Immunology & Internal Medicine & Pediatrics & Family Medicine
Total IgG
Immunoglobulin G (IgG) is the most abundant antibody class in human serum - representing 70-80 % of total circulating immunoglobulins, with normal values ranging from 6.0 to 16.0 g/L in adults, depending on the laboratory. They are the main mediators of long-term humoral immune memory, produced during the secondary immune response (vaccine boosters + repeated infections) by memory B lymphocytes under the influence of helper T lymphocytes (CD4+). IgG is subdivided into four subclasses (IgG1 + IgG2 + IgG3 + IgG4) which differ in their effector functions, relative abundance and associated diseases. Total IgG measurement is a key element in the assessment of humoral immune deficiencies, recurrent infections and certain inflammatory and autoimmune diseases. Low IgG - hypogammaglobulinemia - may indicate a primary immune deficiency (Variable Common Immune Deficiency - VCD, X-linked agammaglobulinemia - Bruton's disease, or IgG subclass deficiency) or a secondary one (myeloma, lymphoma, drugs, renal or digestive losses). Elevated IgG - hypergammaglobulinemia - is characteristic of chronic inflammatory conditions, autoimmune diseases and chronic infections, and may point to monoclonal gammopathy (MGUS, myeloma). Intravenous immunoglobulin (IVIG) or subcutaneous immunoglobulin (SCIG) substitution is the standard treatment for severe primary humoral immunodeficiency, helping to maintain protective IgG levels and prevent recurrent bacterial infections.
Biology of IgG, subclasses, and pathophysiology of deficiencies
- Structure, subclasses, and biological functions of IgG: general structure of IgG: γ-type immunoglobulin → 2 γ heavy chains + 2 light chains (κ or λ) linked by disulfide bridges → Fab region (Fragment Antigen Binding): specific binding to antigen → Fc region (Fragment Crystallizable): interaction with Fc receptors on immune cells + complement activation + long half-life: 21-28 days for IgG1 + IgG4 → 7-10 days for IgG3 → half-life regulated by FcRn (neonatal Fc Receptor) which recycles IgG from endosomes to circulation → transplacental passage of IgG: via FcRn → immunological protection of fetus and newborn up to 6 months; four subclasses and their functions: IgG1 (60-70 % of total IgG): strongly activate complement (classical pathway) + bind to FcγR of phagocytes → opsonization + neutralization of viral + bacterial antigenic proteins → main subclass responsible for anti-protein responses (vaccine boosters + viral + bacterial infections) → IgG2 (20-30 % of total IgG): response to polysaccharide antigens (23-valent pneumococcal vaccine + polysaccharide meningococcal vaccine) → less efficient for complement activation + binding to FcγRIIA (H131 variant) → IgG2 deficiency → recurrent infections with S. pneumoniae + H. influenzae (encapsulated + polysaccharide pathogens) → IgG3 (5-8 % of total IgG): most potent complement activator → response to viral + bacterial proteins → short half-life (7-10 days) → marker of recent immune response → IgG4 (1-6 % of total IgG): anti-inflammatory properties → block IgE-dependent allergic responses + little complement activation + no binding to FcγR → IgG4 diseases (IgG4-Related Disease - IgG4-RD): IgG4+ plasma cell fibro-inflammatory disease → multi-organ involvement (pancreas + salivary glands + orbit + kidneys + aorta) → IgG4 >1.35 g/L + IgG4/IgG ratio >5 % + tissue infiltrates → corticosensitive → Stone 2012 - NEJM; total IgG reference values by age: term newborn: maternal IgG → 7-16 g/L (transplacental) → nadir at 3-6 months (<3 g/L — physiological trough) → progressive rise → adult: 6–16 g/L → standards vary between laboratories + assay methods (nephelometry + turbidimetry) → IgG subclasses (adult): IgG1: 4.2–12.9 g/L + IgG2: 1.2–6.6 g/L + IgG3: 0.18–1.63 g/L + IgG4: 0.01–1.35 g/L
