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Biomedical subjects

J J Iacuone

Publications and source records attributed to J J Iacuone.

6 recordsLinked to original sources
PubMed1999

Intact sensory fusion in a child with divergence paresis caused by a pontine glioma.

PURPOSE: To describe a child with divergence paresis esotropia caused by a brain tumor with intact sensory and motor fusion. METHOD: Case report. RESULTS: A 9-year-old boy who had one episode of double vision was initially seen with a small, variably present esophoria at near vision, an intermittent 10 prism diopter esotropia at distance, and stereopsis of 80 arc seconds. A magnetic resonance imaging examination disclosed a 4.0 x 4.5-cm pontine glioma. CONCLUSIONS: Ophthalmologists should recognize that the presence of intact sensory and motor fusion in a child with acute, comitant esotropia of the divergence paresis type does not preclude intracranial abnormality. If immediate neuroimaging is deferred, repeated thorough ocular motility examinations are warranted to detect progression.

Brain Neoplasms↗
PubMed1989

A lineage switch in acute monocytic leukemia. A case report.

A case of congenital monocytic leukemia that underwent a lineage switch to acute lymphocytic leukemia (ALL) is described. The original leukemia had typical monocytic features, as evidenced by morphology (FAB M5), cytochemistry (nonspecific esterase) and immunophenotype (My4 positive). Cytogenetic study showed a pseudodiploid clone t(9;11)(p22;q21) that could be interpreted as a variant of the t(9;11)(p22;q23) reported in patients with the M5 type of leukemia. After successful remission induction with single-agent chemotherapy (VM-26) and subsequent sustained remission for 12 months with alternating VM-26 and VP-16-213, lineage switch to ALL (FAB L1) occurred. The presence of both lymphoid and myeloid markers on leukemic cells at lineage switch suggested the biphenotypic character of the patient's ALL. Our observation indicates that a lineage switch can occur from monocytic leukemia to ALL, although most of the cases previously reported have been in the reverse direction. This case emphasizes again the need to carry out careful and comprehensive marker studies to gain insight into the possible prognostic significance and the application of appropriate therapy.

Bone Marrow↗
PubMed1977

Acute respiratory illness in children with acute lymphoblastic leukemia.

Ten of 70 children (14%) with acute lymphoblastic leukemia developed severe interstitial pneumonitis within three weeks after induction of central nervous system prophylactic therapy. The clinical picture was characterized by fever, cough, progressive dyspnea, and hypoxemia with complete resolution in one to three weeks, except in one patient who died during the acute illness from respiratory failure. P. carinii organisms were found in the lung tissue of only one patient. The etiology of the pneumonitis in the other nine children was probably viral, acquired or activated during a period of lymphopenia and immunosuppression. The morbidity and potential mortality from the pneumonitis warrants early recognition by open lung biopsy and intensive supportive therapy.

Central Nervous System Diseases↗
PubMed1976

Accidental digitoxin poisoning.

A healthy 141/2-month-old child ingested 1.5 mg of digitoxin by accident. Digitoxin was wrongly identified as digoxin, the initial electrocardiogram was misinterpreted, and the vomiting was underestimated as an important symptom of toxicity. Symptoms persisted and the patient was hospitalized. Serial digitoxin levels were obtained and correlated with ECG and clinical course. It appears that serial digitoxin levels can be a useful adjunct in diagnosis, assessment of severity, and indication of recovery from digitoxin poisoning. In each patient, it is imperative that ECG, pharmacologic, and clinical indicators of digitalis toxicity be accurately identified for proper assessment of severity and appropriate management.

Absorption↗
PubMed1975

Acquired agammaglobulinemia after a life-threatening illness with clinical and laboratory features of infectious mononucleosis in three related male children.

Three males in one family (two siblings and one maternal cousin) had an illness with cervical adenopathy, hepatosplenomegaly, and a fulminant febrile course. In the two survivors agammaglobulinemia developed. One of them became ill at the age of six months and had an Epstein-Barr-virus antibody titer of 1:10 during illness and convalescence. The white-cell count was 120,000 with 90 per cent lymphocytes, most being atypical and forming increased numbers of sheep erythrocyte rosettes. IgM was elevated, IgA normal and IgG decreased. Subsequently, all immunoglobulins were absent, and the Epstein-Barr-virus antibody titer became negative. Peripheral B-cell number remained normal, but abnormal lymph-node architecture associated with failure to respond to antigenic challenge indicated B-cell dysfunction. The pathogenesis of this entity may involve an abnormal T-cell response to transformation of B cells by Epstein-Barr virus, leading to B-cell dysfunction and agammaglobulinemia.

Agammaglobulinemia↗