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This is the first case, hitherto described, of benign essential gammopathy, presenting symptoms and histological evidence of peripheral neuropathy. Furthermore, in no previous case, has a specific localization of immunoglobulin (type IgM) to the areas of nerves involved by the lymphocytes been demonstrated. After six months' treatment with chlorambucil the neurological symptoms disappeared and in a biopsy from the right n saphenus no endoneural lymphocytes or local IgM could be found.

Bone marrow biopsies of 137 patients with Waldenström's macroglobulinaemia (WM), 26 with non-secretory immunocytoma and 32 with benign monoclonal gammopathy were processed for histologic evaluation. Bone marrow involvement was found in 110 (80%) initially, and in 24 (18%) in sequential biopsies. 3 types were distinguished: lymphoplasmacytoid (47%), lymphoplasmacytic (42%) and polymorphous (11%) with median survivals of 74, 25 and 12 months, respectively. When grouped according to the tumour cell mass in the biopsies, the median survivals were 55, 21 and 8 months for less than 20 vol%, 20-50 vol% and greater than 50 vol% respectively; in each subtype, the tumour cell mass correlated with the disease progression. 6 clinical variables were also found prognostically significant. These results demonstrate that (i) 98% of patients with WM have bone marrow involvement; (ii) the lymph node sub-classification is applicable to the bone marrow and has both clinical and prognostic significance; (iii) patients may be staged according to the tumour cell burden in the bone marrow biopsy.

Summary. Peripheral neuropathy has been described in malignant plasma cell dyscrasias such as multiple myeloma and Waldenstrom's macroglobulinaemia. Since it is not known whether the neuropathy is related to the plasma cell disorder or is a paramalignant phenomenon, 21 consecutive out-patients with benign monoclonal gammopathy (BMG) were analysed for peripheral neuropathies. Eleven patients had noticed slight motor and/or sensory extremity symptoms. Clinical examination, electromyographic and electroneurographic studies of the upper and lower extremities were performed. In five patients all results indicated a neuropathy, six other patients had clinical signs of neuropathy and four additional patients had positive electromyographic and/or electroneurographic results. Thus, a total of 15 patients had clinical and/or electrophysiological results compatible with neuropathy. There were no significant differences in haematological parameters between the group where all results indicated a neuropathy and the totally negative group or between the two groups with and without clinical neuropathy. Thus, the benign form of plasma cell dyscrasias seems also to be associated with mild clinical or subclinical peripheral neuropathy.

Based on the observation of a patient with a causal relationship between hyperparathyroidism and development of both autoimmune disease and paraproteinemia, we hypothesize a novel cause of autoimmunity triggered in the context of hyperparathyroidism. © Cañas et al.; Licensee Bentham Open.

Benign monoclonal gammopathy (MG) is an MG that is not accompanied by clinical manifestations of plasma cell dyscrasia, such as multiple myeloma, macroglobulinemia, amyloidosis, or other related disorders. Benign MG can progress to malignancy, but seldom causes organ damage.We presented a case denied any underlying disease who visited our hospital as acute uremia syndrome. Laboratory data indicated renal failure and abnormal paraprotein in the serum and urine. Renal biopsy indicated acute tubular necrosis and cast in the renal tubule. The plasma cell counts were normal in his bone marrow biopsy. The patient had received maintenance hemodialysis for the irreversible renal failure.Benign MG might progress to malignancy or other related disorders in a risk of 1% per year. It also might cause secondary organ impairment, such as kidney.