- Humoral Immune Deficiencies — Mechanisms and Classification: Primary immunodeficiencies with low IgG — the main ones: CVID (Common Variable Immunodeficiency): the most frequent symptomatic primary immunodeficiency → prevalence 1/25,000 → low IgG, IgA, IgM <2 SD below norms + lack of vaccine response + after exclusion of other causes → variable presentation: recurrent bacterial infections (pneumonia + sinusitis + bronchitis + encapsulated germ otitis) + gastrointestinal diseases (Giardia + IBD-like) + granulomatous diseases + lymphomas + autoimmune diseases → average diagnostic delay: 5-7 years → Conley 1999 - Clinical Immunology: diagnostic criteria for CVID + genetic mechanisms + Picard 2018 - JACI : IUIS classification → mutations in ICOS + TACI (TNFRSF13B) + BAFFR + CD19 + CD20 + CD81 + X-linked agammaglobulinemia (Bruton disease - XLA) : BTK (Bruton Tyrosine Kinase) gene mutation → blockage of B lymphocyte maturation (pre-B → mature B) → total absence of IgG + IgA + IgM (<0.1 g/L) → absence of B lymphocytes → boys exclusively (X-linked) → severe infections as early as 6-9 months (maternal protection disappears) → S. pneumoniae + H. influenzae + Giardia → enterovirus (chronic meningitis + meningoencephalitis) → treatment: lifelong IVIG substitutes → Vetrie 1993 - Nature: discovery of BTK + XLA → autosomal recessive agammaglobulinemia (ARA): mutations in IGHM + CD79A + CD79B + BLNK + λ5/ψ → picture similar to XLA + boys and girls → isolated IgG subclass deficiency: normal or slightly low total IgG + one or more low IgG subclasses (IgG2 most often) + recurrent encapsulated germ infections + IgG2: <0.5 g/L (adult) or <2 SD relative to age norms → systematic subclass workup if total IgG normal + recurrent infections + Aghamohammadi 2012 - Journal of Clinical Immunology: IgG2 subclass deficiencies + recurrent infections; mechanisms of secondary hypogammaglobulinemias: renal losses: nephrotic syndrome (urinary IgG) → low IgG → infections + lymphatic leakage (lymphoma + intestinal lymphangiectasia) → digestive losses: exudative enteropathy (IBD + lymphangiectasia) → immunosuppressive drugs: rituximab (anti-CD20) → B-cell depletion → prolonged hypogammaglobulinemia + long-term corticosteroids + belimumab + certain chemotherapies + multiple myeloma: production of monoclonal IgG + inhibition of normal IgG (immunosuppression) → normal Ig («background normal immunoglobulins») are low in myeloma → bacterial infections + chronic lymphocytic leukemia (CLL): hypogammaglobulinemia + recurrent infections + rituximab + CLL + biotherapies → Frey 2020 - Journal of Allergy and Clinical Immunology: hypogammaglobulinemias secondary to autoimmune disease treatments.
Diagnosis, treatment, and associated diseases of elevated IgG
| Situation / illness | Data, criteria and procedures | Key studies and recommendations |
|---|---|---|
| Diagnostic workup for low IgG Electrophoresis — immunofixation — IgG subclasses — vaccine response — lymphophenotyping — BTK — DICV evaluation — ESID — recurrent infections |
Structured diagnostic approach to low IgG: step 1 - confirm hypogammaglobulinemia: total IgG <6.0 g/L (adult) → confirm with a 2nd assay at ≥1 month + compare with age norms (child) + exclude hemodilution or global hypoprotidemia (albuminemia + total protidemia) + step 2 - complete immunological workup: total IgG + IgA + IgM + IgE → hypogammaglobulinemia profile: IgG + IgA + IgM all low → CVID or agammaglobulinemia → low IgG + normal IgA + IgM → selective IgG deficiency or insufficient production (liver failure + malnutrition + losses) → IgG subclasses (IgG1 + IgG2 + IgG3 + IgG4): essential if slightly low total IgG + recurrent infections + or normal total IgG but suspected subclass deficiency → lymphophenotyping: CD3+ (T) + CD4+ + CD8+ + CD19+ (B) + CD16+CD56+ (NK) → DICV: B lymphocytes present but not functional + XLA: B lymphocytes absent (<1 % of lymphocytes) → + activated + switched B → CBC + CRP + albuminemia + total protidemia → liver workup (cirrhosis → variable IgG) + step 3 - evaluation of vaccine response: functional indicator of IgG production → level of specific anti-tetanus + anti-pneumococcal (post 23-valent vaccine) + anti-diphtheria antibodies → insufficient