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Biomedical subjects

R Boeri

Publications and source records attributed to R Boeri.

At least 37 records · Page 2Linked to original sources
PubMed1983

Course of chronic cluster headache.

A follow-up study (3.2 years) of 56 patients with chronic cluster headache who had had no remissions for at least a year. They were treated with lithium carbonate, methysergide and prednisone singly and in combination. An assessment of the therapeutic benefits is followed by a discussion on the course of chronic cluster headache.

Adult↗
PubMed1982

Electrophysiologic changes in workers with "low" blood lead levels.

In spite of numerous studies, the minimum level of lead exposure at which "sub-clinical" electrophysiologic abnormalities appear is still under discussion. Furthermore, it has not been clarified whether the electrophysiologic changes are directly related to PbB levels or to duration of exposure. This study was conducted on a group of 62 subjects occupationally exposed to lead with average blood lead levels below 50 microgram/100 ml and durations of exposure of less than 10 years. A reduction of motor and sensory nerve conduction velocities and sensory action potential amplitude of the median nerve was found in the subjects exposed to lead, as compared with a control group. Such abnormalities were already present in workers with the lowest blood lead levels, but were more severe in workers whose blood lead levels had exceeded 70 microgram/100 ml, even if this occurred only once in the last two years. The electrophysiologic changes did not correlate with duration of exposure but occurred very soon after initial exposure to lead.

Adolescent↗
PubMed1982

Electrophysiological study of subjects occupationally exposed to lead and with low levels of lead poisoning.

The relationship between the length of exposure to lead, blood lead level (PbB), and peripheral nerve damage in a population occupationally exposed to low lead levels was evaluated. Sixty-two foundry workers were studied whose length of exposure ranged from 5 months to 10 a; their mean PbB in the last 2 a had not exceeded 50 microgram/100 ml (2.4 mumol/l). The referents were 27 hospital employees, of comparable ages, not occupationally exposed to lead. The electrophysiological examination consisted of the determination of the motor conduction velocity (MCV) of the median, and peroneal nerves, sensory conduction velocity (SCV) of the median and sural nerves, and the latency of the T and H reflexes. The mean MCV, SCV and the amplitude of the sensory action potential (SAP) of the median nerve were significantly lower in the group of exposed workers than in the reference group. When the exposed subjects were divided into three groups according to length of exposure, no difference was observed between the three groups. When they were divided into different groups according to the maximum PbB (max PbB) value, the observed differences with respect to the reference groups were already present in those with a max PbB of less than 50 microgram/100 ml (less than 2.4 mumol/l), but were more evident in the subjects with a max PbB of greater than 70 microgram/100 ml (greater than 3.4 mumol/l). Within the group of subjects with a max PbB of 50-69 microgram/100 ml (2.4-3.3 mumol/l), the differences with respect to the reference values were more evident for subjects with a short length of exposure (less than 2 a). The MCV of the median nerve correlated with the time since the PbB exceeded 50 microgram/100 ml (2.4 mumol/l). In conclusion, the electrophysiological changes observed in lead-exposed subjects do not seem correlated with the length of exposure. Such alterations seem more evident in those subjects whose PbB has been greater than 70 microgram/100 ml (3.4 mumol/l) at least once during the preceding 2 a and in those subjects who, at the time of the neurophysiological examination, have a PbB greater than 50 microgram/100 ml (2.4 mumol/l). The apparently greater sensitivity to lead in new employees, compared to workers with a longer exposure time, remains to be clarified.

Adult↗
PubMed1981

A case of progressive multifocal leukoencephalopathy in preleukemic syndrome.

A case of an apparently primary PML in a 57-ys-old female is reported. The first neurological symptoms appeared about one year before death. The hematological abnormalities observed only during the last two months of life, at postmortem examination, were found to fit the criteria of the preleukemic syndromes.

Brain↗
PubMed1981

Relationship between clinical and electrophysiological findings and indicators of heavy exposure to 2,3,7,8-tetrachlorodibenzo-dioxin.