56歳の男性. セルロース・アセテート膜電気泳動上微量のM-蛋白を検出し, 免疫電気泳動を実施したところ, 抗α鎖抗体と反応してspurを形成する2本の沈降線が観察された. SRID法によるIgAの定量でも2重沈降輪を認めたため, 半分子IgAを疑い検索を進めたが, ゲル濾過法上IgAの分子量には異常を認めなかった. また, 本例のM-蛋白はIgA1と結合するレクチン (Jacalin) と反応しなかったことからIgA2M-蛋白と推察された. このM-蛋白を非還元下SDS-PAGEで分析したところL鎖の2量体の遊離が認められた. IgA2のアロタイプのうちIgA2m(1) はH鎖-L鎖間のS-S結合を欠き, L鎖間がS-S結合しているため, L鎖の2量体が容易に遊離する, このため本例のM-蛋白はIgA2m(1) アロタイプと判定した. 以上, 比較的まれにしか認められないIgA2m(1) アロタイプの良性M-蛋白血症の一例について検討した結果を報告した.

This is a review of the monoclonal gammopathies, including a discussion of cause. The role of T lymphocytes and B lymphocytes is presented. The recognition of a monoclonal protein in the serum and urine is presented in detail. The frequency of benign and malignant monoclonal gammopathies is provided. A long-term follow-up of 241 patients with apparently benign monoclonal gammopathy is examined closely. In this series, multiple myeloma, macroglobulinaemia, amyloidosis, or related disorders developed in 22% of the 241 patients with long-term disease. The median duration from the recognition of the monoclonal protein until the development of serious disease was approximately eight to ten years. The differentiation of benign from malignant monoclonal gammopathics is examinad in detail. The point is made that paticnu must be folld indefinitely because malignancy may develop more than 20 years later. The association of monoclonal gammopathies with other apparently unrelated diseases discussed. (Aust NZ J Med 1992; 22: 291–302.)

Purpose: Two cases of corneal crystal deposition are reported, both caused by a benign monoclonal gammopathy. Methods: Similar corneal pathology is identified in these two patients, both of whom presented with visual acuities of 6/6 or better Consideration of possible causes involved biochemical and haematological testing and assessment. Results: Potential for malignant transformation of monoclonal gammopathy was recognized, hence the need for ongoing haematological follow-up. Conclusion: Corneal crystals may be the initial presentation in a patient with monoclonal gammopathy, a rare, but significant, clinical finding.

Monoclonal gammopathy of undetermined significance (MGUS) and peripheral neuropathy may be causally linked. In most cases, the M-protein is of IgG or IgM type. Peripheral neuropathy associated with IgA MGUS is uncommon, and there are limited reports. Here, we report a case of a 55-year-old male who was diagnosed to have symmetrical sensorimotor peripheral neuropathy associated with IgA MGUS with deposits of IgA-monoclonal protein in the myelin sheath.

Bisalbuminemia (or alloalbuminemia) is characterized by the presence of two albumin components (in equal or unequal amounts) on serum protein electrophoresis (1). Bisalbuminemia may be inherited (genetic) or acquired. The cumulative frequency of inherited bisalbuminemia is typically 1:10 000 to 1:1000 (2)(3)(4), with inheritance showing an autosomal codominant pattern (5). Inherited bisalbuminemia has no pathologic or therapeutic consequences, but it is of interest for investigations of the evolution of functional differences in the protein, including altered affinity for steroid hormones, thyroxine, and several dyes (6). An acquired or transient form has been described that usually has a faster mobility (1)(7)(8). The faster form may be seen in patients who receive large amounts of β-lactam antibiotics or have pancreatic diseases, usually complicated by a ruptured false cyst (9). Acquired bisalbuminemia has been reported as a rare occurrence in patients with myeloma (10) or in nephrotic syndrome (1). We recently …

A 69 year old woman with inclusion body myositis is described. She presented with benign monoclonal gammopathy. She was resistant to steroid therapy, but responded to repeated immunoabsorption. Up to now, there has been no established therapy for inclusion body myositis, including IVIg. It is suggested that immunoabsorption could be an alternative therapy for inclusion body myositis, when it was accompanied by immunological abnormality.

