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Biomedical subjects

D L Solanki

Publications and source records attributed to D L Solanki.

At least 19 recordsLinked to original sources
PubMed1995

A phase II trial of continuous-infusion recombinant interleukin-2 in patients with advanced renal cell carcinoma: a Southwest Oncology Group study.

A multicenter, phase II trial of continuous-infusion interleukin 2 (IL-2) was done in the Southwest Oncology Group to evaluate the efficacy and safety of this treatment in a broad-based population of patients with metastatic renal-cell carcinoma. Forty-seven patients from 11 different institutions were entered in this study, with 43 eligible. Two technically ineligible patients who received treatment and for whom records are available are included in the data analysis. Thus, there are 45 analyzable patients. Of these patients, performance status was 0 in 58% and 1 in 42%. Thirty-one patients had a prior nephrectomy, and 12 patients had received prior therapy. IL-2 was initially given at a dose of 4.5 x 10(6) Roche U/m2/day, 4 days a week, for 4 weeks in a row, followed by a 3-week rest period. Because of the difficulty in obtaining reimbursement for the hospitalization required on the days of IL-2 administration, after 10 patients had been entered, the treatment regimen was changed to 6 x 10(6) Roche U/m2/day for 4 days as an inpatient, followed by 2 weeks of potential outpatient treatment at a dose of 3 x 10(6) Roche U/m2/day for 4 days each week. This was followed by a 2-week rest period. Within the 45 analyzable patients, there were 0 complete responses and 6 partial responses, for a response rate of 13% (95% confidence interval 5.1-27%). Responses occurred in lung metastases, nodal disease, and in one patient with bone metastases and the primary kidney tumor. Response durations were 1 month, 1 month, 14+ months, 19 months, 26+ months, and 27 months. Of 12 patients with a nephrectomy and only lung metastases, 4 showed partial responses. Medial survival for all analyzable patients is 15 months (95% confidence interval 8-20 months). Toxicity was significant, with nausea and vomiting, diarrhea, fever and chills, dermatologic changes, and fatigue the most frequent. There were 18 instances of grade 4 toxicity, with the most common grade 4 toxicity, respiratory, found in 8 patients. There were two early deaths of probable heart-related causes while receiving treatment. A continuous-infusion IL-2 regimen that allows some potential outpatient treatment shows effectiveness and toxicity similar to that in other multicenter IL-2 infusion trials and high-dose intravenous bolus regimens.

Adult↗
PubMed1989

Refractory potassium repletion due to cisplatin-induced magnesium depletion.

Cisplatin is a common cause of hypomagnesemia and hypokalemia due to renal magnesium (Mg) and potassium (K) losses. Magnesium plays an important role in the maintenance of intracellular K. An unrecognized and untreated Mg depletion can lead to a refractory K repletion. We describe two patients with hypomagnesemia-associated refractory hypokalemia following cisplatin following cisplatin therapy. Potassium supplementation failed to replace the K deficit. Profound hypokalemia persisted until hypomagnesemia was recognized and corrected. In neither patient was the concurrent hypomagnesemia recognized until the 11th and 9th hospital days. These two cases demonstrated the association of a refractory K repletion and an Mg deficiency. Thus, both serum K ion and Mg levels should routinely be assessed in patients who require cisplatin therapy.

Adult↗
PubMed1988

Dyserythropoiesis and erythroblast-phagocytosis preceding pure red cell aplasia.

A 50-year-old woman with typical acquired primary pure red cell aplasia (PRCA) was successfully treated with prednisone. A later relapse was preceded by a period of ineffective erythropoiesis characterized by a reticulocyte response inappropriately low for the degree of anemia, serum iron of 189 micrograms/dl, total iron-binding capacity (TIBC) of 213 micrograms/dl, and erythroid hyperplasia. In addition there was marked dyserythropoiesis and erythroblast-phagocytosis. One month later, bone marrow examination showed classic PRCA. This rarely reported evolutionary stage of PRCA has several implications: 1) it suggests antibody induced erythroblast cytotoxicity as one mechanism of PRCA; 2) at a particular time in the development of PRCA there is potential for misdiagnosis as primary refractory anemia (PRA); and 3) some cases of PRA with similar morphologic and laboratory findings may be pathogenetically related to PRCA and may benefit from evaluation for immune-mediated suppression of erythropoiesis.