vaccine response + low IgG → confirmed functional deficit → Gold standard for diagnosis of CVID + immunofixation + electrophoresis: rule out monoclonal gammopathy (M peak) + polyclonal hypogammaglobulinemia profile → BTK sequencing (Bruton's tyrosine kinase gene): if XLA suspected (boy + IgG + IgA + near-zero IgM + absence of B lymphocytes) → other genes according to clinic + immune deficiency gene panel if typical CVID <30 years (ICOS + TACI + BAFFR + CD19 + LRBA + NFKB1 + NFKB2 + PIK3CD) + step 4 - search for secondary causes if unlikely primitive : proteinuria (nephrotic syndrome) + ECBU + 24h urinary protein assay + liver workup (cirrhosis + hepatitis) + immunosuppressive drugs (rituximab + corticoids + chemotherapy + belimumab) + CBC + blood smear (CLL + lymphoma) + HIV serology → LDH + beta-2-microglobulin + TAP scan (lymphoma + thymic tumor) + step 5 - ESID criteria for diagnosis of CVID: IgG <2 SD below norms + ≥1 of : IgA <2 SD + IgM <2 SD + no normal vaccine response + reduced switched B lymphocytes + after exclusion of other causes | Picard 2018 - Journal of Allergy and Clinical Immunology (IUIS): 2017 IUIS classification of primary immune deficiencies → diagnostic criteria + DICV + XLA + subclass deficiencies + Conley 1999 - Clinical Immunology: diagnostic criteria for DICV + infections + associated diseases + Cunningham-Rundles 2007 - Journal of Allergy and Clinical Immunology: DICV → infections + autoimmune diseases + granulomas + lymphomas → comprehensive review + Vetrie 1993 - Nature: BTK → XLA gene discovery → major impact on genetic diagnosis + Notarangelo 2014 - JACI: ESID criteria for CVID + + Frey 2020 - JACI: hypogammaglobulinemia secondary to biotherapies → rituximab + corticosteroids + monitoring protocols + CAAIF (Canadian Allergy Asthma and Immunology Foundation) + Immunodeficiency Canada: Canadian guidelines for primary immunodeficiencies + vaccine response assessment + ESID 2023: European Society for Immunodeficiencies - guidelines for CVID + XLA |
| Immunoglobulin Replacement Therapy (IVIG and SCIG) IVIG — SCIG — indications — dose — IgG target — trough level — frequency — adverse effects — reimbursement — Régie de l'assurance maladie du Québec |
Intravenous immunoglobulin (IVIG) - indications and protocols in primary deficiencies: definite indications for IVIG according to the Guide to the use of IVIG (Health Canada + INESSS): CVID (ESID criteria met) + XLA + autosomal recessive agammaglobulinemia + other primary immune deficiencies with low IgG + documented recurrent infections + secondary hypogammaglobulinemia with severe or recurrent infections (CLL + rituximab + myeloma + post marrow transplant) → indication not certain: isolated IgG subclass deficiency without documented infections → debatable + substitution dose for primary deficiencies (CVID + XLA): 400-600 mg/kg/4 weeks (adult) + adjust according to residual IgG level (trough level) → target trough level: residual IgG before next infusion ≥6-8 g/L for most patients → higher target (>8 g/L) if: chronic lung infections + bronchiectasis + recurrent sepsis + children + Bonilla 2015 - Journal of Allergy and Clinical Immunology : review of IVIG substitution in immune deficiencies → trough level objectives + frequency → infusion frequency: every 3-4 weeks IV → or every 1-2 weeks SC (SCIG) → products available in Canada: Gammagard (Baxter/Takeda) + Privigen (CSL Behring) + Gamunex-C (Grifols) + Panzyga + Octagam → IgG content >95 % + very low IgA in some preparations (Privigen + Octagam - important if anti-IgA positive) → subcutaneous immunoglobulins (SCIG) - home ambulatory alternative : advantages vs IVIG: more stable IgG levels (no peak → no trough) + fewer systemic effects + home administration (pump + or facilisette) + better quality of life → Gardulf 1991 - Lancet: SCIG → stable levels + fewer reactions → first demonstration + Chapel 2000 - Lancet: SCIG vs IVIG → comparable infection rates + Duse 2009 - Journal of Clinical Immunology: SCIG → improved quality of life + superior