calcium receptor, which is a G-protein coupled calcium sensor.
[Idiopathic hypereosinophilic syndrome].
The idiopathic hypereosinophilic syndrome is a heterogeneous group of disorders characterized by persistent eosinophilia of undetected cause, and multiple organ system involvement. The systems affected include the central and peripheral nervous, cardiovascular, respiratory and gastrointestinal systems and the kidneys, skin, muscles and joints. Treatment is mainly by immunosuppressive drugs to prevent organ system complications. Prognosis is variable, depending mainly on heart involvement.
Acute colchicine intoxication--possible role of erythromycin administration.
A 29-year-old patient with familial Mediterranean fever and amyloidosis involving the kidney, liver, and gastrointestinal tract received longterm colchicine, 1 mg daily. In the last year she developed diarrhea and abdominal pain, that coincided with toxic colchicine blood levels. After 2 weeks of oral erythromycin therapy she was hospitalized for acute, life threatening colchicine toxicity, with fever, diarrhea, abdominal pain, myalgia and lower extremity parasthesias and later convulsions and alopecia. Pancytopenia evolved into rebound leukocytosis, disturbed liver function and hypoglycemia. After a long stormy course she improved. Colchicine toxicity with combined liver and renal impairment and the role of erythromycin in her colchicine toxicity are discussed.