[Parvovirus B19-induced aplastic crisis in a patient with iron deficiency anemia].

A 38-year-old female was referred to Takaoka City Hospital for treatment of common-cold-like symptom and an episode of transient unconsciousness. Physical examination on admission revealed severe anemia and an ejection heart murmur. Complete blood count revealed microcytic hypochromic anemia (Hb 4.1 g/dl), leukocytopenia (2.600/microliters), thrombocytopenia (7.1 x 10(4)/microliters) and reticulocytopenia (17,000/microliters). The bone marrow cellularity was within normal limits. Cells in the erythroid series were decreased to 5% of total bone marrow nucleated cells with maturation arrest at the level of proerythroblasts. Giant proerythroblasts were observed in 0.2% of marrow nucleated cells. No stainable iron was seen. Both anti-parvovirus B19 IgM antibody and IgG antibody were positive in the serum and parvovirus B19 DNA was detected in the bone marrow cells by polymerase chain reaction. From these results, iron deficiency anemia complicated with pure red cell aplasia secondary to parvovirus B19-induced infection was diagnosed. The anemia gradually improved with administration of sodium ferrous citrate one month after admission. Parvovirus B19 has been reported to cause an aplastic crisis in the patients who has a rapid red cell turn over such as hemolytic anemia or acute blood loss. This report suggested that severe aplastic crisis is also induced in patients with iron deficiency anemia by parvovirus B19-induced infection and warns that careful observation is necessary for the follow up of patients with iron deficiency anemia.

Leukemic meningitis in a patient with splenic lymphoma with villous lymphocytes (SLVL). Meningitis as a possible initial manifestation of SLVL.

BACKGROUND: Splenic lymphoma with villous lymphocytes (SLVL) is a low grade, non-Hodgkin's lymphoma with a stable or slowly progressive clinical course. To the authors' knowledge, central nervous system involvement has not been described previously in patients with SLVL. METHODS: Morphologic, immunocytochemical, and immunohistochemical analyses were conducted to determine the nature of villous lymphocytes in the peripheral blood, spleen, and cerebrospinal fluid (CSF) of a patient with massive splenomegaly. RESULTS: A diagnosis of SLVL was made, based on tartrate-resistant acid phosphatase-negative peripheral villous lymphocytosis with CD19+, CD20+, HLA-DR+ phenotypes, and the involvement of spleen white pulp with these cells. Mononuclear cells in the CSF showed the same morphologic and immunocytochemical features seen in the villous lymphocytes in the peripheral blood and spleen. Splenectomy and intrathecal chemotherapy were successful in clearing leukemic cells from the CSF. CONCLUSION: In this patient with SLVL in whom leukemic meningitis developed, meningitis was found to be a possible initial manifestation of SLVL.

[Immunohistochemical studies of paraneoplastic subacute sensory neuropathy--an analysis of antineuronal antibody and infiltrated lymphocytes].

In order to clarify the pathogenesis of paraneoplastic syndrome, immunohistochemical studies were performed in a patient with subacute sensory neuropathy secondary to a small cell lung cancer. The case was a 73-year-old ex-farmer, whose chief complaints were pins and needles sensation of distal limbs and gait difficulty. After 6 weeks prodromata of pain in the upper limbs and numbness in all the limbs, he became unable to stand up without assistance. Neurological examinations on admission revealed marked sensory disturbances with glove and stocking type hypalgesia to pin prick and the loss of position and vibration senses in the distal extremities. His deep tendon reflexes also decreased in all the limbs. A chest X-ray showed a mass in the left upper lung field. A transbronchial lung biopsy of the mass revealed a small cell carcinoma. He was treated with anti-cancer drugs and radiation but he died of pneumonia after 8 months illness. Autopsy revealed a marked demyelination of the entire posterior column of the spinal cord. Dorsal root ganglia were infiltrated by lymphocytes with significant neuronal loss. Immunohistochemically, most of the infiltrated cells around the neurons were classified as CD8+ with fewer CD4+ lymphocytes. No B-lymphocytes were detected in the ganglia. The HLA-ABC and HLA-DR positive cells were found only among the satellite cells, not in the neurons. The serum and CSF from the patient were immunohistologically reacted with the nuclei and cytoplasm of all neurons of human as well as of rats, indicating the presence of anti-Hu type antineuronal antibody in the patient's CSF as well as serum.(ABSTRACT TRUNCATED AT 250 WORDS)

The expression of a cerebellar degeneration-associated neural antigen in human tumor line cells.