compliance → SCIG on the rise in Canada (home SCIG program reimbursed in several provinces) → SCIG dose: equivalent to or slightly higher than IVIG dose (better bioavailability) + 100-200 mg/kg/week → injection sites: abdomen + thighs + back → IVIG side effects: systemic reactions (headache + fever + chills + myalgias): frequent with first infusions → premedication: acetaminophen + diphenhydramine + methylprednisolone if history of reactions + thromboembolism (IVIG + elderly patients + thrombotic FdR) → slow the flow rate + hydration + acute renal failure: particularly with sucrose preparations → prefer sucrose-free preparations in renal failure patients + aseptic meningitis (rare) + hemolysis (rare - anti-red blood cell antibodies in IVIG) → reimbursement in Quebec (RAMQ): IVIG reimbursed in certain indications of primary immune deficiencies + severe secondary hypogammaglobulinemia → prior authorization request + INESSS: Guide d'utilisation clinique des immunoglobulines IV au Québec → consult for reimbursed indications + frequency + doses + monitoring | Bonilla 2015 - Journal of Allergy and Clinical Immunology: review IVIG in immune deficiencies → trough level targets + frequency + safety + Gardulf 1991 - Lancet: SCIG at home → stable levels + fewer reactions + Chapel 2000 - Lancet: SCIG vs IVIG → comparable infection rates → SCIG = valid alternative + Duse 2009 - Journal of Clinical Immunology: SCIG → quality of life + superior compliance vs IVIG + Cunningham-Rundles 2010 - Journal of Allergy and Clinical Immunology: trough level IgG → correlates with protection against infections → target >6-8 g/L → + INESSS 2020: Guide d'utilisation des immunoglobulines IV au Québec → indications + doses + reimbursement → mandatory Quebec reference + Health Canada: national guidelines on the use of immunoglobulins → CAAIF + Immunodeficiency Canada: substitution protocols + follow-up + National Blood Authority Australia 2021 (Canadian equivalent INESSS) + Picard 2018 - JACI: IUIS classification of deficiencies → IVIG indications clearly defined |
| Elevated IgG — polyclonal and monoclonal hypergammaglobulinemia Autoimmune diseases — chronic infections — cirrhosis — HIV — monoclonal gammopathy — IgG4-RD — MGUS IgG — IgG myeloma — electrophoresis — immunofixation |
Elevated IgG (>16 g/L) - causes and orientation: polyclonal hypergammaglobulinemia (diffuse increase in all IgG subclasses + often all elevated Ig + EPS: diffuse polyclonal peak in γ region): systemic autoimmune diseases: SLE (often elevated IgG + consumed C3/C4 complement + anti-DNA) + autoimmune hepatitis (IgG >16-20 g/L → diagnostic criterion + massive hypergammaglobulinemia) + Sjögren's syndrome (elevated IgG + IgA + IgM + positive rheumatoid factor) + rheumatoid arthritis + SAPL + dermato/polymyositis → chronic infectious diseases: HIV (polyclonal IgG increase - up to 20-30 g/L in untreated forms) + active tuberculosis + chronic hepatitis B or C + malaria (chronic) + visceral leishmaniasis (kala-azar - massive IgG 30-50 g/L) + syphilis + chronic liver diseases: cirrhosis (elevated IgG + IgA - stimulation by intestinal bacterial antigens via the portal system) + autoimmune hepatitis +++ → chronic inflammatory diseases: sarcoidosis + Crohn's disease + drug-induced causes + IgG4 diseases: IgG4 >1.35 g/L in appropriate clinical context (Stone 2012 - NEJM) → diagnosis of IgG4-RD by biopsy (lymphoplasmacytic infiltrates + storiform fibrosis + obliterative vasculitis) + response to corticosteroids; monoclonal hypergammaglobulinemia (narrow peak on EPS in β or γ region + immunofixation: specific heavy chain + light chain) : IgG MGUS (Monoclonal Gammopathy of Undetermined Significance): monoclonal IgG <30 g/L + bone marrow plasma cells 30 g/L + plasma cells ≥10 % + organ involvement (CRAB) → IMWG 2014 criteria → Kyle 2003 - NEJM: series of 1,027 myelomas → IgG = most frequent subtype (52 %) → see multiple myeloma fact sheet + Waldenström macroglobulinemia: monoclonal IgM (not IgG) + lympho-plasmocytes → hyperviscosity syndrome → different