The condition, also known as benign monoclonal gammopathy, is characterized by the presence of a monoclonal immunoglobulin or light chain on immunofixation of the patient’s serum or urine.[1][1],[2][2] Such a diagnosis can only be considered if underlying causes, most notably multiple myeloma, are

The presence of a serum IgD monoclonal protein (M-protein) is usually indicative of a malignant plasma cell disorder. However, one case of well-documented benign monoclonal gammopathy (BMG) of IgD type has been reported. We describe another patient with IgD monoclonal gammopathy of undetermined significance (MGUS) with long-term follow-up. In this patient an IgD lambda M-protein was found on routine serum electrophoresis. She is alive and has no evidence of multiple myeloma or amyloidosis after 8 years of follow-up. Although IgD MGUS is exceedingly rare, this case demonstrates that the presence of a serum IgD M-protein is not necessarily synonymous with a malignant plasma cell process.

Interleukin 6 (IL6) plasma levels were measured in 63 patients with multiple myeloma and 8 individuals with benign monoclonal gammopathy. 15 of these 71 samples showed by an enzyme linked immunosorbent assay (ELISA) detectable levels that ranged from 5 to 107 pg of IL6/ml. The IL6 levels of patients with multiple myeloma did not differ significantly from those of normal individuals (N = 25, range 5-27 pg IL6/ml) (Student's t-test, p = 0.295). The samples were negative for IL4; 3 were found positive for IL1 beta. A correlation between IL6, IL4 and IL1 beta levels and disease status was not observed for this group of patients.

The C57BL/KaLwRij mice have been shown to spontaneously develop a variety of B-cell proliferative disorders with aging. Over 80% of mice of this strain develop benign monoclonal gammopathy (BMG) which in most aspects is indistinguishable from that described in humans (for reviews see Radl,1981, 1986, 1989). About one third of old mice at necropsy and histopathology examination were shown to suffer from lymphoma, mainly of the follicle center cell type, the majority of which is most likely of the B cell origin (unpublished results). Nearly 1% of mice older than two years develop Waldenstrom’s macroglobulinaemia-like lymophoma (WM) (Radl et al. 1989) or multiple myeloma (MM) (Radl et al. 1988).

Monoclonal gammopathy of uncertain significance (MGUS) may present the clinician with diagnostic difficulties. This paper reviews the literature relating to MGUS, presents findings of a local prevalence study, and provides advice on monitoring.

Paraproteinaemia may be associated with xanthomatous skin deposits and these can arise in the absence of elevated lipid levels. Two cases of benign monoclonal gammopathy with diffuse plane xanthomatosis are reported. Case 1 exhibited hypolipidaemia and a functional deficiency of C1 esterase inhibitor. Case 2 showed a normal lipoprotein profile, abnormal platelet aggregation, and a cutaneous vasculitis with evidence of complement consumption via the classical pathway. The significance of these abnormalities is discussed.

A case of isolated lambda-light chain proteinemia and proteinuria is reported. During a 42-month follow-up, no sign of myelomatosis or amyloidosis developed and Bence Jones proteinuria remained nearly of the same magnitude. This case of apparently idiopathic Bence Jones gammopathy, the first lambda-type so far reported, is added to similar observations to give further support to the contention that a benign counterparty to light-chain myeloma may exist.

The number and mode of distribution of immunoglobulin containing cells in human bone marrow were investigated immunohistochemically using paraffin sections of bone marrow aspirates. In individuals without specific diseases, the number of immunoglobulin containing cells per unit field in bone marrow increased with advancing age until the 3rd decade and leveled off thereafter. The magnitude of the increase was great for Ig-G and Ig-A, but very slight for Ig-M. Such age-related change in the number of Ig-G and Ig-M containing cells in bone marrow was almost comparable to the age-related change of serum level of Ig-G and Ig-M. However, the magnitude of age-related increase of Ig-A containing cells in bone marrow was apparently higher than that of the serum level of Ig-A. Cluster formation of immunoglobulin containing cells increased with age in terms of both incidence and size. Three points were suggested for differentiation of benign monoclonal gammopathy (BMG) from multiple myeloma (MM). First, the ratio of serum level of M-component divided by the average number of immunoglobulin containing cells per unit field was higher in BMG than in MM; second, the number of cells per cluster of immunoglobulin containing cells was more than 50 in MM, but that in BMG less than 20; third, the small immunoglobulin containing cells with narrow cytoplasm were more prominent in MM than in BMG.