Bone Marrow↗
PubMed1988

Hemolysis in sickle cell disease as measured by endogenous carbon monoxide production. A preliminary report.

To detect and quantitate temporal variations of the hemolytic rate in sickle cell disease, the authors measured endogenous carbon monoxide (CO) production in five normal subjects, nine patients with sickle cell anemia (SS) in steady clinical state, and two patients with sickle cell-hemoglobin C (SC) disease in and out of pain crises. The red blood cell life span calculated from these data (RCLSco) ranged from 81.2 to 102.9 days (mean +/- standard deviation [SD] 88.0 +/- 9.2, coefficient of variation [CV] 10.2%) for the normal subjects and 8.0-24.7 days (mean +/- SD 12.1 +/- 5.1, CV 42.1%) for those with SS. Although the individual figures for RCLSco for the normal subjects and those with SS fell within the range previously obtained by radioisotopic techniques for the respective groups, the mean values calculated from the CO technique were slightly (though not significantly) shorter for the normal subjects and about 25% shorter for the subjects with SS (P less than 0.01). Repetitive studies were performed in four subjects with SS who were clinically stable; the temporal variability in the calculated hemolytic rate differed considerably from patient to patient (CV 3.6%, 7.0%, 17.0%, 28.0%). In two patients concurrent RCLS studies were performed by the CO technique and 51Cr tagged red blood cells. In one patient, the RCLS was similar by the two techniques, in the other, a two exponent 51Cr curve did not permit calculation of RCLS. In the two patients with SC disease there was no difference in RCLSco during and after recovery from pain crisis. Although the CO technique may overestimate the turnover of circulating heme mass, especially in the presence of hemolysis, the results of serial studies in a small number of patients with SS suggest but do not prove temporal variations in hemolytic rate in SS.

Anemia, Sickle Cell↗
PubMed1987

Peripheral blood remission of hairy cell leukemia after transfusion hepatitis.

Hairy cell leukemia is a chronic lymphoproliferative disorder characterized clinically by splenomegaly and cytopenias. Spontaneous remissions are rare and splenectomy is often performed when the blood counts worsen and cause symptoms. Three of our patients with hairy cell leukemia developed recurrent pancytopenia and transfusion-dependent anemia after splenectomy. Each subsequently acquired transfusion hepatitis and in two patients marked hematologic improvement was noted within 2 months. Complete peripheral blood remission occurred within 17 months in all patients although bone marrow infiltration with hairy cells persisted. One patient remains in remission for 12 years; the other two succumbed to infectious illnesses but with normal blood counts. The mechanism by which hepatitis virus induces hematologic recovery in patients with hairy cell leukemia is unknown but may involve augmentation of the interferon system.

Aged↗
PubMed1986

Acute splenic sequestration crises in adults with sickle cell disease.

Reports of acute splenic sequestration crises in adults with sickle cell hemoglobin C disease or sickle cell thalassemia are rare, although an enlarged and distensible spleen persists in half of these patients. Seven episodes of acute splenic sequestration crises in four adults, two with sickle C disease and two with sickle thalassemia, are described. The crises were life-threatening and recurrent in all, but there were no fatalities. One patient had mild steady-state thrombocytopenia suggesting hypersplenism. Technetium 99m/sulfur colloid scanning of the spleen during the acute splenic sequestration crises in three patients showed almost total lack of splenic uptake or decreased uptake with intrasplenic filling defects thought to be splenic infarcts or hematomas on follow-up computed tomographic scanning. The scanning abnormalities resolved following recovery from the crises. Acute splenic sequestration crises probably are common in adults with sickle C disease and sickle thalassemia but may be underdiagnosed or misdiagnosed as splenic infarctions. The hematologic and splenic findings during acute splenic sequestration crises resemble those following splenic vein ligation in animals.

Acute Disease↗
PubMed1985

Erythrophagocytosis in vivo in sickle cell anemia.