from IgG myeloma + algorithm in front of an IgG monoclonal peak: EPS → suspicious peak → immunofixation → confirms monoclonal IgG kappa or lambda → determination of total IgG + free light chains (FLC - Free Light Chain kappa/lambda) → CBC + renal workup + calcemia + skeletal X-rays + if CRAB → myelogram → if no CRAB + IgG <30 g/L + plasma cells <10 % → MGUS → annual monitoring (CBC + protidemia + FLC) | Stone 2012 — NEJM : IgG4-Related Disease → diagnostic criteria + IgG >1.35 g/L + biopsy + corticosteroid therapy + Kyle 2002 — NEJM : MGUS → progression → 1 %/year → risk factors + monitoring → Rajkumar 2014 — NEJM : IMWG 2014 myeloma criteria → CRAB + malignancy biomarker criteria + Kyle 2003 — NEJM : 1,027 myelomas + 52 % IgG + survival + prognostic factors + Dispenzieri 2021 — Mayo Clinic Proceedings : MGUS → follow-up + progression + Cunningham-Rundles 2007 — JACI : DICV + low IgG + autoimmune diseases → context + Amati 2020 — Clinical Immunology : hypergammaglobulinemia in autoimmune and infectious diseases → mechanisms + interpretation + IMWG 2014 (International Myeloma Working Group) + IMWG 2022 : myeloma diagnostic criteria + MGUS → absolute reference + Leung 2020 — American Journal of Medicine : spectrum of polyclonal hypergammaglobulinemias + diagnostic approach |
| DICV — complications and long-term follow-up Lymphomas — autoimmune diseases — granulomas — bronchiectasis — enteropathy — quality of life — monitoring — DICV biotherapies — rituximab complications |
Long-term complications of CVID - multidisciplinary monitoring essential: chronic lung infections and bronchiectasis : consequence of unprevented recurrent infections → high-resolution chest CT (HRCT) at baseline + every 5 years → spirometry + respiratory function monitoring + early treatment of infections + intensification of trough level if bronchiectasis + Cunningham-Rundles 2007 - JACI: bronchiectasis in 33-50 % of CVID → major prognostic factor + gastrointestinal diseases: Giardia lamblia (treatment: metronidazole 250 mg × 3/d × 5-7 days) + inflammatory-like colonopathy (30 % of CVIDs) + celiac-like villous atrophy (often HLA-DQ2/DQ8 negative + anti-tTG negative) + lymphangiectasia → duodenal biopsy + colonoscopy if persistent digestive symptoms → pulmonary + hepatic + splenic granulomas: 10-20 % of CVID → similar to sarcoidosis histologically → no infectious cause + no link with Ig → treatment: corticoids + methotrexate + sirolimus depending on severity + autoimmune diseases: ITP (immune thrombocytopenia) + autoimmune hemolytic anemia + polyarthritis + lupus-like + thyroiditis → frequency 20-30 % → treatment: corticoids + rituximab cautious (worsens hypogammaglobulinemia) + Cunningham-Rundles 2012 - Clinical Immunology: autoimmunity + CVID + lymphomas: risk × 5-10 vs general population → diffuse large B-cell lymphoma + MALT lymphoma + Hodgkin lymphoma → annual surveillance (CBC + LDH + β2M + CT scan if abnormalities) + nodular lymphoid hyperplasia (NLH): increased non-commutative B lymphocytes + lymphoid nodules in the gastrointestinal tract → benign but distinguish from lymphoma + biopsies + endoscopic follow-up + biological follow-up of CVID: total IgG before each infusion (trough level) → target >6-8 g/L → adjust dose → CBC + lymphophenotyping every 1-2 years + liver workup → chest CT scan every 5 years → colonoscopy if digestive symptoms + INESSS: Quebec IVIG/SCIG program + biotherapies in CVID: rituximab (autoimmune diseases in CVID): use with extreme caution → massively worsens hypogammaglobulinemia → if necessary → increase IVIG + monitor IgG monthly → sirolimus (mTOR inhibitor): granulomas + refractory HNL → Cols 2019 - NEJM EVIDENCE: sirolimus in CVID + granulomas → promising data + abatacept (CTLA-4-Ig): modulator of T costimulation → trial in CVID + autoimmune diseases → under evaluation; CVID + vaccination: inactivated vaccines (influenza + pneumococcal + COVID-19): limited benefit if almost no vaccine response → but recommended as some patients still produce specific antibodies + live attenuated vaccines (MMR + varicella + BCG): CONTRAINDICATED if IgG <4 g/L + if B lymphocytes almost absent → risk of infection by live vaccine → inform patient + unvaccinated entourage → herd immunity | Cunningham-Rundles 2007 — JACI: Common variable immunodeficiency (CVID) → infections + autoimmunity + granulomas + lymphomas → reference review + Cunningham-Rundles 2012 — Clinical Immunology: autoimmunity in CVID → mechanisms + treatment → cautious rituximab + Bonilla 2015 — JACI: IVIG replacement in primary deficiencies → trough level + targets + Cols 2019 — NEJM EVIDENCE: sirolimus in CVID + granulomas → early clinical trial data → Picard 2018 — JACI: IUIS classification 2017 → CVID + mutations + biotherapies + Aghamohammadi 2012 — JCI: IgG subclass deficiency + infections + INESSS 2020: Quebec guide IVIG → indications + monitoring + doses → regulatory and medical reference in Quebec + ESID 2023 guidelines CVID + Immunodeficiency Canada: resources for patients + physicians + Garber 2020 — Journal of Clinical Immunology: long-term CVID complications → USIDNET North American cohort results |
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An unexpectedly low IgG in an adult with recurrent infections should suggest CVID — the diagnosis is often delayed by 5 to 7 years: Common variable immunodeficiency is the most frequent form of symptomatic primary immunodeficiency. Its diagnosis is based on low IgG levels<6 g/L), low IgA and/or IgM, and insufficient vaccine response, after exclusion of secondary causes. Treatment with replacement IVIG or SCIG normalizes IgG levels and prevents serious infections and bronchiectasis. Failure to diagnose CVID is a major missed opportunity for the patient.
Situations requiring urgent or specialized consultation
Boy (under 2 years old) with recurrent severe bacterial infections (pneumonia + sepsis + meningitis) since 6–9 months old, absence of B lymphocytes on lymphophenotyping, and near-zero IgG, IgA, and IgM. → X-linked agammaglobulinemia (Bruton's disease) → Pediatric immunology emergency → BTK sequencing + immediate replacement IVIG → Pediatric immunologist consultation + center of excellence for immunodeficiencies.
Patient with IgG 2/year) + chronic sinusitis + no secondary cause found → Probable DICV → immunologist consultation → complete workup (IgG subclasses + lymphophenotyping + vaccine response + ESP + IFX) → if DICV confirmed → IVIG replacement therapy → RAMQ file for reimbursement (INESSS).
Total IgG >25 g/L + EPS showing a narrow monoclonal peak + hypercalcemia + renal failure + normochromic normocytic anemia → probable IgG myeloma (CRAB criteria) → hematologic-oncologic emergencies → immunofixation + serum free light chains + CBC + creatinine + calcium + β2M + bone marrow aspirate → immediate treatment.
Patient on rituximab for autoimmune rheumatism for 2 years + progressively low IgG (from 10 g/L → 5 g/L → 3 g/L) + S. pneumoniae pneumonia → secondary hypogammaglobulinemia due to rituximab + severe infection → medical emergencies + discussion with rheumatologist to stop or space out rituximab → substitute IVIG if INESSS criteria met + consult immunologist.
Consult at Clinique Omicron
Clinique Omicron physicians prescribe and interpret total IgG and subclass dosages in appropriate contexts (recurrent infections, immunological assessment, monitoring of biotherapies), screen for primary immunodeficiencies, refer to immunologists for specialized assessments and initiation of IVIG/SCIG, and collaborate with hemato-oncologists for monoclonal hypergammaglobulinemia. Consultations are available at several service points in Quebec and via telemedicine. To make an appointment, visit cliniqueomicron.ca.
The content of this page is for informational purposes only and does not substitute for the advice of a physician or immunologist. An IgG deficiency with recurrent infections requires specialist evaluation and should not be treated empirically without a complete assessment.
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