A report of a patient with the rare syndrome of sinus histiocytosis with massive lymphadenopathy is presented here. This patient is unusual in several respects, including his longevity after diagnosis, the presence of a benign monoclonal gammopathy, and the characterization of his cutaneous infiltrates by immunofluorescent monoclonal antibody markers. A review of the literature on sinus histiocytosis with massive lymphadenopathy, with particular emphasis on cutaneous manifestations, is given.

Peripheral blood leukocytes (PBL) from myeloma patients were studied for their capacity to lyse plasma cells from myeloma patients, benign monoclonal gammopathy (BMG) patients, and nonneoplastic disease patients. Plasma cells were isolated from bone marrow, labeled with 51Cr, and cultured with PBL isolated from patients with myeloma, BMG, or nonneoplastic disease, as well as normal individuals. PBL from patients with multiple myeloma demonstrated responses to autologous or allogeneic myeloma plasma cells. Optimum conditions for cytotoxic response included a responder-to-stimulator ratio of 1:1 and an effector-to-target ratio of 20:1. PBL from normal individuals or patients with BMG failed to demonstrate this response. However, PBL from BMG patients, but not normal individuals, could be induced to kill myeloma plasma cells (but not nonmyeloma plasma cells) by simultaneous stimulation with allogeneic lymphocytes and myeloma plasma cells.

Peripheral nerve biopsies from two patients with chronic sensorimotor neuropathy were studied. The first case was a non-Hodgkin malignant lymphoma and did not show any dysglobulinemia. The second case had a benign monoclonal gammopathy IgG, Lambda type. Direct immunofluorescence showed no deposits in the first case and slight deposits of anti IgG sera on a few myelinated fibers in the second case. There were numerous fibers showing uncompacted myelin lamellae, 7% in the first case and 4% in the second case. Some of these fibers had axons containing more tubules than filaments. The very few cases reported on neuropathies showing that uncompacted myelin lamellae were frequently associated with dysglobulinemic neuropathy. However, this ultrastructural abnormality of the myelin sheath can be observed without any dysglobulinemia.

In 42 patients with untreated or treated multiple myeloma (MM) or benign monoclonal gammopathy (BMG) the lymphocytes and T lymphocyte subsets were determined by monoclonal antibodies and other surface markers. In untreated MM, the T cells (1077/microliters vs 1439/microliters, P less than 0.01) and especially the OKT4+ lymphocytes (700/microliters vs 950/microliters, P less than 0.05) were significantly reduced compared with a control group. The OKT8+ cells were slightly but not significantly decreased. In previously treated MM, the loss of T cells was more pronounced than in the untreated group and was primarily caused by a further reduction of OKT4+ cells. Patients with BMG revealed decreased OKT8+ lymphocytes (304/microliters vs 502/microliters, P less than 0.001), whereas the OKT4+ cells were within the normal range. Therefore, the OKT4/OKT8 ratio was significantly elevated compared with that in untreated MM patients and normal controls (3.31 vs 2.06 vs 2.13; P less than 0.005). To sum up, in MM the results revealed a reduction of T cells, mainly of OKT4+ cells, which is intensified by chemotherapy and persists even after a long therapy-free interval. The different findings of T cell subsets in BMG and MM may be a helpful criterion to differentiate between BMG and MM.

Four cases of pernicious anemia developing in association with multiple myeloma are described. The description now of 14 cases demonstrating the association of these two disorders suggest a causative relationship. These observations, in addition to the previously well-documented increased coincidence of pernicious anemia and benign monoclonal gammopathy and pernicious anemia and hypoglobulinemia, suggest that screening for vitamine B12 deficiency in patients with gammopathies and for protein abnormalities in patients with pernicious anemia is indicated.