In this study the prevalence rate of peripheral neuropathy in a population living in an area polluted with 2,3,7,8-tetrachlorodibenzo-dioxin (dioxin-TCDD) was determined. Of the 723 subjects invited to the first screening in 1977, 470 (65%) attended. At the second screening in 1978, of the 710 invited subjects, 319 (45%) attended. Prevalence rate ratios for peripheral neuropathy and the associated 95% confidence limits were calculated for subgroups determined by the presence of (i) predisposing factors to neuropathy (alcoholism, diabetes, occupational exposure to neurotoxic agents, etc) or (ii) conditions thought to result from exposure to dioxin-TCDD such as chloracne or abnormal serum hepatic enzyme levels. The prevalence rate of peripheral neuropathy among those subjects with predisposing factors and among those with chloracne or abnormal serum hepatic enzyme levels was nearly three times greater than among those without these manifestations. The results derived from this study may be useful qualitative pointers for identifying subjects at risk in the neurological follow-up.

Acne Vulgaris↗
PubMed1980

Friedreich's ataxia. I. Clinical, neurophysiological and in vivo biochemical studies.

Eighteen patients with the presumptive diagnosis of Friedreich's ataxia were studied. Clinical, neurophysiological and biochemical data were concordant in 14 patients and led to the diagnosis of typical Friedreich's ataxia in this group of patients: the remaining 4 patients differed from the typical patients in several respects but mainly in the cardiological findings. It is concluded that so far no single clinical or laboratory finding is typical of F.A.. Multidisciplinary approaches are essential to the diagnosis of Friedreich's ataxia.

Adolescent↗
PubMed1980

Friedreich's ataxia in northern Italy: I. Clinical, neurophysiological and in vivo biochemical studies.

Eighteen patients with the presumptive diagnosis of Friedreich's ataxia were studied. Clinical, neurophysiological and biochemical data were concordant in 14 patients and led to the diagnosis of typical Friedreich's ataxia in this group of patients. The remaining 4 patients differed from the typical patients in several respects, but mainly in the cardiological findings. It is concluded that no single clinical or laboratory finding is typical of F.A. Multidisciplinary approaches are essential to the diagnosis of Friedreich's ataxia.

Adolescent↗
PubMedDate not supplied

Cytologic detection of metastatic malignant melanoma in urine. A report of three cases.

BACKGROUND: The presence of melanoma cells in urinary specimens is a rare event in either primary or metastatic melanoma of the genitourinary tract. CASES: Melanoma cells were observed in urinary specimens from three white males aged 50, 67 and 51 years, with a previous history of cutaneous melanoma in the first two cases; in the last one autopsy showed a primary melanoma of the gallbladder. The first patient, treated with palliative therapy, survived 10 months, the second died a few days after the cytologic diagnosis, while the third survived 1 month. All patients had widespread metastases at the time of cytologic diagnosis. CONCLUSION: The presence of melanoma cells in urinary specimens may be an important marker for assessing the spread of metastatic disease. When the cytologic diagnosis is made, widespread dissemination is present, and only palliative treatment is suggested.

Aged↗
PubMedDate not supplied

[ANCA-associated vasculitis].

ANCA-associated vasculitis. The term "antineutrophil cytoplasm antibody (ANCA)- associated vasculitis" (AASV) ihighers generally used to include primary vasculitis syndromes in which circulating ANCA against proteinase 3 (PR3) and myeloperoxidase (MPO) are commonly found. AASV syndromes include Wegener's granulomatosis, microscopic polyangiitis, idiopathic pauci- immune necrotizing crescentic glomerulonephritis and Churg-Strauss syndrome (CSS). AASV syndromes share some general clinical-histological manifestations, such as rapidly progressive renal failure and focal necrotizing glomerulonephritis with extracapillary proliferation in the absence (or in the presence of modest) immunoglobulins deposits (pauci- immune). Untreated AASV follow a progressive course with a fatal outcome due to vital organ failure. The combination of cyclophosphamide and prednisone is now established as the treatment of choice for patients with AASV, but there is considerable debate over the duration of therapy and the best way to administer cyclophosphamide. Treatment of AASV can be divided into two phases: an induction of remission and a maintenance of remission phase. Patients with AASV and renal involvement (serum creatinine less than 500 ml/L or 5.6 mg/dl) should be treated with a combination of oral prednisone with gradual tapering and cyclophosphamide. Once remission is achieved, usually after 3-6 months, azathioprine should replace cyclophosphamide. It is not known for how long treatment should be continued but at least one year of treatment after remission is warranted. When serum creatinine is than 500 ml/L (5.6 mg/dl) and/or oliguria is present, the addition of methylprednisolone pulses and/or plasma exchange should be considered.

Antibodies, Antineutrophil Cytoplasmic↗