We examined the expression of the paraneoplastic cerebellar degeneration-associated autoantigen (PCD-AA) protein in human tumor lines of different origins by using an immunoaffinity-purified antibody from a patient with paraneoplastic cerebellar degeneration (PCD) and uterine adenocarcinoma. Immunocytochemical studies revealed that this antigen is expressed in the cytoplasm of two different uterine carcinoma lines and the tumor lines of neural origin as well as in the cytoplasm of a normal skin fibroblast line. By immunoblot analysis, we detected a 52-kd antigen identical to the PCD-AA protein in all the cell lines studied, including a colon adenocarcinoma line, a small-cell lung carcinoma line, and a squamous cell lung carcinoma line. These results indicate that the PCD-AA protein is expressed in a wide range of tumor cells. In this respect, this antigen is distinguishable from the cerebellar degeneration-related--34 antigen, of which expression is confined to tumor lines of neuroectodermal origin and not detected in colon, breast, or ovarian carcinoma lines derived from patients without PCD. These findings suggest the variability of the immune response to antigens in PCD.

[Intramedullary spinal cord metastasis documented by MR imaging].

A 63-year-old woman with progressive paraparesis was found to have an intramedullary spinal cord metastasis from the primary rectal cancer. Myelography and post myelography CT showed an enlargement of the spinal cord at level of the sixth to seventh thoracic vertebra. MR imaging disclosed a localized mass in the spinal cord at the same level. T2-weighted images showed an oval high signal intensity area with central low intensity, and gadolinium-DTPA-enhanced T1-weighted images demonstrated a ring enhancement. Histological examination of the spinal cord revealed an intramedullary spinal cord metastasis with intra-tumorous necrosis at T7 to T8 cord level.

[A case of unilateral VIIIth, IXth and Xth cranial nerve involvement with herpes zoster].

A 46-year-old healthy man suffered from sore throat, fever and right otalgia. On the next day, he developed hoarseness and difficulty in swallowing. On the 6th day, he suffered from vertigo, nausea and vomiting associated with unsteady gait. He was admitted to the otorhinolaryngology department in our hospital and pointed out to have vesicles at his right ear. On the 13th day, he was referred to our service. On admission, no vesicles were noted at the right ear or pharynx. Neurological examination revealed mild nuchal rigidity and marked hoarseness, associated with poor elevation of soft palate and loss of pharyngeal reflex on the right side. He also had horizontal-clockwise rotatory nystagmus in primary gaze and ataxic gait. There was no hearing loss nor facial palsy. No other abnormal neurological findings were noted. The cerebrospinal fluid showed pleocytosis associated with increased protein. The viral antibody titre for herpes zoster was significantly elevated on 18th day in serum as well as in cerebrospinal fluid. Vertigo, nausea, vomiting, ataxia and difficulty in swallowing were all disappeared by the 25th day, whereas hoarseness was improved but still noted 6 months later. Among cranial nerves, trigeminal and facial nerves are the most commonly affected in patients with herpes zoster, but there have been a few reported cases of the 9th and 10th cranial nerve involvement in the literature. In these previously reported cases, all were written before the era of serological diagnosis, and herpes zoster was diagnosed by the vesicles at the ear or pharynx.(ABSTRACT TRUNCATED AT 250 WORDS)

Pseudohypoparathyroidism (PHP) type II and selective hypoaldosteronism in a patient with retinitis pigmentosa.

A 53-year-old man with retinitis pigmentosa, who had two years' complaints of general malaise and muscle weakness, noticed occasional attacks of the cramps of the lower legs about three months prior to admission. At that time, hypocalcemia (7.6 mg/dl) and hyperphosphatemia (5.2 mg/dl) were pointed out. On admission, serum potassium was high-normal or high (4.4 - 4.9 mEq/l). Endocrinological studies revealed the findings of pseudohypoparathyroidism (PHP) type II, including a normal urinary cyclic AMP but blunted phosphaturic response to synthetic human parathyroid hormone (PTH), a high level of serum amino-terminal fragment of PTH with a low level of serum calcium and its ionized form, and a high-normal level of nephrogenous cyclic AMP. This patient also had selective hypoaldosteronism, as shown by intermittent hyperkalemia, low plasma and urinary levels of aldosterone and normal glucocorticoid levels. Plasma renin activity was normal but responded to a greater extent to furosemide plus upright posture. Plasma aldosterone was low and responded poorly to furosemide plus upright posture and graded angiotensin II infusions. The possible explanations for the association of PHP type II and selective hypoaldosteronism in this patient with retinitis pigmentosa are discussed.