Scleromyxedema is an infiltrative skin disease produced by hyaluronic acid deposition in the dermis. A benign monoclonal gammopathy is usually present. We report 2 patients with scleromyxedema and systemic illnesses. Both patients had muscle weakness, dysphagia, and weight loss in addition to the skin changes. One also had sclerodactyly, telangiectasias, and Raynaud's phenomenon. Scleromyxedema with systemic involvement may mimic rheumatic diseases.

Paraproteins display a characteristic pattern of limited heterogeneity on isoelectric focusing. In a group of 50 patients with various neurological disorders and paraproteinaemia this pattern could be demonstrated in serum and cerebrospinal fluid simultaneously, regardless of the form of nervous system involvement or of the function of the blood-cerebrospinal fluid barrier. Although there were no qualitative differences in the pattern between paraproteins from benign and malignant cases, a distinct quantitative difference was found: Paraproteins from myeloma patients had significantly more subfractions extending over a wider pH range than paraproteins from patients with benign monoclonal gammopathy. Due to the high sensitivity of isoelectric focusing, more paraproteins could be detected in cases where other electrophoretic methods including immunoelectrophoresis were negative. A surprisingly high percentage of patients was found with benign monoclonal gammopathy and vascular lesions of the central nervous system.

Plasma immunoglobulin levels, Bence-Jones proteinuria, and bone marrow cytology were examined in 44 patients with benign monoclonal gammopathy (BMG), in order to study differential diagnostic criteria between this state and multiple myeloma. High immunoglobulin concentrations, in the range usually attributed to multiple myeloma, and subnormal concentrations of uninvolved polyclonal (“background”) immunoglobulin were frequently seen in BMG. Of the BMG patients, 40% had Bence-Jones proteinuria defined as a urinary M component, and myeloma-like accumulations of plasma cells were seen in the bone marrow in several instances. We conclude that criteria used to distinguish between myeloma and BMG are not specific and that differences between the two conditions are quantitative rather than qualitative.

The urinary neopterine levels were measured by HPLC in 417 normal subjects and in 216 patients with haematological diseases. All patients with active malignancies (multiple myeloma, polycythaemia vera, Hodgkin's lymphoma, non-Hodgkin's lymphoma, chronic myelocytic and chronic lymphocytic leukaemia) showed highly elevated mean and median values compared to the control groups. Those of patients with multiple myeloma stage I were only raised to near the upper limit of healthy subjects. Of 123 patients with active disease 105 (85%) were above the upper limit. In contrast, the mean and median values of 56 patients with neoplasias in remission (Hodgkin's and non-Hodgkin's lymphoma, acute leukemia and multiple myeloma) were not different from those of healthy subjects, and only 7 (12.5%) of these patients had levels above the upper limit. In patients with non-malignant diseases (haemolytic anaemia and benign monoclonal paraproteinaemia) the mean and median values were not raised. In patients with non-Hodgkin's lymphoma and with chronic lymphocytic leukemia, the neopterine levels corresponded with the tumor stage. The present data suggest that neopterine assay may supplement laboratory measurements in haematological diseases, providing helpful information.

During a 6 year period, eight instances of familial occurrence of myeloma involving siblings (16 cases of myeloma and 3 of probable benign monoclonal gammopathy) were encountered at the Mayo Clinic. No other monoclonal serum protein abnormalities were found in 70 relatives studied. In view of the infrequency of myeloma, the high familial occurrence of this disease suggests the possibility of genetic factors in its etiology. It is most important that a complete family history be obtained from patients with myeloma.