Recent observations that the sickle RBC are excessively susceptible to phagocytosis by macrophages in vitro prompted me to look for evidence of in vivo erythrophagocytosis (Ep) in patients with sickle cell anemia (SS). Freshly prepared smears of unmanipulated blood of 27 patients with SS in steady state were examined for Ep by a 500-cell differential white blood cell (WBC) count performed in duplicate. Ten of 27 (37%) SS patients showed Ep (1-6/1,000 WBC or 1-10/100 monocytes). By contrast, no Ep was found in similarly prepared blood smears of 25 normal adult controls and nine splenectomized subjects. The mean hemotocrit value of the Ep(+) SS patients was significantly lower than that of the Ep(-) patients (21.0 +/- 1.7% vs 24.0 +/- 2.7% p less than 0.01). Considering the rarity of spontaneous Ep in unmanipulated blood from normal subjects and the relative insensitivity of the method used, the finding of Ep in over one third of SS patients indicates a significant membrane injury of the sickle RBC and serves to validate the in vitro observations. The possible role of the "senescence" mechanism in the induction of Ep is discussed.

Adult↗
PubMed1985

Spurious red blood cell parameters due to serum cold agglutinins: observations on Ortho ELT-8 cell counter.

The pattern of spurious red blood cell parameters caused by serum cold agglutinins has been well characterized for the Coulter counters but not the Ortho ELT-8. The pattern consists of a spurious increase in mean corpuscular volume (MCV), a discrepancy between the hemoglobin and the hematocrit, the latter falsely reduced and consequently a MCHC value greater than 36%. Since MCHC rarely exceeds 36% in health or disease, it is an important clue to the spurious nature of the macrocytosis caused by cold agglutinins. The authors have studied five examples of cold agglutinin induced artefact on the Ortho ELT-8 counter. Although a pattern similar to that for the Coulter counters was anticipated, three of the five patients failed to show the characteristics "internal discrepancy" and a MCHC value greater than 36%, despite a marked spurious elevation of MCV. In two of the three patients a classical pattern of cold agglutinin artefact was observed on a Coulter S Plus IV counter with only a modest elevation of MCV. Possible explanations for the observed pattern on the ELT-8 and its implications are discussed.

Adult↗
PubMed1985

Spurious thrombocytopenia during pregnancy.

Thrombocytopenia in four healthy pregnant women proved to be spurious and caused by in vitro clumping of platelets (three) or adherence of platelets to granulocytes (one) in the presence of edetic acid used to anticoagulate the blood. All had normal vaginal deliveries without unusual bleeding. One of the newborns transiently exhibited the phenomenon of platelet clumping in vitro, probably due to transplacental transfer of the platelet agglutinin from the mother. Recognition of these laboratory artifacts is important to avoid unwarranted investigations and inappropriate management of the mother and infant. Careful examination of a blood smear in all thrombocytopenic patients is the best safeguard against being misled by spurious thrombocytopenia.

Adult↗
PubMed1984

Circulating monoclonal IgM proteins in B cell chronic lymphocytic leukemia: their identification, characterization and relationship to membrane IgM.

Accumulated evidence indicates that there is a circulating monoclonal Ig protein related to the leukemic cell-associated Ig in the majority of patients with B cell chronic lymphocytic leukemia (CLL) despite the failure to demonstrate such a protein by conventional serum electrophoresis. Methodology has been developed to reveal these hidden monoclonal bands and to show that they are related to the leukemia-associated membrane Ig (mIg). Of nine CLL cases with stainable mIgM and without discernable plasma Ig bands, marked hypogammaglobulinemia was evident in six. In the other three, a significant amount of protein was present in the gamma region. IgM was isolated from the plasma of these patients by affinity chromatography with Sepharose-4B, conjugated with affinity purified anti-human IgM antibodies. One to 3 mg were isolated from 20 to 40 ml of plasma. Agarose electrophoresis revealed a monoclonal Ig band in the isolated IgM in all cases. Eight of these IgM proteins were analyzed by high-pressure liquid chromatography. Five were found to be pentameric IgM. In the remaining three, various amounts of monomeric IgM were detected. Attempts to make anti-idiotypic antibodies to the isolated proteins have been successful. Thus far, a rabbit anti-idiotypic antiserum was obtained in one case and two mouse monoclonal anti-idiotypic antibodies in two additional cases. Immunofluorescence analysis revealed that plasma IgM and mIgM shared similar idiotypic determinants. One other monoclonal antibody was shown to be specific for a V region marker of a minor Ig population. These findings indicate that B leukemic lymphocytes do secrete a small amount of IgM and lend further support to the thesis that the maturation defect in CLL is incomplete. It is also feasible to isolate the secreted IgM and to produce anti-idiotypic antibodies to them. In view of the potential therapeutic effect of anti-idiotypic antibodies, this may offer an alternative and efficient approach to generate a large panel of anti-idiotypic antibodies for clinical trials. The possibility also exists that this approach is applicable to other B cell proliferative disorders such as the non-Hodgkin B cell lymphomas.

