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Biomedical subjects

J M Carrillo

Publications and source records attributed to J M Carrillo.

At least 19 recordsLinked to original sources
PubMed1999

Disseminated histoplasmosis in infants.

BACKGROUND: Disseminated histoplasmosis usually occurs in immunocompromised patients who reside in Histoplasma capsulatum-endemic regions. It has also been described in immunocompetent infants after exposure to a large inoculum of the pathogen resulting in case fatality rates of 40 to 50%. METHODS: From 1983 through 1996 all infants with documented disseminated histoplasmosis were treated with amphotericin B followed by daily ketoconazole for 3 months. Immunologic workups were performed at the time of diagnosis and at 4 to 6 weeks of therapy. Surviving patients were followed for at least 1 year. Time to resolution of signs and symptoms was recorded, as were complications. RESULTS: We managed 40 patients with disseminated histoplasmosis. The age in months at diagnosis was 15.3+/-10.2 (mean +/- SD), and 24 were male. All patients were from endemic regions and they presented with fever, spleen and/or liver enlargement and hematologic abnormalities. Diagnosis was made by histology and culture of bone marrow, spleen, lymph node, bronchoalveolar or liver samples. Twenty patients presented with T cell deficiency that resolved at 4 to 6 weeks of therapy in all of the retested patients, and 10 of 12 tested patients had hyperglobulinemia that resolved. Thirty-five (88%) patients were cured by treatment; 4 died and 1 relapsed. CONCLUSIONS: Disseminated histoplasmosis should be considered in infants from endemic areas who present with fever, hepatosplenomegaly and hematologic abnormalities. These patients develop transient hyperglobulinemia and T cell deficiency that resolve with treatment. Treatment with amphotericin B followed by an oral azole for 3 months is effective in most patients.

Amphotericin B↗
PubMed1995

High-dose intravenous methylprednisolone therapy for patients with Diamond-Blackfan anemia refractory to conventional doses of prednisone.

OBJECTIVES: To assess the efficacy and toxicity of very high doses of glucocorticoids in patients with congenital pure red cell aplasia (Diamond-Blackfan anemia) who did not respond to standard doses of prednisone. STUDY DESIGNS: We prospectively treated eight patients with transfusion-dependent Diamond-Blackfan anemia with high intravenous doses of methylprednisolone. All patients had previously not responded to one or more oral courses of prednisone in standard doses and were dependent on erythrocyte transfusions. Every patient initially received methylprednisolone at a dose of 30 mg/kg per day, followed by slow tapering for 4 weeks, but none responded. All patients then received a second treatment course starting at 100 mg of methylprednisolone per kilogram per day, again followed by slow tapering of the dosage. RESULTS: Three patients had a complete response that has been sustained for 21+, 31+, and 41+ months, respectively. One patient had a partial response. Toxic effects included a rise in serum alanine aminotransferase activity in all patients, transient diabetes mellitus in one child, and three episodes of bacteremia in two patients with intravenous access devices. CONCLUSIONS: We conclude that very high doses of methylprednisolone may induce sustained remission in some patients with transfusion-dependent Diamond-Blackfan anemia refractory to standard-dose prednisone therapy.

Adolescent↗
PubMed1988

Neurologic, endocrinologic, and pathologic findings associated with large pituitary tumors in dogs: eight cases (1976-1984).

Invasive tumors of the pituitary gland were diagnosed in 8 dogs. Seven of the dogs had been treated for pituitary-dependent hyperadrenocorticism before the onset of neurologic signs. All 8 dogs had behavior abnormalities and similar neurologic signs: 6 dogs had rotary nystagmus and 7 dogs had symmetric tetraparesis. Once neurologic signs developed, the clinical course in all 8 dogs had a mean duration of 4.7 +/- 2.0 months before death or euthanasia; 5 dogs had a clinical course of less than or equal to 2 months. Necropsy was performed in 7 dogs. The histologic diagnosis was malignant pituitary adenocarcinoma in 2 dogs and pituitary adenoma in 5 dogs.

Adenocarcinoma↗
PubMed1987

Cerebral astrocytoma in four cats: clinical and pathologic findings.

Cerebral astrocytoma was diagnosed in 4 cats. A long-standing history of seizures followed by an increase in frequency of uncontrolled seizures were prominent features in these cats. Anticonvulsants provided effective seizure control in 3 cats for a period of 1 to 3 years. On initial and subsequent neurologic examinations, all cats were postictal and had focal neurologic deficits. In 2 cats, there were focal EEG patterns consistent with the neuroanatomic diagnosis of the tumor. White blood cell pleomorphism of the CSF was determined in the cats that underwent CSF analysis. Pathologic findings in all cats included tumor necrosis and edema, compression of the opposite hemisphere, and invasion of the third and lateral ventricles.

Animals↗
PubMed1986

Differential diagnosis of granulomatous meningoencephalomyelitis, distemper, and suppurative meningoencephalitis in the dog.

Clinical differences were determined between granulomatous meningoencephalomyelitis, distemper, and suppurative meningoencephalitis in the dog. Dogs with granulomatous meningoencephalomyelitis had "head" signs on examination, which progressed to profound caudal fossa abnormalities, changes in mental status, and tetraparesis. Dogs with distemper had a gradual onset of posterior paresis; tetraparesis and occasional vestibular signs developed later in the course of disease. Dogs with suppurative meningoencephalitis had lethargy and anorexia at the time of examination, which progressed to nuchal rigidity, mental depression, tetraparesis, and profound alterations in consciousness. Analysis of cerebral spinal fluid was useful in distinguishing suppurative meningoencephalitis from the other 2 diseases. Twenty-seven cases of inflammatory disease of the CNS in dogs were reviewed. Comparisons of history, results of physical and neurologic examinations, ancillary data, and response to treatment were made. It appeared that certain clinical and neurologic features contributed to the diagnosis of these diseases.

Animals↗
PubMed1980

[Prethrombosis in child malnutrition].

Antithrombin III (AT III) and heparin antithrombin assay were estimated in 30 severely malnourished children and 40 normal children. The AT III was found significatively depressed and the heparin antithrombin assay showed a flat curve in the patients, which reflects a prethrombotic pattern in this group of children. Those findings agree with the high incidence of thrombosis reported in childhood malnutrition.

Antithrombin III↗
PubMed1979

Primary hyperparathyroidism in a dog.

A 6-year-old male Standard Poodle had hypercalcemia, hypophosphatemia, and a urinary concentrating defect. A parathyroid adenoma involving the left caudal parathyroid gland was surgically removed. Transient hypocalcemia followed, which resolved without treatment. A renal biopsy did not demonstrate renal parenchymal mineral deposition. Urinary concentrating ability returned after surgery.

Adenoma↗
PubMed1979

Antithrombin activities in childhood malnutrition.

Antithrombin activities in 30 severely malnourished children and 40 normal children were estimated in clotting tests by thrombin neutralisation as anti-Xa and by a heparin antithrombin assay; and by immunodiffusion as alpha 2-globulin and alpha 1-antitrypsin. The patients' mean alpha 2-globulin was severely depressed, and there were less marked depletions in mean values for thrombin neutralisation, anti-Xa, and in the heparin antithrombin assay (which showed the flat curve thought to reflect a thrombotic tendency). The alpha 1-antitrypsin values were normal. The findings support the concept of antithrombin as the summation of alpha 2-globulin and alpha 1-antitrypsin (with alpha 2-macroglobulin); and the low values may be related to the high incidence of thrombosis reported in childhood malnutrition, although it was not seen in these patients.

Antithrombins↗