Disease associations of clonally restricted serum immunoglobulin (Ig) abnormalities were examined using methods for detecting and characterizing homogeneous Ig that are approximately forty times more sensitive than either cellulose acetate zone electrophoresis or immunoelectrophoresis. Medical records of three hundred five patients with clonally-restricted serum immunoglobulins, including 100 monoclonal gammopathies, and 205 immune complex/oligoclonal patterns were reviewed to obtain the attending physician's discharge diagnosis. Our data confirm lymphoproliferative disorders as the most frequent cause of monoclonal gammopathy (63% of our cases). However, in contrast to earlier reports, we found little evidence to support an association between monoclonal gammopathy and non-reticular malignancy. This does not mean our patients with these disorders had normal serum immunoglobulin patterns; rather, their qualitative abnormalities were, for the most part, not monoclonal. Instead, patients with these diseases had a high incidence of serum immune complexes and their antibody excess sequelae, oligoclonal patterns. Oligoclonal responses are noteworthy because Ig products of the individual clones do not always achieve equivalent serum concentrations, nor are the various clonal products synchronized with respect to the time at which they attain peak concentration. This creates a number of problems for laboratories attempting to characterize such abnormalities; 1) some analytical methods may only be capable of detecting the dominant clone of an oligoclonal pattern, and 2) analysis of a single specimen may yield erroneous results because the unique waxing and waning kinetic pattern of oligoclonal responses may preclude identification of all components at a single time point. We conclude that benign "monoclonal" gammopathies and circulating immune complex/oligoclonal Ig abnormalities occur in the same clinical situations and may be synonymous. The sensitivity of an individual laboratory's analytical methods would then determine which name is applied.

We describe a patient in whom classic clinical multiple myeloma did not develop until eighteen years after discovery of an elevated erythrocyte sedimentation rate, hyperglobulinemia and increased plasma cells in the bone marrow. The patient exhibited a tall, sharp peak in the serum electrophoretic pattern, no appreciable change in the amount of serum γ-globulin (which was less than 3.0 gm. per 100 ml.), and a constant slight plasmacytosis in the bone marrow for nearly eighteen years, thus fulfilling the criteria for "benign monoclonal gammopathy." This illustrates the possibility that this "chronic benign process" can erupt into a progressive and serious phase at a much later date, and extends our understanding of plasmaproliferative disease.

52 patients with benign monoclonal gammopathy were HLA typed and compared withe 48 patients with malignant monoclonal gammopathy. Antigen B40 was more frequent within the first sample. This association is discussed, together with the results of familial investigations. For systematic serum electrophoresis detected 5 benign monoclonal gammopathies in 172 relatives of 37 patients suffering from multiple myeloma or Waldenström's macroglobulinemia.

In over 1200 cases examined by isoelectric focusing of CSF and serum proteins, 4 patients had benign monoclonal gammopathy. These patients were affected by amyotrophic lateral sclerosis of bulbar onset, sensitive neuropathy of Thevenard type, myasthenia gravis, and limb-girdle muscular dystrophy, respectively. The difficulty to relate the differences in the clinical features of these cases to a common physiopathological mechanism and the incidence of this finding (0.4% in 873 cases ranging from 21-60 years of age) do not seem to suggest any pathogenetic relationship between benign monoclonal gammopathy and the different neurological disorders encountered in these patients.

Bilateral superficial corneal deposits and scleromyxedema, an uncommon dermatosis caused by the accumulation of acid mucopolysaccharide in the skin often associated with a benign monoclonal gammopathy developed in a 71-year-old man. A biopsy specimen of the cornea showed that the deposits stained strongly positive for IgG and lambda chains. Ultrastructurally, the deposits consisted of amorphous granular material. Scleromyxedema should be considered in the differential diagnosis of noninflammatory superficial keratopathies associated with benign gammopathies.