Animals↗
PubMed1983

Spurious leukocytosis and thrombocytopenia. A dual phenomenon caused by clumping of platelets in vitro.

Three patients with spurious thrombocytopenia caused by in vitro clumping of platelets also had leukocytosis that was inappropriate for their clinical state and could not be verified on examination of a blood smear. Serial blood counts and analysis of the platelet and WBC histograms proved the "leukocytosis" to be spurious and caused by platelet clumps erroneously "recognized" by the counter as white blood cells. In three additional patients, the WBC counts increased concomitantly with a decrease in their platelet counts but remained within the normal range. Abnormal platelet and WBC counts generated by automated cell counters must be verified by examination of a blood smear before patients are subjected to unwarranted investigations and therapy.

Adult↗
PubMed1982

Chronic lymphocytic leukemia: a monoclonal disease.

A black woman with chronic lymphocytic leukemia (CLL) was found to have monoclonal B lymphocytes with one type of surface immunoglobulin and one variant of G6PD (glucose-6-phosphate dehydrogenase) (G6PD A). Erythrocytes and T cells contained both G6PD A and G6PD B and hence were of polyclonal origin. The CLL cells in this patient likely arose from a developmental stage later than the step of differentiation into T and B lymphocytes. Furthermore, her erythrocytes did not arise from a stem cell affected by the CLL process.

Aged↗
PubMed1981

Pernicious anemia in blacks. A study of 64 patients from Washington, D. C., and Johannesburg, South Africa.

In a collaborative study from Washington, D. C., and Johannesburg, South Africa, the clinical, laboratory, and immunologic features of 64 black patients (25 male, 39 female) who had pernicious anemia were studied. Mean age at diagnosis was 53 +/- 20 years (mean +/- SD); 29.6% of the patients were under 40 years of age, and 14% were 30 years of age or younger. This suggests that there may be an earlier age of onset of pernicious anemia amongst blacks than the reported age incidence in whites. Serum anti-intrinsic factor blocking antibodies were found in 25 of 37 patients tested (67.5%). There was a significantly higher incidence of the antibody in women (85%) than in men (50%) (P < 0.01).

Adolescent↗
PubMed1980

Oat cell carcinoma mimicking leukemia.

A patient with oat cell carcinoma had circulating carcinoma cells, which initially suggested a diagnosis of acute leukemia. The correct diagnosis was made only by histopathologic examination of the bone marrow. A case of a similar bone marrow disorder, which developed after diagnosis of oat cell carcinoma, is also presented.

Bone Marrow Examination↗
PubMed1980

Left ventricular function in sickle cell anemia: a noninvasive evaluation.

There is controversy in the medical literature regarding the significance of "sickle cell cardiomyopathy." In an attempt to clarify this, we studied 14 patients with sickle cell anemia (age range 16 to 36 years) using simultaneous echocardiography and phonocardiography. The values of systolic time intervals and echocardiographic indices of left ventricular performance were similar to those reported for normal subjects and those with comparable degrees of anemia. We confirm a previous report of normal left ventricular function at rest in patients with sickle cell anemia and concur with the suggestion that a concomitant heart disease be considered in these patients when cardiac failure supervenes.

Adolescent↗
PubMed1980

Thromboembolism in patients with hereditary deficiency of coagulation factors.

Despite significantly prolonged prothrombin time endogenously caused by factor VII deficiency, a 65-year-old woman suffered a fatal pulmonary embolism. This seemingly paradoxic phenomenon prompted our review of 14 other patients with various coagulation factor deficiencies who also had thromboembolic events. It is postulated that certain factor deficiencies may protect against venous and/or arterial thrombosis. A large-scale prospective study of this population may help define the relative importance of the various coagulation factors, platelets, and the vessel wall in thrombosis and atherogenesis and allow a rational evaluation of anticoagulant therapy.

Aged↗