To the Editor. —We are writing in regard to the article entitled "Posterior Corneal Crystalline Deposits in Benign Monoclonal Gammopathy" by Rodrigues et al, which appeared in the January issue of theArchives(97:124-128, 1979). Using a modification of the peroxidase-antiperoxidase technique of Sternberger et al, 1 the crystalline deposits in the corneal button stained with antiserum to IgG, IgA, and IgM heavy chains and both κ and λ light chains. Both the control slides—one where the primary antiserum is replaced by normal rabbit serum and the second where the primary antiserum is omitted—were positive. Thus, the crystalline deposits were not identified as deposits of IgG κ immunoglobulin, as stated by the authors. The findings seem to indicate that the crystalline deposits are composed of a material with rheumatoid-factor-like activity. Rheumatoid factors are immunoglobulins, usually of the IgM class, that react with the Fc fragments of various immunoglobulins. It should

A panel of monoclonal antibodies that identify various antigens present on T and B cells was used to characterize circulating blood lymphocyte subsets in multiple myeloma [(MM) - 13 patients] and benign monoclonal gammopathy [(BMG) - 5 patients]. In MM and BMG an increase in B cell proportions (BA 1 positive cells) was observed, whereas T cells (Lyt 3 positive cells) were reduced compared to normal controls. However, with respect to the T cell subset distribution, a marked diversity between MM and BMG was noted. This may help to differentiate BMG from MM. In MM a relative decrease in inducer/helper T cells (OKT 4 positive cells) and increase in suppressor/cytotoxic T cells (OKT 8 positive cells) as well as in NK/K T cells (Leu 7 positive cells) was observed. On the other hand, in BMG the relative T cell subset distribution was comparable to those seen in normal subjects.

A newly observed case of asymptomatic multiple myeloma in which phagocytic myeloma cells were observed is described. Bone marrow aspirates contained 16% myeloma cells, 2% of which engulfed red blood cells, lymphocytes, and platelets. The possibility is discussed that phagocytizing ability may be one of the markers for malignant plasma cells. Nothing is so far known of the phagocytosis by plasma cells in benign monoclonal gammopathy which is strictly defined.

This study was carried out in order to investigate a possible relationship between multiple myeloma and the occurrence of material exhibiting the properties of amyloid within renal tubules. Two groups of autopsied patients, with myelomatosis and benign monoclonal gammopathy were examined for the presence of amyloid deposits in renal and extra-renal sites. Urines were analysed for the presence and amount of Bence Jones protein and the pattern of the associated proteinuria was characterized. Renal tubular casts exhibiting the histochemical characteristics of immuno-amyloid were found exclusively in myeloma patients with Bence Jones proteinuria but without the renal lesions classically described as “myeloma kidney”. This finding was independent of the occurrence of immuno-amyloid deposits in other renal and extra-renal sites, suggesting involvement of local factors in the pathogenesis of amyloid formation and deposition within renal tubular lumina. The results of present study suggest the conclusion that the presence of amyloid intratubular casts is to be regarded as a peculiar finding in myelomatosis.

A patient with monoclonal gammopathy and renal failure due to kappa light chain deposition in the glomerular basement membrane is reported. After 8 months, he developed a progressive and severe renal failure requiring haemodialysis. 30 months later, the monoclonal gammopathy was unchanged. Clinical features, as well as kinetic and immunological studies, were consistent with a diagnosis of benign monoclonal gammopathy (BMG). This case suggests that the renal failure complicating a monoclonal gammopathy is not related to its malignancy.

Sera from 111 patients with IgG myeloma (MM) and 76 patients with IgG benign monoclonal gammopathy (BMG) were examined for the presence of anti-IgG antibodies. Forty-nine and five-tenths percent of MM patients were positive as compared to 26.3% of patients with BMG and 28% of age-matched controls (P < 0.005). Anti-IgG antibodies were most easily detected using Rh-positive cells coated with various human incomplete antibodies. Anti-IgG antibodies showed specificity for determinants present on whole IgG and, in some instances, Fc. No clear evidence for anti-idiotypic reactivity with autologous M components could be obtained. In most sera, anti-IgG factors appeared to be present in low-molecular-weight fractions (3.5–5.0S). The apparent increase in anti-Ig factors in MM as opposed to BMG may reflect a basic difference in control mechanisms.